Presenilin modulates EGFR signaling and cell transformation by regulating the ubiquitin ligase Fbw7

The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-d...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Oncogene Jg. 29; H. 20; S. 2950 - 2961
Hauptverfasser: Rocher-Ros, V, Marco, S, Mao, J-H, Gines, S, Metzger, D, Chambon, P, Balmain, A, Saura, C A
Format: Journal Article
Sprache:Englisch
Veröffentlicht: London Nature Publishing Group UK 20.05.2010
Nature Publishing Group
Nature Publishing Group [1987-....]
Schlagworte:
631/208/200
631/80/86
692/420/755
Animals
Apoptosis
Biochemistry, Molecular Biology
Biological and medical sciences
Blotting, Western
Carcinogenesis
Catalysis
Cell Biology
Cell physiology
Cell Proliferation
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Cell Transformation, Neoplastic
Cells, Cultured
Cellular signal transduction
Embryo, Mammalian - cytology
Embryo, Mammalian - metabolism
Epidermal growth factor
Epidermal growth factor receptors
Epidermis
F-Box Proteins - metabolism
F-Box-WD Repeat-Containing Protein 7
Fibroblasts - cytology
Fibroblasts - metabolism
Fluorescent Antibody Technique
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
Genetic aspects
Genetic regulation
Genetics
Growth factor receptors
Human Genetics
Hyperplasia
Immunoenzyme Techniques
Integrases - metabolism
Internal Medicine
Intracellular signalling
Keratinocytes
Keratinocytes - cytology
Keratinocytes - metabolism
Life Sciences
Ligases
Medicine
Medicine & Public Health
Mice
Mice, Knockout
Molecular and cellular biology
Molecular biology
Molecular modelling
Notch1 protein
Oncology
original-article
Physiological aspects
Presenilin
Presenilins - physiology
Proteasomes
Receptor, Epidermal Growth Factor - metabolism
Secretase
Signal transduction
Signal Transduction - physiology
Transcription
Ubiquitin
Ubiquitin - metabolism
Ubiquitin-protein ligase
Ubiquitin-Protein Ligases - metabolism
Ubiquitination
France
Spain
carcinogenesis
γ-secretase
Fbw7
Notch
epidermis
Carbon-nitrogen ligases
Enzyme
Ligases
Presenilin
Epidermis
Carcinogenesis
Ubiquitin-protein ligase
Cell signaling
ISSN:0950-9232, 1476-5594, 1476-5594
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Abstract The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of γ-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves γ-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7α, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo , we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7.
AbstractList The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of gamma-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves gamma-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7alpha, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo, we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7.
The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of gamma-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves gamma-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7alpha, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo, we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7. [PUBLICATION ABSTRACT]
The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of γ-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves γ-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7α, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo , we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7.
The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of γ-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves γ-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7α, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo, we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7.
The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of g-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves g-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7a, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo, we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7.
The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of gamma-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves gamma-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7alpha, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo, we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7.The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of gamma-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves gamma-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7alpha, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo, we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7.
The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The molecular mechanisms regulating the crosstalk between EGFR and Notch during epidermal transformation are largely unknown. We found enhanced EGFR-dependent signaling, proliferation and oncogenic transformation caused by loss of presenilins (PS), the catalytic components of γ-secretase that generates the Notch1 intracellular domain (NICD). The underlying mechanism for abnormal EGFR signaling in PS-deficient cells involves γ-secretase-independent transcriptional upregulation of the E3 ubiquitin ligase Fbw7. Fbw7α, which targets NICD for degradation, regulates positively EGFR by affecting a proteasome-dependent ubiquitination step essential for constitutive degradation and stability of EGFR. To investigate the pathological relevance of this findings in vivo, we generated a novel epidermal conditional PS-deficient (ePS cDKO) mouse by deleting both PS in keratinocytes of the basal layer of the epidermis. The ePS cDKO mice develop epidermal hyperplasia associated with enhanced expression of both EGFR and Fbw7 and reduced NICD levels in keratinocytes. These findings establish a novel role for PS on epidermal growth and transformation by reciprocally regulating the EGFR and Notch signaling pathways through Fbw7. Oncogene (2010) 29, 2950-2961; doi: 10.1038/onc.2010.57; published online 8 March 2010 Keywords: carcinogenesis; epidermis; Fbw7; Notch; γ-secretase
Audience Academic
Author Marco, S
Metzger, D
Chambon, P
Balmain, A
Saura, C A
Rocher-Ros, V
Mao, J-H
Gines, S
AuthorAffiliation 4 Department of Functional Genomics, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Inserm U964, CNRS, Collège de France, Illkirch; Université de Strasbourg, Strasbourg, France
1 Institut de Neurociències, Department de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat Autònoma de Barcelona, Barcelona, Spain
3 Department de Biologia Cellular, Inmunologia i Neurociències, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat de Barcelona, Barcelona, Spain
2 Cancer Research Institute, University of California at San Francisco, San Francisco, CA, USA
AuthorAffiliation_xml – name: 1 Institut de Neurociències, Department de Bioquímica i Biologia Molecular, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat Autònoma de Barcelona, Barcelona, Spain
– name: 2 Cancer Research Institute, University of California at San Francisco, San Francisco, CA, USA
– name: 3 Department de Biologia Cellular, Inmunologia i Neurociències, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat de Barcelona, Barcelona, Spain
– name: 4 Department of Functional Genomics, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Inserm U964, CNRS, Collège de France, Illkirch; Université de Strasbourg, Strasbourg, France
Author_xml – sequence: 1
  givenname: V
  surname: Rocher-Ros
  fullname: Rocher-Ros, V
  organization: Department de Bioquímica i Biologia Molecular, Institut de Neurociències, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat Autònoma de Barcelona
– sequence: 2
  givenname: S
  surname: Marco
  fullname: Marco, S
  organization: Department de Bioquímica i Biologia Molecular, Institut de Neurociències, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat Autònoma de Barcelona
– sequence: 3
  givenname: J-H
  surname: Mao
  fullname: Mao, J-H
  organization: Cancer Research Institute, University of California at San Francisco
– sequence: 4
  givenname: S
  surname: Gines
  fullname: Gines, S
  organization: Department de Biologia Cellular, Inmunologia i Neurociències, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat de Barcelona
– sequence: 5
  givenname: D
  surname: Metzger
  fullname: Metzger, D
  organization: Department of Functional Genomics, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Inserm U964, CNRS, Collège de France, Illkirch; Université de Strasbourg
– sequence: 6
  givenname: P
  surname: Chambon
  fullname: Chambon, P
  organization: Department of Functional Genomics, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Inserm U964, CNRS, Collège de France, Illkirch; Université de Strasbourg
– sequence: 7
  givenname: A
  surname: Balmain
  fullname: Balmain, A
  organization: Cancer Research Institute, University of California at San Francisco
– sequence: 8
  givenname: C A
  surname: Saura
  fullname: Saura, C A
  email: carlos.saura@uab.es
  organization: Department de Bioquímica i Biologia Molecular, Institut de Neurociències, Centro de Investigación Biomédica en Red Enfermedades Neurodegenerativas, Universitat Autònoma de Barcelona
BackLink http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=22838445$$DView record in Pascal Francis
https://www.ncbi.nlm.nih.gov/pubmed/20208556$$D View this record in MEDLINE/PubMed
https://hal.science/hal-04087161$$DView record in HAL
BookMark eNqFkttrFDEUxoNU7EWffJfBIiK6a-6ZeRGW0m2FBUX0OWQymdmUmaRNZir9703ctZelRfIQcvL7zjk5-Q7BnvPOAPAawTmCpPzsnZ5jmE5MPAMHiAo-Y6yie-AAVgzOKkzwPjiM8QJCKCqIX4B9DDEsGeMHQH8PJhpne-uKwTdTr0YTi9Oz5Y8i2s6pFO8K5ZpCm74vxqBcbH0Y1Gi9K-qbIpguazI1rk0x1fZqsulY9LZT0RTL-rd4CZ63qo_m1XY_Ar-Wpz9Pzmerb2dfTxarmeaEjTNueKWERqysNWSGMSZwbSituYINM1rAuqECGdU0uK2g1hQJVCKiMVMtJogcgS-bvJdTPZhGG5f67eVlsIMKN9IrKx_eOLuWnb-WFHFMYZkSfNgkWO_IzhcrmWMwUQJxdJ2Lvd8WC_5qMnGUg415SMoZP0UpKOWIcQz_TxJCKBWYJfLtDnnhp5A-IUqCMOakIhk6fgrCnCIKCeP3qE71RlrX-vRinQvLBcYiEWWZW5s_QqXVmMHqZLPWpvgDwZv7I74d0j9DJeDdFlBRq75NhtE23nG4JCWlub-PG04HH2Mw7S2CoMy2lsnWMttaMpFotENrO_71YOrX9k9oPm00MWV2nQl3c3oM_wOk2AYb
CODEN ONCNES
CitedBy_id crossref_primary_10_3390_md20100596
crossref_primary_10_1016_j_pharmthera_2014_11_005
crossref_primary_10_1038_s41419_022_05229_2
crossref_primary_10_1371_journal_ppat_1008541
crossref_primary_10_3389_fnins_2020_586108
crossref_primary_10_1007_s00432_011_1128_4
crossref_primary_10_1371_journal_pone_0183500
crossref_primary_10_3892_ijo_2015_2983
crossref_primary_10_1016_j_febslet_2012_03_017
crossref_primary_10_1038_embor_2011_231
crossref_primary_10_1158_0008_5472_CAN_16_2456
crossref_primary_10_1016_j_semcancer_2015_09_005
crossref_primary_10_1038_cddis_2016_123
crossref_primary_10_1038_onc_2014_128
crossref_primary_10_1186_s12943_018_0857_2
crossref_primary_10_1016_j_cellsig_2015_10_006
crossref_primary_10_1038_s41388_019_0746_1
crossref_primary_10_1371_journal_pone_0079249
crossref_primary_10_1002_bies_201100101
crossref_primary_10_1097_MD_0000000000002496
crossref_primary_10_4161_cc_26591
crossref_primary_10_1007_s10555_011_9330_z
crossref_primary_10_1016_j_semcancer_2015_09_006
crossref_primary_10_1158_0008_5472_CAN_16_2246
crossref_primary_10_1002_cnr2_1369
crossref_primary_10_1038_srep21207
crossref_primary_10_1042_BST20170002
crossref_primary_10_1096_fj_15_270645
Cites_doi 10.1073/pnas.191284198
10.1128/MCB.21.21.7403-7415.2001
10.1158/0008-5472.CAN-06-0793
10.1038/nature03155
10.1046/j.1471-4159.2002.01105.x
10.1074/jbc.C300096200
10.1016/j.molcel.2006.02.018
10.1186/1747-1028-2-7
10.1016/S0167-4781(03)00156-8
10.1038/ncb1750
10.1038/19083
10.1083/jcb.200802076
10.1073/pnas.0706057105
10.1093/nar/27.22.4324
10.1200/JCO.2005.04.8306
10.1074/jbc.M301326200
10.1074/jbc.M703649200
10.1038/nature01234
10.1093/hmg/ddh151
10.1016/j.devcel.2004.09.014
10.1073/pnas.96.15.8551
10.1158/0008-5472.CAN-05-1294
10.1073/pnas.0703903104
10.1038/35036595
10.1016/j.molcel.2009.01.014
10.1074/jbc.M101343200
10.1084/jem.20070876
10.1016/0092-8674(87)90592-7
10.1101/gad.1477606
10.1038/nrc2290
10.1073/pnas.95.26.15787
10.1371/journal.pbio.0060123
10.1016/j.semcancer.2004.04.017
10.1073/pnas.93.4.1683
10.1016/S0896-6273(04)00182-5
10.1083/jcb.152.4.785
10.1038/sj.embor.7400897
10.1016/S0092-8674(00)80244-5
10.1016/S0092-8674(02)00970-4
10.1038/sj.onc.1207567
10.1038/sj.onc.1209397
10.1073/pnas.0707416104
10.1074/jbc.M909624199
10.1038/nm1065
10.1523/JNEUROSCI.5384-05.2006
10.1083/jcb.98.3.1048
10.1073/pnas.0402770101
10.1083/jcb.200106056
10.1242/dev.02767
10.1038/ng1099
10.1074/jbc.M704273200
10.1038/sj.onc.1207390
ContentType Journal Article
Copyright Macmillan Publishers Limited 2010
2015 INIST-CNRS
COPYRIGHT 2010 Nature Publishing Group
Macmillan Publishers Limited 2010.
Copyright Nature Publishing Group May 20, 2010
Distributed under a Creative Commons Attribution 4.0 International License
2010 Macmillan Publishers Limited All rights reserved 2010
Copyright_xml – notice: Macmillan Publishers Limited 2010
– notice: 2015 INIST-CNRS
– notice: COPYRIGHT 2010 Nature Publishing Group
– notice: Macmillan Publishers Limited 2010.
– notice: Copyright Nature Publishing Group May 20, 2010
– notice: Distributed under a Creative Commons Attribution 4.0 International License
– notice: 2010 Macmillan Publishers Limited All rights reserved 2010
DBID AAYXX
CITATION
IQODW
CGR
CUY
CVF
ECM
EIF
NPM
3V.
7TM
7TO
7U9
7X7
7XB
88A
88E
8AO
8C1
8FD
8FE
8FH
8FI
8FJ
8FK
8G5
ABUWG
AFKRA
AZQEC
BBNVY
BENPR
BHPHI
CCPQU
DWQXO
FR3
FYUFA
GHDGH
GNUQQ
GUQSH
H94
HCIFZ
K9.
LK8
M0S
M1P
M2O
M7P
MBDVC
P64
PHGZM
PHGZT
PJZUB
PKEHL
PPXIY
PQEST
PQGLB
PQQKQ
PQUKI
PRINS
Q9U
RC3
7X8
1XC
5PM
DOI 10.1038/onc.2010.57
DatabaseName CrossRef
Pascal-Francis
Medline
MEDLINE
MEDLINE (Ovid)
MEDLINE
MEDLINE
PubMed
ProQuest Central (Corporate)
Nucleic Acids Abstracts
Oncogenes and Growth Factors Abstracts
Virology and AIDS Abstracts
Health & Medical Collection (ProQuest)
ProQuest Central (purchase pre-March 2016)
Biology Database (Alumni Edition)
Medical Database (Alumni Edition)
ProQuest Pharma Collection
Public Health Database (ProQuest)
Technology Research Database
ProQuest SciTech Collection
ProQuest Natural Science Collection
Hospital Premium Collection
Hospital Premium Collection (Alumni Edition)
ProQuest Central (Alumni) (purchase pre-March 2016)
Research Library (Alumni)
ProQuest Central (Alumni)
ProQuest Central UK/Ireland
ProQuest Central Essentials
Biological Science Collection
ProQuest Central
Natural Science Collection
ProQuest One Community College
ProQuest Central Korea
Engineering Research Database
Proquest Health Research Premium Collection
Health Research Premium Collection (Alumni)
ProQuest Central Student
Research Library Prep
AIDS and Cancer Research Abstracts
SciTech Premium Collection
ProQuest Health & Medical Complete (Alumni)
ProQuest Biological Science Collection
ProQuest Health & Medical Collection
Medical Database
Research Library (ProQuest)
Biological Science Database
Research Library (Corporate)
Biotechnology and BioEngineering Abstracts
ProQuest Central Premium
ProQuest One Academic (New)
ProQuest Health & Medical Research Collection
ProQuest One Academic Middle East (New)
ProQuest One Health & Nursing
ProQuest One Academic Eastern Edition (DO NOT USE)
ProQuest One Applied & Life Sciences
ProQuest One Academic (retired)
ProQuest One Academic UKI Edition
ProQuest Central China
ProQuest Central Basic
Genetics Abstracts
MEDLINE - Academic
Hyper Article en Ligne (HAL)
PubMed Central (Full Participant titles)
DatabaseTitle CrossRef
MEDLINE
Medline Complete
MEDLINE with Full Text
PubMed
MEDLINE (Ovid)
Research Library Prep
ProQuest Central Student
Oncogenes and Growth Factors Abstracts
ProQuest Central Essentials
Nucleic Acids Abstracts
SciTech Premium Collection
ProQuest Central China
ProQuest One Applied & Life Sciences
Health Research Premium Collection
Natural Science Collection
Health & Medical Research Collection
Biological Science Collection
ProQuest Central (New)
ProQuest Medical Library (Alumni)
Virology and AIDS Abstracts
ProQuest Biological Science Collection
ProQuest One Academic Eastern Edition
ProQuest Hospital Collection
Health Research Premium Collection (Alumni)
Biological Science Database
ProQuest Hospital Collection (Alumni)
Biotechnology and BioEngineering Abstracts
ProQuest Health & Medical Complete
ProQuest One Academic UKI Edition
Engineering Research Database
ProQuest One Academic
ProQuest One Academic (New)
Technology Research Database
ProQuest One Academic Middle East (New)
ProQuest Health & Medical Complete (Alumni)
ProQuest Central (Alumni Edition)
ProQuest One Community College
ProQuest One Health & Nursing
Research Library (Alumni Edition)
ProQuest Natural Science Collection
ProQuest Pharma Collection
ProQuest Biology Journals (Alumni Edition)
ProQuest Central
ProQuest Health & Medical Research Collection
Genetics Abstracts
Health and Medicine Complete (Alumni Edition)
ProQuest Central Korea
AIDS and Cancer Research Abstracts
ProQuest Research Library
ProQuest Public Health
ProQuest Central Basic
ProQuest SciTech Collection
ProQuest Medical Library
ProQuest Central (Alumni)
MEDLINE - Academic
DatabaseTitleList
Research Library Prep


AIDS and Cancer Research Abstracts
MEDLINE - Academic


MEDLINE
Research Library Prep
Database_xml – sequence: 1
  dbid: NPM
  name: PubMed
  url: http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed
  sourceTypes: Index Database
– sequence: 2
  dbid: BENPR
  name: ProQuest Central
  url: https://www.proquest.com/central
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
Chemistry
Biology
EISSN 1476-5594
EndPage 2961
ExternalDocumentID PMC4162408
oai:HAL:hal-04087161v1
2039237161
A227653880
20208556
22838445
10_1038_onc_2010_57
Genre Research Support, Non-U.S. Gov't
Journal Article
GeographicLocations France
Spain
GeographicLocations_xml – name: Spain
– name: France
GrantInformation_xml – fundername: NCI NIH HHS
  grantid: R01 CA116481
GroupedDBID ---
-Q-
0R~
123
29N
2WC
36B
39C
3O-
3V.
4.4
406
53G
5RE
70F
7X7
88A
88E
8AO
8C1
8FE
8FH
8FI
8FJ
8G5
8R4
8R5
AANZL
AAYZH
AAZLF
ABAKF
ABAWZ
ABDBF
ABJNI
ABLJU
ABUWG
ABZZP
ACAOD
ACGFO
ACGFS
ACKTT
ACMJI
ACPRK
ACRQY
ACUHS
ACZOJ
ADBBV
ADFRT
ADHDB
AEJRE
AEMSY
AENEX
AEVLU
AEXYK
AFBBN
AFKRA
AFSHS
AGHAI
AGQEE
AHMBA
AHSBF
AILAN
AJRNO
ALFFA
ALIPV
ALMA_UNASSIGNED_HOLDINGS
AMYLF
ASPBG
AVWKF
AXYYD
AZFZN
AZQEC
B0M
BBNVY
BENPR
BHPHI
BKKNO
BPHCQ
BVXVI
CAG
CCPQU
COF
CS3
DIK
DNIVK
DPUIP
DU5
DWQXO
E3Z
EAD
EAP
EBC
EBD
EBLON
EBS
EE.
EIOEI
EJD
EMB
EMK
EMOBN
EPL
ESX
F5P
FDQFY
FEDTE
FERAY
FIZPM
FRP
FSGXE
FYUFA
GNUQQ
GUQSH
HCIFZ
HMCUK
HVGLF
HZ~
IAO
IHR
INH
INR
ITC
IWAJR
JSO
JZLTJ
KQ8
L7B
LK8
M0L
M1P
M2O
M7P
N9A
NAO
NQJWS
NXXTH
O9-
OK1
OVD
P2P
PQQKQ
PROAC
PSQYO
Q2X
RNT
RNTTT
ROL
SNX
SNYQT
SOHCF
SOJ
SRMVM
SV3
SWTZT
TAOOD
TBHMF
TDRGL
TEORI
TSG
TUS
UKHRP
W2D
WH7
~8M
AASML
AATNV
AAYXX
ABBRH
ABDBE
ABFSG
ABRTQ
ACSTC
AEFQL
AEZWR
AFDZB
AFFHD
AFHIU
AHWEU
AIGIU
AIXLP
ATHPR
AYFIA
CITATION
PHGZM
PHGZT
PJZUB
PPXIY
PQGLB
.55
.GJ
AACDK
ABEFU
AFFNX
BAWUL
FIGPU
IQODW
LGEZI
LOTEE
NADUK
RNS
TR2
UDS
X7M
ZXP
CGR
CUY
CVF
ECM
EIF
NPM
7TM
7TO
7U9
7XB
8FD
8FK
FR3
H94
K9.
MBDVC
P64
PKEHL
PQEST
PQUKI
PRINS
Q9U
RC3
7X8
1XC
5PM
ID FETCH-LOGICAL-c635t-6e69a7c158bc05e55572be44b6a0d5ec70bd471eadd2f90cc4171813c25af2313
IEDL.DBID M7P
ISICitedReferencesCount 35
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000277890400006&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 0950-9232
1476-5594
IngestDate Tue Nov 04 01:55:39 EST 2025
Tue Oct 14 20:44:46 EDT 2025
Sun Nov 09 14:05:24 EST 2025
Sun Nov 09 13:49:02 EST 2025
Mon Oct 06 18:11:14 EDT 2025
Tue Oct 07 05:27:53 EDT 2025
Sat Nov 29 13:25:06 EST 2025
Sat Nov 29 09:57:59 EST 2025
Mon Jul 21 06:04:07 EDT 2025
Mon Jul 21 09:17:59 EDT 2025
Sat Nov 29 03:40:49 EST 2025
Tue Nov 18 22:16:33 EST 2025
Fri Feb 21 02:39:38 EST 2025
IsDoiOpenAccess false
IsOpenAccess true
IsPeerReviewed true
IsScholarly true
Issue 20
Keywords carcinogenesis
γ-secretase
Fbw7
Notch
epidermis
Carbon-nitrogen ligases
Enzyme
Ligases
Presenilin
Epidermis
Carcinogenesis
Ubiquitin-protein ligase
Cell signaling
Language English
License CC BY 4.0
Distributed under a Creative Commons Attribution 4.0 International License: http://creativecommons.org/licenses/by/4.0
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c635t-6e69a7c158bc05e55572be44b6a0d5ec70bd471eadd2f90cc4171813c25af2313
Notes ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ORCID 0000-0002-5555-046X
OpenAccessLink http://doi.org/10.1038/onc.2010.57
PMID 20208556
PQID 2641403565
PQPubID 36330
PageCount 12
ParticipantIDs pubmedcentral_primary_oai_pubmedcentral_nih_gov_4162408
hal_primary_oai_HAL_hal_04087161v1
proquest_miscellaneous_744615620
proquest_miscellaneous_733344725
proquest_journals_312263935
proquest_journals_2641403565
gale_infotracmisc_A227653880
gale_infotracacademiconefile_A227653880
pubmed_primary_20208556
pascalfrancis_primary_22838445
crossref_primary_10_1038_onc_2010_57
crossref_citationtrail_10_1038_onc_2010_57
springer_journals_10_1038_onc_2010_57
PublicationCentury 2000
PublicationDate 20100520
PublicationDateYYYYMMDD 2010-05-20
PublicationDate_xml – month: 5
  year: 2010
  text: 20100520
  day: 20
PublicationDecade 2010
PublicationPlace London
PublicationPlace_xml – name: London
– name: Basingstoke
– name: England
– name: New York
PublicationTitle Oncogene
PublicationTitleAbbrev Oncogene
PublicationTitleAlternate Oncogene
PublicationYear 2010
Publisher Nature Publishing Group UK
Nature Publishing Group
Nature Publishing Group [1987-....]
Publisher_xml – name: Nature Publishing Group UK
– name: Nature Publishing Group
– name: Nature Publishing Group [1987-....]
References Jost, Kari, Rodeck (CR16) 2000; 10
Kalyankrishna, Grandis (CR17) 2006; 24
Welcker, Clurman (CR48) 2007; 2
Rikiyama, Curtis, Oikawa, Zimonjic, Popescu, Murphy (CR37) 2003; 1629
Blanpain, Lowry, Pasolli, Fuchs (CR3) 2006; 20
Huang, Goh, Sorkin (CR13) 2007; 104
Gupta-Rossi, Le Bail, Gonen, Brou, Logeat, Six (CR12) 2001; 276
Kopan, Schroeter, Weintraub, Nye (CR21) 1996; 93
Mosesson, Shtiegman, Katz, Zwang, Vereb, Szollosi (CR29) 2003; 278
Nicolas, Wolfer, Raj, Kummer, Mill, van Noort (CR30) 2003; 33
De Strooper (CR6) 2007; 8
Kang, Soriano, Xia, Eberhart, De Strooper, Zheng (CR18) 2002; 110
Longva, Blystad, Stang, Larsen, Johannessen, Madshus (CR26) 2002; 156
Alwan, van Zoelen, van Leeuwen (CR1) 2003; 278
Saura, Choi, Beglopoulos, Malkani, Zhang, Shankaranarayana Rao (CR38) 2004; 42
Li, Indra, Warot, Brocard, Messaddeq, Kato (CR24) 2000; 407
Saura, Tomita, Soriano, Takahashi, Leem, Honda (CR39) 2000; 275
Welcker, Orian, Jin, Grim, Harper, Eisenman (CR50) 2004; 101
Soriano, Kang, Fu, Pestell, Chevallier, Zheng (CR42) 2001; 152
Wu, Hubbard, Kitajewski, Greenwald (CR51) 1998; 95
Li, Wen, Brayton, Das, Smithson, Fauq (CR25) 2007; 282
Bhoumik, Fichtman, DeRossi, Breitwieser, Kluger, Davis (CR2) 2008; 105
Indra, Warot, Brocard, Bornert, Xiao, Chambon (CR15) 1999; 27
Kolev, Mandinova, Guinea-Viniegra, Hu, Lefort, Lambertini (CR19) 2008; 10
Shen, Bronson, Chen, Xia, Selkoe, Tonegawa (CR41) 1997; 89
Deng, Tarassishin, Kallhoff, Peethumnongsin, Wu, Li (CR9) 2006; 26
To, Gokgoz, Doyle, Donoviel, Knight, Hyslop (CR44) 2006; 25
Vasioukhin, Degenstein, Wise, Fuchs (CR46) 1999; 96
de Souza, Vallier, Fares, Greenwald (CR5) 2007; 134
Zhang, Wang, Liu, Zhang, Liao, Xu (CR54) 2007; 104
Stoscheck, Carpenter (CR43) 1984; 98
Koo, Kopan (CR20) 2004; 10
Shaye, Greenwald (CR40) 2002; 420
Chen, Sun (CR4) 2009; 33
Pirrone, Hager, Fleckman (CR34) 2005; 289
Grim, Gustafson, Hirata, Hagar, Swanger, Welcker (CR11) 2008; 181
Pan, Lin, Tian, Cheng, Gridley, Shen (CR32) 2004; 7
Welcker, Clurman (CR49) 2008; 8
Mao, Perez-Losada, Wu, Delrosario, Tsunematsu, Nakayama (CR27) 2004; 432
Wu, Lyapina, Das, Li, Gurney, Pauley (CR52) 2001; 21
O'Neil, Grim, Strack, Rao, Tibbitts, Winter (CR31) 2007; 204
Marmor, Yarden (CR28) 2004; 23
Repetto, Yoon, Zheng, Zhang (CR36) 2007; 282
Xia, Qian, Soriano, Wu, Fletcher, Wang (CR53) 2001; 98
Di Fiore, Pierce, Fleming, Hazan, Ullrich, King (CR10) 1987; 51
Proweller, Tu, Lepore, Cheng, Lu, Seykora (CR35) 2006; 66
Demehri, Liu, Lee, Lin, Crosby, Roberts (CR8) 2008; 6
Lefort, Dotto (CR22) 2004; 14
Huang, Kirkpatrick, Jiang, Gygi, Sorkin (CR14) 2006; 21
Perez-Losada, Mao, Balmain (CR33) 2005; 65
Tournoy, Bossuyt, Snellinx, Regent, Garmyn, Serneels (CR45) 2004; 13
Wang, Gamsby, Highfill, Mora, Bloom, Yeatman (CR47) 2004; 23
De Strooper, Annaert, Cupers, Saftig, Craessaerts, Mumm (CR7) 1999; 398
Li, Pauley, Myers, Shuang, Brashler, Yan (CR23) 2002; 82
A Pirrone (BFonc201057_CR34) 2005; 289
S Soriano (BFonc201057_CR42) 2001; 152
JW Wang (BFonc201057_CR47) 2004; 23
HA Alwan (BFonc201057_CR1) 2003; 278
K Lefort (BFonc201057_CR22) 2004; 14
B De Strooper (BFonc201057_CR6) 2007; 8
J Li (BFonc201057_CR23) 2002; 82
J Tournoy (BFonc201057_CR45) 2004; 13
J O'Neil (BFonc201057_CR31) 2007; 204
M Welcker (BFonc201057_CR49) 2008; 8
DD Shaye (BFonc201057_CR40) 2002; 420
T Rikiyama (BFonc201057_CR37) 2003; 1629
J Perez-Losada (BFonc201057_CR33) 2005; 65
CA Saura (BFonc201057_CR39) 2000; 275
T Li (BFonc201057_CR25) 2007; 282
PP Di Fiore (BFonc201057_CR10) 1987; 51
KE Longva (BFonc201057_CR26) 2002; 156
DE Kang (BFonc201057_CR18) 2002; 110
Y Pan (BFonc201057_CR32) 2004; 7
F Huang (BFonc201057_CR13) 2007; 104
N de Souza (BFonc201057_CR5) 2007; 134
V Kolev (BFonc201057_CR19) 2008; 10
JH Mao (BFonc201057_CR27) 2004; 432
M Nicolas (BFonc201057_CR30) 2003; 33
CA Saura (BFonc201057_CR38) 2004; 42
X Xia (BFonc201057_CR53) 2001; 98
S Demehri (BFonc201057_CR8) 2008; 6
M Welcker (BFonc201057_CR50) 2004; 101
EH Koo (BFonc201057_CR20) 2004; 10
Y Mosesson (BFonc201057_CR29) 2003; 278
C Blanpain (BFonc201057_CR3) 2006; 20
CM Stoscheck (BFonc201057_CR43) 1984; 98
M Jost (BFonc201057_CR16) 2000; 10
N Gupta-Rossi (BFonc201057_CR12) 2001; 276
MD To (BFonc201057_CR44) 2006; 25
F Huang (BFonc201057_CR14) 2006; 21
M Li (BFonc201057_CR24) 2000; 407
Y Deng (BFonc201057_CR9) 2006; 26
G Wu (BFonc201057_CR51) 1998; 95
MD Marmor (BFonc201057_CR28) 2004; 23
Y-W Zhang (BFonc201057_CR54) 2007; 104
V Vasioukhin (BFonc201057_CR46) 1999; 96
B De Strooper (BFonc201057_CR7) 1999; 398
A Proweller (BFonc201057_CR35) 2006; 66
M Welcker (BFonc201057_CR48) 2007; 2
R Kopan (BFonc201057_CR21) 1996; 93
ZJ Chen (BFonc201057_CR4) 2009; 33
E Repetto (BFonc201057_CR36) 2007; 282
A Bhoumik (BFonc201057_CR2) 2008; 105
G Wu (BFonc201057_CR52) 2001; 21
A Indra (BFonc201057_CR15) 1999; 27
J Shen (BFonc201057_CR41) 1997; 89
J Grim (BFonc201057_CR11) 2008; 181
S Kalyankrishna (BFonc201057_CR17) 2006; 24
11517342 - Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10863-8
11266469 - J Cell Biol. 2001 Feb 19;152(4):785-94
18227516 - Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1674-9
15066262 - Neuron. 2004 Apr 8;42(1):23-36
15288263 - Semin Cancer Biol. 2004 Oct;14(5):374-86
12829707 - J Biol Chem. 2003 Sep 12;278(37):35781-90
16597739 - J Neurosci. 2006 Apr 5;26(14):3845-54
15150404 - Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):9085-90
10411913 - Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8551-6
18507503 - PLoS Biol. 2008 May 27;6(5):e123
16474849 - Oncogene. 2006 Jun 15;25(25):3557-64
9861048 - Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15787-91
11864992 - J Cell Biol. 2002 Mar 4;156(5):843-54
11425854 - J Biol Chem. 2001 Sep 14;276(37):34371-8
19217402 - Mol Cell. 2009 Feb 13;33(3):275-86
12297048 - Cell. 2002 Sep 20;110(6):751-62
9160754 - Cell. 1997 May 16;89(4):629-39
10748144 - J Biol Chem. 2000 Jun 2;275(22):17136-42
11585921 - Mol Cell Biol. 2001 Nov;21(21):7403-15
10536138 - Nucleic Acids Res. 1999 Nov 15;27(22):4324-7
15525534 - Dev Cell. 2004 Nov;7(5):731-43
15272268 - Nat Med. 2004 Jul;10 Suppl:S26-33
16885339 - Cancer Res. 2006 Aug 1;66(15):7438-44
17646409 - J Exp Med. 2007 Aug 6;204(8):1813-24
14522076 - Biochim Biophys Acta. 2003 Oct 1;1629(1-3):15-25
12719435 - J Biol Chem. 2003 Jun 13;278(24):21323-6
17716970 - J Biol Chem. 2007 Oct 26;282(43):31504-16
12590261 - Nat Genet. 2003 Mar;33(3):416-21
3500791 - Cell. 1987 Dec 24;51(6):1063-70
17827153 - J Biol Chem. 2007 Nov 2;282(44):32264-73
17298674 - Cell Div. 2007 Feb 13;2:7
11056418 - Eur J Dermatol. 2000 Oct-Nov;10(7):505-10
16543144 - Mol Cell. 2006 Mar 17;21(6):737-48
16763281 - J Clin Oncol. 2006 Jun 10;24(17):2666-72
18604200 - Nat Cell Biol. 2008 Aug;10(8):902-11
17079689 - Genes Dev. 2006 Nov 1;20(21):3022-35
12478297 - Nature. 2002 Dec 12;420(6916):686-90
15064745 - Oncogene. 2004 May 20;23(23):4089-97
17556541 - Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10613-8
16061623 - Cancer Res. 2005 Aug 1;65(15):6488-92
15592418 - Nature. 2004 Dec 9;432(7018):775-9
15128703 - Hum Mol Genet. 2004 Jul 1;13(13):1321-31
10206645 - Nature. 1999 Apr 8;398(6727):518-22
15021893 - Oncogene. 2004 Mar 15;23(11):2057-70
12354302 - J Neurochem. 2002 Sep;82(6):1540-8
18094723 - Nat Rev Cancer. 2008 Feb;8(2):83-93
17215302 - Development. 2007 Feb;134(4):691-702
8643690 - Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1683-8
17940017 - Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):16904-9
18559665 - J Cell Biol. 2008 Jun 16;181(6):913-20
11034212 - Nature. 2000 Oct 5;407(6804):633-6
6321514 - J Cell Biol. 1984 Mar;98(3):1048-53
15502164 - Methods Mol Biol. 2005;289:3-14
17268505 - EMBO Rep. 2007 Feb;8(2):141-6
References_xml – volume: 98
  start-page: 10863
  year: 2001
  end-page: 10868
  ident: CR53
  article-title: Loss of presenilin 1 is associated with enhanced β-catenin signaling and skin tumorigenesis
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.191284198
– volume: 21
  start-page: 7403
  year: 2001
  end-page: 7415
  ident: CR52
  article-title: Sel-10 is an inhibitor of Notch signaling that targets Notch for ubiquitin-mediated protein degradation
  publication-title: Mol Biol Cell
  doi: 10.1128/MCB.21.21.7403-7415.2001
– volume: 66
  start-page: 7438
  year: 2006
  end-page: 7444
  ident: CR35
  article-title: Impaired Notch signaling promotes squamous cell carcinoma formation
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-06-0793
– volume: 432
  start-page: 775
  year: 2004
  end-page: 779
  ident: CR27
  article-title: Fbxw7/Cdc4 is a p53-dependent, haploinsufficient tumour suppressor gene
  publication-title: Nature
  doi: 10.1038/nature03155
– volume: 82
  start-page: 1540
  year: 2002
  end-page: 1548
  ident: CR23
  article-title: SEL-10 interacts with presenilin 1, facilitates its ubiquitination, and alters A-beta peptide production
  publication-title: J Neurochem
  doi: 10.1046/j.1471-4159.2002.01105.x
– volume: 278
  start-page: 21323
  year: 2003
  end-page: 21326
  ident: CR29
  article-title: Endocytosis of receptor tyrosine kinases is driven by monoubiquitylation, not polyubiquitylation
  publication-title: J Biol Chem
  doi: 10.1074/jbc.C300096200
– volume: 21
  start-page: 737
  year: 2006
  end-page: 748
  ident: CR14
  article-title: Differential regulation of EGF receptor internalization and degradation by multiubiquitination within the kinase domain
  publication-title: Mol Cell
  doi: 10.1016/j.molcel.2006.02.018
– volume: 2
  start-page: 7
  year: 2007
  ident: CR48
  article-title: Fbw7/hCDC4 dimerization regulates its substrate interactions
  publication-title: Cell Division
  doi: 10.1186/1747-1028-2-7
– volume: 1629
  start-page: 15
  year: 2003
  end-page: 25
  ident: CR37
  article-title: GCF2: expression and molecular analysis of repression
  publication-title: Biochim Biophys Acta
  doi: 10.1016/S0167-4781(03)00156-8
– volume: 10
  start-page: 902
  year: 2008
  end-page: 911
  ident: CR19
  article-title: EGFR signalling as a negative regulator of Notch1 gene transcription and function in proliferating keratinocytes and cancer
  publication-title: Nat Cell Biol
  doi: 10.1038/ncb1750
– volume: 398
  start-page: 518
  year: 1999
  end-page: 522
  ident: CR7
  article-title: A presenilin-1-dependent γ-secretase-like protease mediates release of Notch intracellular domain
  publication-title: Nature
  doi: 10.1038/19083
– volume: 181
  start-page: 913
  year: 2008
  end-page: 920
  ident: CR11
  article-title: Isoform- and cell cycle-dependent substrate degradation by the Fbw7 ubiquitin ligase
  publication-title: J Cell Biol
  doi: 10.1083/jcb.200802076
– volume: 105
  start-page: 1674
  year: 2008
  end-page: 1679
  ident: CR2
  article-title: Suppressor role of activating transcription factor 2 (ATF2) in skin cancer
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0706057105
– volume: 27
  start-page: 4324
  year: 1999
  end-page: 4327
  ident: CR15
  article-title: Temporally-controlled site-specific mutagenesis in the basal layer of the epidermis: comparison of the recombinase activity of the tamoxifen-inducible Cre-ER and Cre-ER recombinases
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/27.22.4324
– volume: 24
  start-page: 2666
  year: 2006
  end-page: 2672
  ident: CR17
  article-title: Epidermal growth factor receptor biology in head and neck cancer
  publication-title: J Clin Oncol
  doi: 10.1200/JCO.2005.04.8306
– volume: 278
  start-page: 35781
  year: 2003
  end-page: 35790
  ident: CR1
  article-title: Ligand-induced lysosomal epidermal growth factor receptor (EGFR) degradation is preceded by proteasome-dependent EGFR de-ubiquitination
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M301326200
– volume: 282
  start-page: 32264
  year: 2007
  end-page: 32273
  ident: CR25
  article-title: Epidermal growth factor receptor and notch pathways participate in the tumor suppressor function of γ-secretase
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M703649200
– volume: 420
  start-page: 686
  year: 2002
  end-page: 690
  ident: CR40
  article-title: Endocytosis-mediated downregulation of LIN-12/Notch upon Ras activation in
  publication-title: Nature
  doi: 10.1038/nature01234
– volume: 13
  start-page: 1321
  year: 2004
  end-page: 1331
  ident: CR45
  article-title: Partial loss of presenilins causes seborrheic keratosis and autoimmune disease in mice
  publication-title: Hum Mol Genet
  doi: 10.1093/hmg/ddh151
– volume: 7
  start-page: 731
  year: 2004
  end-page: 743
  ident: CR32
  article-title: γ-Secretase functions through Notch signaling to maintain skin appendages but is not required for their patterning or initial morphogenesis
  publication-title: Dev Cell
  doi: 10.1016/j.devcel.2004.09.014
– volume: 96
  start-page: 8551
  year: 1999
  end-page: 8556
  ident: CR46
  article-title: The magical touch: genome targeting in epidermal stem cells induced by tamoxifen application to mouse skin
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.96.15.8551
– volume: 65
  start-page: 6488
  year: 2005
  end-page: 6492
  ident: CR33
  article-title: Control of genomic instability and epithelial tumor development by the p53-Fbxw7/Cdc4 pathway
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-05-1294
– volume: 104
  start-page: 10613
  year: 2007
  end-page: 10618
  ident: CR54
  article-title: Presenilin/γ-secretase-dependent processing of β-amyloid precursor protein regulates EGF receptor expression
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0703903104
– volume: 407
  start-page: 633
  year: 2000
  end-page: 636
  ident: CR24
  article-title: Skin abnormalities generated by temporally controlled RXRalpha mutations in mouse epidermis
  publication-title: Nature
  doi: 10.1038/35036595
– volume: 10
  start-page: 505
  year: 2000
  end-page: 510
  ident: CR16
  article-title: The EGF receptor—an essential regulator of multiple epidermal functions
  publication-title: Eur J Dermatol
– volume: 33
  start-page: 275
  year: 2009
  end-page: 286
  ident: CR4
  article-title: Nonproteolytic functions of ubiquitin in cell signaling
  publication-title: Mol Cell
  doi: 10.1016/j.molcel.2009.01.014
– volume: 276
  start-page: 34371
  year: 2001
  end-page: 34378
  ident: CR12
  article-title: Functional interaction between SEL-10, an F-box protein, and the nuclear form of activated Notch1 receptor
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M101343200
– volume: 204
  start-page: 1813
  year: 2007
  end-page: 1824
  ident: CR31
  article-title: FBW7 mutations in leukemic cells mediate NOTCH pathway activation and resistance to γ-secretase inhibitors
  publication-title: J Exp Med
  doi: 10.1084/jem.20070876
– volume: 51
  start-page: 1063
  year: 1987
  end-page: 1070
  ident: CR10
  article-title: Overexpression of the human EGF receptor confers an EGF-dependent transformed phenotype to NIH 3T3 cells
  publication-title: Cell
  doi: 10.1016/0092-8674(87)90592-7
– volume: 20
  start-page: 3022
  year: 2006
  end-page: 3035
  ident: CR3
  article-title: Canonical notch signaling functions as a commitment switch in the epidermal lineage
  publication-title: Genes Dev
  doi: 10.1101/gad.1477606
– volume: 8
  start-page: 83
  year: 2008
  end-page: 93
  ident: CR49
  article-title: FBW7 ubiquitin ligase: a tumour suppressor at the crossroads of cell division, growth and differentiation
  publication-title: Nat Rev Cancer
  doi: 10.1038/nrc2290
– volume: 95
  start-page: 15787
  year: 1998
  end-page: 15791
  ident: CR51
  article-title: Evidence for functional and physical association between SEL-10, a Cdc4p-related protein, and SEL-12 presenilin
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.95.26.15787
– volume: 6
  start-page: e123
  year: 2008
  ident: CR8
  article-title: Notch-deficient skin induces a lethal systemic B-lymphoproliferative disorder by secreting TSLP, a sentinel for epidermal integrity
  publication-title: PLoS Biol
  doi: 10.1371/journal.pbio.0060123
– volume: 14
  start-page: 374
  year: 2004
  end-page: 386
  ident: CR22
  article-title: Notch signaling in the integrated control of keratinocyte growth/differentiation and tumor suppression
  publication-title: Semin Cancer Biol
  doi: 10.1016/j.semcancer.2004.04.017
– volume: 93
  start-page: 1683
  year: 1996
  end-page: 1688
  ident: CR21
  article-title: Signal transduction by activated mNotch: importance of proteolytic processing and its regulation by the extracellular domain
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.93.4.1683
– volume: 42
  start-page: 23
  year: 2004
  end-page: 36
  ident: CR38
  article-title: Loss of presenilin function causes impairments of memory and synaptic plasticity followed by age-dependent neurodegeneration
  publication-title: Neuron
  doi: 10.1016/S0896-6273(04)00182-5
– volume: 152
  start-page: 785
  year: 2001
  end-page: 794
  ident: CR42
  article-title: Presenilin 1 negatively regulates beta-catenin/T cell factor/lymphoid enhancer factor-1 signaling independently of β-amyloid precursor protein and notch processing
  publication-title: J Cell Biol
  doi: 10.1083/jcb.152.4.785
– volume: 8
  start-page: 141
  year: 2007
  end-page: 146
  ident: CR6
  article-title: Loss-of-function presenilin mutations in Alzheimer disease
  publication-title: EMBO Rep
  doi: 10.1038/sj.embor.7400897
– volume: 89
  start-page: 629
  year: 1997
  end-page: 639
  ident: CR41
  article-title: Skeletal and CNS defects in presenilin-1 deficient mice
  publication-title: Cell
  doi: 10.1016/S0092-8674(00)80244-5
– volume: 110
  start-page: 751
  year: 2002
  end-page: 762
  ident: CR18
  article-title: Presenilin couples the paired phosphorylation of β-catenin independent of axin: implications for β-catenin activation in tumorigenesis
  publication-title: Cell
  doi: 10.1016/S0092-8674(02)00970-4
– volume: 23
  start-page: 4089
  year: 2004
  end-page: 4097
  ident: CR47
  article-title: Deregulated expression of LRBA facilitates cancer cell growth
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1207567
– volume: 25
  start-page: 3557
  year: 2006
  end-page: 3564
  ident: CR44
  article-title: Functional characterization of novel presenilin-2 variants in human breast cancers
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1209397
– volume: 104
  start-page: 16904
  year: 2007
  end-page: 16909
  ident: CR13
  article-title: EGF receptor ubiquitination is not necessary for its internalization
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0707416104
– volume: 275
  start-page: 17136
  year: 2000
  end-page: 17142
  ident: CR39
  article-title: The nonconserved hydrophilic loop domain of presenilin (PS) is not required for PS endoproteolysis or enhanced Aβ42 production mediated by familial early onset Alzheimer/s disease-linked PS variants
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M909624199
– volume: 10
  start-page: S26
  issue: Suppl
  year: 2004
  end-page: S33
  ident: CR20
  article-title: Potential role of presenilin-regulated signaling pathways in sporadic neurodegeneration
  publication-title: Nat Med
  doi: 10.1038/nm1065
– volume: 26
  start-page: 3845
  year: 2006
  end-page: 3854
  ident: CR9
  article-title: Deletion of presenilin 1 hydrophilic loop sequence leads to impaired γ-secretase activity and exacerbated amyloid pathology
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.5384-05.2006
– volume: 289
  start-page: 3
  year: 2005
  end-page: 14
  ident: CR34
  article-title: Primary mouse keratinocyte culture
  publication-title: Methods Mol Biol
– volume: 98
  start-page: 1048
  year: 1984
  end-page: 1053
  ident: CR43
  article-title: Down regulation of epidermal growth factor receptors: direct demonstration of receptor degradation in human fibroblasts
  publication-title: J Cell Biol
  doi: 10.1083/jcb.98.3.1048
– volume: 101
  start-page: 9085
  year: 2004
  end-page: 9090
  ident: CR50
  article-title: The Fbw7 tumor suppressor regulates glycogen synthase kinase 3 phosphorylation-dependent c-Myc protein degradation
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0402770101
– volume: 156
  start-page: 843
  year: 2002
  end-page: 854
  ident: CR26
  article-title: Ubiquitination and proteasomal activity is required for transport of the EGF receptor to inner membranes of multivesicular bodies
  publication-title: J Cell Biol
  doi: 10.1083/jcb.200106056
– volume: 134
  start-page: 691
  year: 2007
  end-page: 702
  ident: CR5
  article-title: SEL-2, the neurobeachin/LRBA homolog, is a negative regulator of lin-12/Notch activity and affects endosomal traffic in polarized epithelial cells
  publication-title: Development
  doi: 10.1242/dev.02767
– volume: 33
  start-page: 416
  year: 2003
  end-page: 421
  ident: CR30
  article-title: Notch1 functions as a tumor suppressor in mouse skin
  publication-title: Nat Genet
  doi: 10.1038/ng1099
– volume: 282
  start-page: 31504
  year: 2007
  end-page: 31516
  ident: CR36
  article-title: Presenilin-1 regulates epidermal growth factor receptor turnover and signaling in the endosomal-lysosomal pathway
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M704273200
– volume: 23
  start-page: 2057
  year: 2004
  end-page: 2070
  ident: CR28
  article-title: Role of protein ubiquitylation in regulating endocytosis of receptor tyrosine kinases
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1207390
– volume: 2
  start-page: 7
  year: 2007
  ident: BFonc201057_CR48
  publication-title: Cell Division
  doi: 10.1186/1747-1028-2-7
– volume: 26
  start-page: 3845
  year: 2006
  ident: BFonc201057_CR9
  publication-title: J Neurosci
  doi: 10.1523/JNEUROSCI.5384-05.2006
– volume: 275
  start-page: 17136
  year: 2000
  ident: BFonc201057_CR39
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M909624199
– volume: 7
  start-page: 731
  year: 2004
  ident: BFonc201057_CR32
  publication-title: Dev Cell
  doi: 10.1016/j.devcel.2004.09.014
– volume: 8
  start-page: 141
  year: 2007
  ident: BFonc201057_CR6
  publication-title: EMBO Rep
  doi: 10.1038/sj.embor.7400897
– volume: 181
  start-page: 913
  year: 2008
  ident: BFonc201057_CR11
  publication-title: J Cell Biol
  doi: 10.1083/jcb.200802076
– volume: 104
  start-page: 16904
  year: 2007
  ident: BFonc201057_CR13
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0707416104
– volume: 432
  start-page: 775
  year: 2004
  ident: BFonc201057_CR27
  publication-title: Nature
  doi: 10.1038/nature03155
– volume: 101
  start-page: 9085
  year: 2004
  ident: BFonc201057_CR50
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0402770101
– volume: 33
  start-page: 275
  year: 2009
  ident: BFonc201057_CR4
  publication-title: Mol Cell
  doi: 10.1016/j.molcel.2009.01.014
– volume: 10
  start-page: S26
  issue: Suppl
  year: 2004
  ident: BFonc201057_CR20
  publication-title: Nat Med
  doi: 10.1038/nm1065
– volume: 23
  start-page: 2057
  year: 2004
  ident: BFonc201057_CR28
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1207390
– volume: 282
  start-page: 31504
  year: 2007
  ident: BFonc201057_CR36
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M704273200
– volume: 21
  start-page: 7403
  year: 2001
  ident: BFonc201057_CR52
  publication-title: Mol Biol Cell
  doi: 10.1128/MCB.21.21.7403-7415.2001
– volume: 276
  start-page: 34371
  year: 2001
  ident: BFonc201057_CR12
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M101343200
– volume: 24
  start-page: 2666
  year: 2006
  ident: BFonc201057_CR17
  publication-title: J Clin Oncol
  doi: 10.1200/JCO.2005.04.8306
– volume: 152
  start-page: 785
  year: 2001
  ident: BFonc201057_CR42
  publication-title: J Cell Biol
  doi: 10.1083/jcb.152.4.785
– volume: 10
  start-page: 505
  year: 2000
  ident: BFonc201057_CR16
  publication-title: Eur J Dermatol
– volume: 33
  start-page: 416
  year: 2003
  ident: BFonc201057_CR30
  publication-title: Nat Genet
  doi: 10.1038/ng1099
– volume: 98
  start-page: 1048
  year: 1984
  ident: BFonc201057_CR43
  publication-title: J Cell Biol
  doi: 10.1083/jcb.98.3.1048
– volume: 20
  start-page: 3022
  year: 2006
  ident: BFonc201057_CR3
  publication-title: Genes Dev
  doi: 10.1101/gad.1477606
– volume: 278
  start-page: 21323
  year: 2003
  ident: BFonc201057_CR29
  publication-title: J Biol Chem
  doi: 10.1074/jbc.C300096200
– volume: 8
  start-page: 83
  year: 2008
  ident: BFonc201057_CR49
  publication-title: Nat Rev Cancer
  doi: 10.1038/nrc2290
– volume: 96
  start-page: 8551
  year: 1999
  ident: BFonc201057_CR46
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.96.15.8551
– volume: 93
  start-page: 1683
  year: 1996
  ident: BFonc201057_CR21
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.93.4.1683
– volume: 14
  start-page: 374
  year: 2004
  ident: BFonc201057_CR22
  publication-title: Semin Cancer Biol
  doi: 10.1016/j.semcancer.2004.04.017
– volume: 134
  start-page: 691
  year: 2007
  ident: BFonc201057_CR5
  publication-title: Development
  doi: 10.1242/dev.02767
– volume: 110
  start-page: 751
  year: 2002
  ident: BFonc201057_CR18
  publication-title: Cell
  doi: 10.1016/S0092-8674(02)00970-4
– volume: 82
  start-page: 1540
  year: 2002
  ident: BFonc201057_CR23
  publication-title: J Neurochem
  doi: 10.1046/j.1471-4159.2002.01105.x
– volume: 156
  start-page: 843
  year: 2002
  ident: BFonc201057_CR26
  publication-title: J Cell Biol
  doi: 10.1083/jcb.200106056
– volume: 98
  start-page: 10863
  year: 2001
  ident: BFonc201057_CR53
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.191284198
– volume: 104
  start-page: 10613
  year: 2007
  ident: BFonc201057_CR54
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0703903104
– volume: 27
  start-page: 4324
  year: 1999
  ident: BFonc201057_CR15
  publication-title: Nucleic Acids Res
  doi: 10.1093/nar/27.22.4324
– volume: 23
  start-page: 4089
  year: 2004
  ident: BFonc201057_CR47
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1207567
– volume: 282
  start-page: 32264
  year: 2007
  ident: BFonc201057_CR25
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M703649200
– volume: 66
  start-page: 7438
  year: 2006
  ident: BFonc201057_CR35
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-06-0793
– volume: 105
  start-page: 1674
  year: 2008
  ident: BFonc201057_CR2
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.0706057105
– volume: 13
  start-page: 1321
  year: 2004
  ident: BFonc201057_CR45
  publication-title: Hum Mol Genet
  doi: 10.1093/hmg/ddh151
– volume: 65
  start-page: 6488
  year: 2005
  ident: BFonc201057_CR33
  publication-title: Cancer Res
  doi: 10.1158/0008-5472.CAN-05-1294
– volume: 95
  start-page: 15787
  year: 1998
  ident: BFonc201057_CR51
  publication-title: Proc Natl Acad Sci USA
  doi: 10.1073/pnas.95.26.15787
– volume: 89
  start-page: 629
  year: 1997
  ident: BFonc201057_CR41
  publication-title: Cell
  doi: 10.1016/S0092-8674(00)80244-5
– volume: 407
  start-page: 633
  year: 2000
  ident: BFonc201057_CR24
  publication-title: Nature
  doi: 10.1038/35036595
– volume: 420
  start-page: 686
  year: 2002
  ident: BFonc201057_CR40
  publication-title: Nature
  doi: 10.1038/nature01234
– volume: 25
  start-page: 3557
  year: 2006
  ident: BFonc201057_CR44
  publication-title: Oncogene
  doi: 10.1038/sj.onc.1209397
– volume: 278
  start-page: 35781
  year: 2003
  ident: BFonc201057_CR1
  publication-title: J Biol Chem
  doi: 10.1074/jbc.M301326200
– volume: 289
  start-page: 3
  year: 2005
  ident: BFonc201057_CR34
  publication-title: Methods Mol Biol
– volume: 1629
  start-page: 15
  year: 2003
  ident: BFonc201057_CR37
  publication-title: Biochim Biophys Acta
  doi: 10.1016/S0167-4781(03)00156-8
– volume: 204
  start-page: 1813
  year: 2007
  ident: BFonc201057_CR31
  publication-title: J Exp Med
  doi: 10.1084/jem.20070876
– volume: 10
  start-page: 902
  year: 2008
  ident: BFonc201057_CR19
  publication-title: Nat Cell Biol
  doi: 10.1038/ncb1750
– volume: 51
  start-page: 1063
  year: 1987
  ident: BFonc201057_CR10
  publication-title: Cell
  doi: 10.1016/0092-8674(87)90592-7
– volume: 398
  start-page: 518
  year: 1999
  ident: BFonc201057_CR7
  publication-title: Nature
  doi: 10.1038/19083
– volume: 6
  start-page: e123
  year: 2008
  ident: BFonc201057_CR8
  publication-title: PLoS Biol
  doi: 10.1371/journal.pbio.0060123
– volume: 21
  start-page: 737
  year: 2006
  ident: BFonc201057_CR14
  publication-title: Mol Cell
  doi: 10.1016/j.molcel.2006.02.018
– volume: 42
  start-page: 23
  year: 2004
  ident: BFonc201057_CR38
  publication-title: Neuron
  doi: 10.1016/S0896-6273(04)00182-5
– reference: 10748144 - J Biol Chem. 2000 Jun 2;275(22):17136-42
– reference: 16597739 - J Neurosci. 2006 Apr 5;26(14):3845-54
– reference: 14522076 - Biochim Biophys Acta. 2003 Oct 1;1629(1-3):15-25
– reference: 15150404 - Proc Natl Acad Sci U S A. 2004 Jun 15;101(24):9085-90
– reference: 15128703 - Hum Mol Genet. 2004 Jul 1;13(13):1321-31
– reference: 9861048 - Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15787-91
– reference: 17716970 - J Biol Chem. 2007 Oct 26;282(43):31504-16
– reference: 17827153 - J Biol Chem. 2007 Nov 2;282(44):32264-73
– reference: 6321514 - J Cell Biol. 1984 Mar;98(3):1048-53
– reference: 19217402 - Mol Cell. 2009 Feb 13;33(3):275-86
– reference: 16885339 - Cancer Res. 2006 Aug 1;66(15):7438-44
– reference: 10411913 - Proc Natl Acad Sci U S A. 1999 Jul 20;96(15):8551-6
– reference: 11517342 - Proc Natl Acad Sci U S A. 2001 Sep 11;98(19):10863-8
– reference: 18559665 - J Cell Biol. 2008 Jun 16;181(6):913-20
– reference: 11425854 - J Biol Chem. 2001 Sep 14;276(37):34371-8
– reference: 18094723 - Nat Rev Cancer. 2008 Feb;8(2):83-93
– reference: 16543144 - Mol Cell. 2006 Mar 17;21(6):737-48
– reference: 10206645 - Nature. 1999 Apr 8;398(6727):518-22
– reference: 15021893 - Oncogene. 2004 Mar 15;23(11):2057-70
– reference: 17268505 - EMBO Rep. 2007 Feb;8(2):141-6
– reference: 11585921 - Mol Cell Biol. 2001 Nov;21(21):7403-15
– reference: 18507503 - PLoS Biol. 2008 May 27;6(5):e123
– reference: 11034212 - Nature. 2000 Oct 5;407(6804):633-6
– reference: 12829707 - J Biol Chem. 2003 Sep 12;278(37):35781-90
– reference: 17940017 - Proc Natl Acad Sci U S A. 2007 Oct 23;104(43):16904-9
– reference: 15064745 - Oncogene. 2004 May 20;23(23):4089-97
– reference: 12478297 - Nature. 2002 Dec 12;420(6916):686-90
– reference: 12590261 - Nat Genet. 2003 Mar;33(3):416-21
– reference: 15525534 - Dev Cell. 2004 Nov;7(5):731-43
– reference: 10536138 - Nucleic Acids Res. 1999 Nov 15;27(22):4324-7
– reference: 15066262 - Neuron. 2004 Apr 8;42(1):23-36
– reference: 18604200 - Nat Cell Biol. 2008 Aug;10(8):902-11
– reference: 8643690 - Proc Natl Acad Sci U S A. 1996 Feb 20;93(4):1683-8
– reference: 17215302 - Development. 2007 Feb;134(4):691-702
– reference: 15272268 - Nat Med. 2004 Jul;10 Suppl:S26-33
– reference: 12719435 - J Biol Chem. 2003 Jun 13;278(24):21323-6
– reference: 17298674 - Cell Div. 2007 Feb 13;2:7
– reference: 12354302 - J Neurochem. 2002 Sep;82(6):1540-8
– reference: 18227516 - Proc Natl Acad Sci U S A. 2008 Feb 5;105(5):1674-9
– reference: 3500791 - Cell. 1987 Dec 24;51(6):1063-70
– reference: 17556541 - Proc Natl Acad Sci U S A. 2007 Jun 19;104(25):10613-8
– reference: 17079689 - Genes Dev. 2006 Nov 1;20(21):3022-35
– reference: 15288263 - Semin Cancer Biol. 2004 Oct;14(5):374-86
– reference: 16763281 - J Clin Oncol. 2006 Jun 10;24(17):2666-72
– reference: 16474849 - Oncogene. 2006 Jun 15;25(25):3557-64
– reference: 16061623 - Cancer Res. 2005 Aug 1;65(15):6488-92
– reference: 9160754 - Cell. 1997 May 16;89(4):629-39
– reference: 11056418 - Eur J Dermatol. 2000 Oct-Nov;10(7):505-10
– reference: 15592418 - Nature. 2004 Dec 9;432(7018):775-9
– reference: 12297048 - Cell. 2002 Sep 20;110(6):751-62
– reference: 15502164 - Methods Mol Biol. 2005;289:3-14
– reference: 11864992 - J Cell Biol. 2002 Mar 4;156(5):843-54
– reference: 17646409 - J Exp Med. 2007 Aug 6;204(8):1813-24
– reference: 11266469 - J Cell Biol. 2001 Feb 19;152(4):785-94
SSID ssj0007902
Score 2.1711102
Snippet The epidermal growth factor receptor (EGFR) and Notch signaling pathways have antagonistic roles during epidermal differentiation and carcinogenesis. The...
SourceID pubmedcentral
hal
proquest
gale
pubmed
pascalfrancis
crossref
springer
SourceType Open Access Repository
Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 2950
SubjectTerms 631/208/200
631/80/86
692/420/755
Animals
Apoptosis
Biochemistry, Molecular Biology
Biological and medical sciences
Blotting, Western
Carcinogenesis
Catalysis
Cell Biology
Cell physiology
Cell Proliferation
Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes
Cell Transformation, Neoplastic
Cells, Cultured
Cellular signal transduction
Embryo, Mammalian - cytology
Embryo, Mammalian - metabolism
Epidermal growth factor
Epidermal growth factor receptors
Epidermis
F-Box Proteins - metabolism
F-Box-WD Repeat-Containing Protein 7
Fibroblasts - cytology
Fibroblasts - metabolism
Fluorescent Antibody Technique
Fundamental and applied biological sciences. Psychology
Gene Expression Regulation
Genetic aspects
Genetic regulation
Genetics
Growth factor receptors
Human Genetics
Hyperplasia
Immunoenzyme Techniques
Integrases - metabolism
Internal Medicine
Intracellular signalling
Keratinocytes
Keratinocytes - cytology
Keratinocytes - metabolism
Life Sciences
Ligases
Medicine
Medicine & Public Health
Mice
Mice, Knockout
Molecular and cellular biology
Molecular biology
Molecular modelling
Notch1 protein
Oncology
original-article
Physiological aspects
Presenilin
Presenilins - physiology
Proteasomes
Receptor, Epidermal Growth Factor - metabolism
Secretase
Signal transduction
Signal Transduction - physiology
Transcription
Ubiquitin
Ubiquitin - metabolism
Ubiquitin-protein ligase
Ubiquitin-Protein Ligases - metabolism
Ubiquitination
Title Presenilin modulates EGFR signaling and cell transformation by regulating the ubiquitin ligase Fbw7
URI https://link.springer.com/article/10.1038/onc.2010.57
https://www.ncbi.nlm.nih.gov/pubmed/20208556
https://www.proquest.com/docview/2641403565
https://www.proquest.com/docview/312263935
https://www.proquest.com/docview/733344725
https://www.proquest.com/docview/744615620
https://hal.science/hal-04087161
https://pubmed.ncbi.nlm.nih.gov/PMC4162408
Volume 29
WOSCitedRecordID wos000277890400006&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
hasFullText 1
inHoldings 1
isFullTextHit
isPrint
journalDatabaseRights – providerCode: PRVPQU
  databaseName: Biological Science Database (ProQuest)
  customDbUrl:
  eissn: 1476-5594
  dateEnd: 20191231
  omitProxy: false
  ssIdentifier: ssj0007902
  issn: 0950-9232
  databaseCode: M7P
  dateStart: 19970101
  isFulltext: true
  titleUrlDefault: http://search.proquest.com/biologicalscijournals
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Health & Medical Collection
  customDbUrl:
  eissn: 1476-5594
  dateEnd: 20191231
  omitProxy: false
  ssIdentifier: ssj0007902
  issn: 0950-9232
  databaseCode: 7X7
  dateStart: 19970101
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/healthcomplete
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: ProQuest Central
  customDbUrl:
  eissn: 1476-5594
  dateEnd: 20191231
  omitProxy: false
  ssIdentifier: ssj0007902
  issn: 0950-9232
  databaseCode: BENPR
  dateStart: 19970101
  isFulltext: true
  titleUrlDefault: https://www.proquest.com/central
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Public Health Database
  customDbUrl:
  eissn: 1476-5594
  dateEnd: 20191231
  omitProxy: false
  ssIdentifier: ssj0007902
  issn: 0950-9232
  databaseCode: 8C1
  dateStart: 19970101
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/publichealth
  providerName: ProQuest
– providerCode: PRVPQU
  databaseName: Research Library
  customDbUrl:
  eissn: 1476-5594
  dateEnd: 20191231
  omitProxy: false
  ssIdentifier: ssj0007902
  issn: 0950-9232
  databaseCode: M2O
  dateStart: 19970101
  isFulltext: true
  titleUrlDefault: https://search.proquest.com/pqrl
  providerName: ProQuest
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3db5swED-t7b6kaR_ZF2sXWVOnSpNQwYANT1MWJetDm0XVJuUNgQ0tUgdpSDr1v98dEFrWqC97sQQ-gR2f737Ed78D2Lc0ugURBKbjJNx03dQ1IxsbiXBDaeELO6oo84_lZOLPZsG0ic0pm7DKtU2sDLUuFP1HfujYCBQoj_Tr_NKkolF0uNpU0NiCHSJJ4FXk3rQ1xLIOOUQQYZmIY3iTnmc5_mGRqzqsi9zSLYfUmOWtc4qKfDaPSvyh0rrCxSYIejeS8p_j1MpLjV_85_xewvMGnrJBrU-v4EGS9-BRXbDyugdPhuv6cD14fNIcy78GNa2SmDKErOx3oakiWFKy0ffxKaP4kIhS3lmUa0bHBGx5CysXOYuv2SI5q6qIoRTiUbaKs8tVhpfsIjtDL8vG8R_5Bn6NRz-HR2ZTvcFUCGKWpkhEEElle36sLC_xPE_yOHHdWESW9hIlrVijZ0RN1jwNLKVcG_0kagj3ohRRp_MWtvMiT94Di6xAB1qI1PZRytFBKnTge3EaIz7UfmrAl_UShqqhNqcKGxdhdcTu-CGud0jrHXrSgP1WeF4zemwWOyBdCGmf47NU1KQr4IiIMSsccC6FR1Q6Bux1JHEZVKf7E2pT-yqi8z4aHId0Dw0ofa_aV7YB_Y6yteLETuS7rocvWatN2FiZMkQwS3SLiMkN2L3b3aqUAaztpdFRXF2eFKsylI5DlI_8PhHXRdQrOE7kXa3sN4OrKrx6wgDZ2QadyXZ78uy84jBHA0HkegZ8Xm-Ym3FvWI0P985vF56ugzq4tQfby8Uq-QgP1dUyKxd92JIzWbU-tv7Q7sPOt9FkeopXJ_xHvzIafwEkkW4I
linkProvider ProQuest
linkToHtml http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1ZT9tAEB4BPahU9UgvF0pXFahSJQt7fT9UVURJgwgpqqjE29betcEStUOcgPKj-h874wtSIt546IuleEf2rnd25tvsNzMAm4ZCt-AGgW5ZMddtO7H10MSLh3BDKtd3zbBMmT_whkP_-Dg4XII_TSwM0Sobm1gaapVL-o982zIRKFAc6ZfRuU5Fo-hwtamgUWnFfjy7xB1b8XnvK07vFue93aOdvl4XFdAl-taJ7sZuEHrSdPxIGk7sOI7Ho9i2Izc0lBNLz4gUGmz8wIongSGlbaL5xo5zJ0wQDFn43GW4Z9NGiJiC_Htr-L2K4oigxdARN_E6HNCw_O08kxWNjNzgNQdYu4HlU2JhPh6FBU5MUlXUWAR5bzI3_zm-Lb1i7-l_9j2fwZMafrNutV6ew1KcdeBBVZBz1oHVnab-XQceHtS0gxcgD8sgrRQhOfudK6p4Fhds91vvByP-S0gh_SzMFKNjEDa5thfIMxbN2Dg-KaukoRTibTaN0vNpij_ZWXqCKIL1okvvJfy8k4G_gpUsz-I3wEIjUIFy3cT0UcpSQeKqwHeiJEL8q_xEg0-NyghZp26nCiJnoqQQWL5A_RKkX8LxNNhshUdVxpLFYh9J9wTZMXyWDOtwDOwRZQQTXc4916FUQRqsz0niNMi55g-ove2rKF15vzsQdA8dBO3HzQtTg4055W7FKfuSb9sOvqRRU1Fb0UIgWKd0krjn0GDtZnOrwhqwtpV6R7zBLM6nhfAsi1Ja8ttEbBtRvctxIK-rxXXVubKCreNq4M0tu7nBzrdk6WmZox0NICUP1GCrWaBX_V4wG29vHd97WO0fHQzEYG-4vwaPGgILN9ZhZTKexu_gvryYpMV4ozRIDH7d9Yr9CyZLxc8
linkToPdf http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1ZT9tAEB5BaGmlqkd6uVC6qkCVKlnxfTxUVQpJQaRRhKjE29betcEStUOcgPLT-u864wtSIt546EukZEf2rneOb-NvZgC2NYlhwfF91TQjQ7Ws2FIDHT9chBtCOp6jB0XJ_IE7HHonJ_5oBf7UuTBEq6x9YuGoZSboP_KOqSNQoDzSTlyxIkZ7_a_jC5UaSNGL1rqbRqkhh9H8Ck9v-ZeDPdzqHcPo945399WqwYAqMM5OVSdy_MAVuu2FQrMj27ZdI4wsK3QCTdqRcLVQovPGhy2N2NeEsHR05bgIww5iBEYmXncV1lzEGFYL1r71hqOjJgy4JeERIYymIooyquRAzfQ6WSpKUhkFxRvhsAoKq2fEyXwyDnLcprjsr7EMAN_mcf7zMreIkf1n__HTfQ5PK2DOuqUlvYCVKG3Dw7JV57wNj3brznhtWP9RERJeghgV6VsJgnX2O5PUCy3KWe97_4gRMyagZH8WpJLRCxI2vXFKyFIWztkkOi36p6EUInE2C5OLWYJf2XlyiviC9cMr9xX8vJeFv4ZWmqXRW2CB5ktfOk6seyhlSj92pO_ZYRwiMpZerMDnWn24qIq6U2-Rc16QC0yPo65x0jVuuwpsN8LjspbJcrFPpIecPBxeSwRVogbOiGqF8a5huI5NRYQU2FyQxG0QC8MfUZObW1Eh8_3ugNNvGDropK5f6gpsLSh6I051mTzLsvEmtcryyr_mHGE8FZrE04gCG7eHG3VWgDWjNDtiFKZRNsu5a5pU7NK4S8SyEO87Bi7kTWlo15MretvajgLuggkuLHZxJE3Oiurt6BqprKACO7WxXs97yW68u3N9H2AdDZUPDoaHG_C4ZrYY2ia0ppNZ9B4eiMtpkk-2Ku_E4Nd9m-xfq43P7A
openUrl ctx_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF-8&rfr_id=info%3Asid%2Fsummon.serialssolutions.com&rft_val_fmt=info%3Aofi%2Ffmt%3Akev%3Amtx%3Ajournal&rft.genre=article&rft.atitle=Presenilin+modulates+EGFR+signaling+and+cell+transformation+by+regulating+the+ubiquitin+ligase+Fbw7&rft.jtitle=Oncogene&rft.au=ROCHER-ROS%2C+V&rft.au=MARCO%2C+S&rft.au=MAO%2C+J.-H&rft.au=GINES%2C+S&rft.date=2010-05-20&rft.pub=Nature+Publishing+Group&rft.issn=0950-9232&rft.volume=29&rft.issue=20&rft.spage=2950&rft.epage=2961&rft_id=info:doi/10.1038%2Fonc.2010.57&rft.externalDBID=n%2Fa&rft.externalDocID=22838445
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0950-9232&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0950-9232&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0950-9232&client=summon