Epigenetic coordination of signaling pathways during the epithelial-mesenchymal transition

Background The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EM...

Celý popis

Uložené v:

Podrobná bibliografia
Vydané v:	Epigenetics & chromatin Ročník 6; číslo 1; s. 28
Hlavní autori:	Cieślik, Marcin, Hoang, Stephen A, Baranova, Natalya, Chodaparambil, Sanjay, Kumar, Manish, Allison, David F, Xu, Xiaojiang, Wamsley, J Jacob, Gray, Lisa, Jones, David R, Mayo, Marty W, Bekiranov, Stefan
Médium:	Journal Article
Jazyk:	English
Vydavateľské údaje:	London BioMed Central 02.09.2013 BioMed Central Ltd Springer Nature B.V
Predmet:	Activator protein 1 Algorithms Analysis Animal Genetics and Genomics Biomedical and Life Sciences Cancer Cell Biology Cellular signal transduction Chromatin Colleges & universities DNA binding proteins Epigenetic inheritance Epigenetics Gene Expression Gene Function Genes Genetic aspects Genetic transcription Genomes Genotype & phenotype Human Genetics Hypotheses Life Sciences Metastasis Plant Genetics and Genomics Protein-protein interactions Proteins Seeds United Kingdom Epigenetics Chromatin Reprogramming Feedback EMT
ISSN:	1756-8935, 1756-8935
On-line prístup:	Získať plný text
Tagy:	Pridať tag Žiadne tagy, Buďte prvý, kto otaguje tento záznam!

Abstract	Background The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-κB activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways. Results We mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the ‘EMT-signature’ we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the ‘EMT-signature’ are upstream regulators of NF-κB, but are also bound by NF-κB at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-κB activation. Conclusions There is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-κB, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming.
AbstractList	The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-κB activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways. We mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the 'EMT-signature' we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the 'EMT-signature' are upstream regulators of NF-κB, but are also bound by NF-κB at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-κB activation. There is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-κB, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming. Doc number: 28 Abstract Background: The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-κB activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways. Results: We mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the 'EMT-signature' we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the 'EMT-signature' are upstream regulators of NF-κB, but are also bound by NF-κB at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-κB activation. Conclusions: There is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-κB, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming. Background The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-κB activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways. Results We mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the ‘EMT-signature’ we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the ‘EMT-signature’ are upstream regulators of NF-κB, but are also bound by NF-κB at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-κB activation. Conclusions There is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-κB, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming. Background: The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-[kappa]B activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways. Results: We mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the 'EMT-signature' we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the 'EMT-signature' are upstream regulators of NF-[kappa]B, but are also bound by NF-[kappa]B at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-[kappa]B activation. Conclusions: There is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-[kappa]B, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming. The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-ÎºB activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways. We mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the 'EMT-signature' we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the 'EMT-signature' are upstream regulators of NF-ÎºB, but are also bound by NF-ÎºB at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-ÎºB activation. There is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-ÎºB, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming. Background The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-ÎºB activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways. Results We mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the 'EMT-signature' we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the 'EMT-signature' are upstream regulators of NF-ÎºB, but are also bound by NF-ÎºB at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-ÎºB activation. Conclusions There is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-ÎºB, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming. Keywords: EMT, Epigenetics, Chromatin, Reprogramming, Feedback The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-κB activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways.BACKGROUNDThe epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant induction of EMT contributes to cancer progression and metastasis. Studies have begun to implicate epigenetic reprogramming in EMT; however, the relationship between reprogramming and the coordination of cellular processes is largely unexplored. We have previously developed a system to study EMT in a canonical non-small cell lung cancer (NSCLC) model. In this system we have shown that the induction of EMT results in constitutive NF-κB activity. We hypothesized a role for chromatin remodeling in the sustained deregulation of cellular signaling pathways.We mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the 'EMT-signature' we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the 'EMT-signature' are upstream regulators of NF-κB, but are also bound by NF-κB at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-κB activation.RESULTSWe mapped sixteen histone modifications and two variants for epithelial and mesenchymal states. Combinatorial patterns of epigenetic changes were quantified at gene and enhancer loci. We found a distinct chromatin signature among genes in well-established EMT pathways. Strikingly, these genes are only a small minority of those that are differentially expressed. At putative enhancers of genes with the 'EMT-signature' we observed highly coordinated epigenetic activation or repression. Furthermore, enhancers that are activated are bound by a set of transcription factors that is distinct from those that bind repressed enhancers. Upregulated genes with the 'EMT-signature' are upstream regulators of NF-κB, but are also bound by NF-κB at their promoters and enhancers. These results suggest a chromatin-mediated positive feedback as a likely mechanism for sustained NF-κB activation.There is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-κB, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming.CONCLUSIONSThere is highly specific epigenetic regulation at genes and enhancers across several pathways critical to EMT. The sites of these changes in chromatin state implicate several inducible transcription factors with critical roles in EMT (NF-κB, AP-1 and MYC) as targets of this reprogramming. Furthermore, we find evidence that suggests that these transcription factors are in chromatin-mediated transcriptional feedback loops that regulate critical EMT genes. In sum, we establish an important link between chromatin remodeling and shifts in cellular reprogramming.
ArticleNumber	28
Audience	Academic
Author	Chodaparambil, Sanjay Wamsley, J Jacob Cieślik, Marcin Baranova, Natalya Hoang, Stephen A Kumar, Manish Allison, David F Mayo, Marty W Gray, Lisa Jones, David R Bekiranov, Stefan Xu, Xiaojiang
AuthorAffiliation	2 Department of Surgery, University of Virginia, Charlottesville, VA 22908, USA 1 Department of Biochemistry and Molecular Genetics, University of Virginia, 1340 Jefferson Park Ave, P.O. Box 800733, Charlottesville, VA 22908, USA
AuthorAffiliation_xml	– name: 1 Department of Biochemistry and Molecular Genetics, University of Virginia, 1340 Jefferson Park Ave, P.O. Box 800733, Charlottesville, VA 22908, USA – name: 2 Department of Surgery, University of Virginia, Charlottesville, VA 22908, USA
Author_xml	– sequence: 1 givenname: Marcin surname: Cieślik fullname: Cieślik, Marcin organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 2 givenname: Stephen A surname: Hoang fullname: Hoang, Stephen A organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 3 givenname: Natalya surname: Baranova fullname: Baranova, Natalya organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 4 givenname: Sanjay surname: Chodaparambil fullname: Chodaparambil, Sanjay organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 5 givenname: Manish surname: Kumar fullname: Kumar, Manish organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 6 givenname: David F surname: Allison fullname: Allison, David F organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 7 givenname: Xiaojiang surname: Xu fullname: Xu, Xiaojiang organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 8 givenname: J Jacob surname: Wamsley fullname: Wamsley, J Jacob organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 9 givenname: Lisa surname: Gray fullname: Gray, Lisa organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 10 givenname: David R surname: Jones fullname: Jones, David R organization: Department of Biochemistry and Molecular Genetics, University of Virginia, Department of Surgery, University of Virginia – sequence: 11 givenname: Marty W surname: Mayo fullname: Mayo, Marty W email: mwm3y@virginia.edu organization: Department of Biochemistry and Molecular Genetics, University of Virginia – sequence: 12 givenname: Stefan surname: Bekiranov fullname: Bekiranov, Stefan email: sb3de@virginia.edu organization: Department of Biochemistry and Molecular Genetics, University of Virginia
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/24004852$$D View this record in MEDLINE/PubMed
BookMark	eNqNkktr3DAUhU1JaR7ttsti6KZdONHLtrQphJC2gUAhaTbZCI185VGwJVey086_rzxJpzMhhaKFpKvvHF0u5zDbc95Blr3F6BhjXp3guqwKLmhZVAXhL7KDTWFv67yfHcZ4h1BFOEOvsn3CEGK8JAfZ7flgW3AwWp1r70NjnRqtd7k3ebStU511bT6ocflTrWLeTGG-j0vIYbBp66zqih4iOL1c9arLx6BctLPF6-ylUV2EN4_7UXbz-fz72dfi8tuXi7PTy0KXgoyFqTGrMUdmUTNBmeai0ZrXmpIGlGlqho0CLAzBjAjFQIFS3OiSLMoGiaahR9mnB99hWvTQaHCph04OwfYqrKRXVu6-OLuUrb-XlLOa1CIZfHg0CP7HBHGUvY0auk458FOUmJUClyL1-R8oFYQgQauEvn-C3vkppIGuKYorTKstqlUdSOuMTy3q2VSelpTVnJaEJ-r4GSqtBnqrUyKMTfUdwccdQWJG-DW2aopRXlxf7bLvtue3GdyfkPz9XQcfYwCzQTCScwrlHDQ5B01Wcu3Ingi0HdexSm3b7t-ykwdZHOaUQdia2POK3xJg7j0
CitedBy_id	crossref_primary_10_3389_fphys_2022_937988 crossref_primary_10_1002_advs_202301802 crossref_primary_10_1016_j_freeradbiomed_2016_01_009 crossref_primary_10_2217_epi_2022_0023 crossref_primary_10_1074_jbc_RA118_003662 crossref_primary_10_3390_cancers14071813 crossref_primary_10_3390_cancers9070072 crossref_primary_10_1186_s13578_015_0013_2 crossref_primary_10_1186_s12964_019_0335_5 crossref_primary_10_3390_biology10111200 crossref_primary_10_3390_genes15020144 crossref_primary_10_1158_0008_5472_CAN_13_2702 crossref_primary_10_1111_jcmm_17590 crossref_primary_10_1016_j_cellsig_2020_109593 crossref_primary_10_3389_fonc_2014_00358 crossref_primary_10_1155_2014_253804 crossref_primary_10_1186_s13148_017_0380_0 crossref_primary_10_1002_cam4_719 crossref_primary_10_1016_j_ydbio_2021_06_008 crossref_primary_10_1038_s41467_020_16066_2 crossref_primary_10_1371_journal_pone_0101931 crossref_primary_10_1002_cso2_1021 crossref_primary_10_1038_s41416_020_01178_9 crossref_primary_10_2147_CMAR_S317922 crossref_primary_10_1016_j_yexcr_2017_03_051 crossref_primary_10_1016_j_acup_2015_01_004 crossref_primary_10_1038_s41419_019_1397_4 crossref_primary_10_1038_nmicrobiol_2017_86 crossref_primary_10_1016_j_trsl_2014_05_007 crossref_primary_10_1002_dvdy_24678 crossref_primary_10_1016_j_molonc_2015_10_002
Cites_doi	10.1007/s12307-011-0080-9 10.1016/j.cell.2009.06.049 10.1007/s10585-008-9200-4 10.1016/j.devcel.2008.05.009 10.1158/1078-0432.CCR-12-1558 10.1074/jbc.M414122200 10.1186/1471-2105-11-396 10.1053/j.gastro.2009.04.004 10.1186/gb-2004-5-10-r80 10.1093/bib/bbs038 10.1038/nature07730 10.1038/nbt.1662 10.1172/JCI65416 10.1158/0008-5472.CAN-07-0874 10.1038/nature09906 10.1073/pnas.1016071107 10.1038/sj.onc.1209954 10.1101/gad.947102 10.1038/sj.bjc.6605530 10.1101/gad.1775509 10.1101/gr.122382.111 10.1038/nrg1272 10.1093/bioinformatics/btr354 10.1002/ijc.2910170110 10.1073/pnas.0402851101 10.1093/bioinformatics/btr260 10.1186/1756-0500-4-288 10.1093/nar/gkq973 10.1016/j.ceb.2003.10.006 10.1016/j.cell.2012.11.018 10.1158/0008-5472.CAN-05-1058 10.1093/carcin/bgi377 10.1038/nature07829 10.1016/j.cyto.2004.03.002 10.1038/nature09725 10.1158/0008-5472.CAN-09-2979 10.1038/ng.322 10.1016/j.cell.2007.12.014 10.1038/nrg2957 10.1073/pnas.0807146105 10.1073/pnas.1017214108 10.1016/j.immuni.2008.12.009 10.1038/ng.759 10.1038/nrm2618 10.1038/47412 10.1016/j.cell.2009.11.007 10.1038/nature08162 10.1093/nar/gkp625 10.2202/1544-6115.1027 10.1016/j.cell.2012.08.033 10.1038/ng1987 10.1126/science.1141319 10.1186/1471-2105-9-559 10.1016/j.cell.2008.03.027 10.1007/s10585-010-9367-3 10.1186/gb-2010-11-10-r106 10.1056/NEJMra1001389 10.1016/j.tig.2012.05.005 10.1016/j.cell.2008.01.018 10.1038/onc.2010.215 10.1007/s10549-011-1482-6 10.1038/cr.2011.146 10.1016/j.devcel.2009.09.011 10.1038/sj.onc.1209254 10.1038/sj.onc.1209808 10.1093/bioinformatics/btp698 10.1038/nbt.1630 10.1002/emmm.200900043 10.1186/1471-2105-11-117 10.1093/bioinformatics/btp340 10.1038/ng.127 10.1016/S0955-0674(03)00013-9 10.1186/1465-9921-6-56 10.1186/1752-0509-1-24 10.1038/ng.1006 10.1038/sj.onc.1206198 10.1016/j.semcancer.2012.06.007 10.1016/j.immuni.2011.06.013 10.1038/nsmb.2084 10.1038/35019019 10.1172/JCI39104 10.1038/sj.bjc.6602996 10.1038/nrm3048 10.1016/j.cell.2007.05.009 10.1186/gb-2003-4-10-r69
ContentType	Journal Article
Copyright	Cieślik et al.; licensee BioMed Central Ltd. 2013 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. COPYRIGHT 2013 BioMed Central Ltd. 2013 Cieslik et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Copyright © 2013 Cieślik et al.; licensee BioMed Central Ltd. 2013 Cieślik et al.; licensee BioMed Central Ltd.
Copyright_xml	– notice: Cieślik et al.; licensee BioMed Central Ltd. 2013 This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: COPYRIGHT 2013 BioMed Central Ltd. – notice: 2013 Cieslik et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. – notice: Copyright © 2013 Cieślik et al.; licensee BioMed Central Ltd. 2013 Cieślik et al.; licensee BioMed Central Ltd.
DBID	C6C AAYXX CITATION NPM ISR 3V. 7TM 7X7 7XB 88E 8FD 8FE 8FH 8FI 8FJ 8FK ABUWG AFKRA AZQEC BBNVY BENPR BHPHI CCPQU DWQXO FR3 FYUFA GHDGH GNUQQ HCIFZ K9. LK8 M0S M1P M7P P64 PHGZM PHGZT PIMPY PJZUB PKEHL PPXIY PQEST PQGLB PQQKQ PQUKI PRINS RC3 7X8 5PM
DOI	10.1186/1756-8935-6-28
DatabaseName	Springer Nature OA Free Journals CrossRef PubMed Gale In Context: Science ProQuest Central (Corporate) Nucleic Acids Abstracts Health & Medical Collection ProQuest Central (purchase pre-March 2016) Medical Database (Alumni Edition) 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) 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 SciTech Premium Collection ProQuest Health & Medical Complete (Alumni) Biological Sciences ProQuest Health & Medical Collection Medical Database ProQuest Biological Science Biotechnology and BioEngineering Abstracts ProQuest Central Premium ProQuest One Academic Publicly Available Content Database 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 Genetics Abstracts MEDLINE - Academic PubMed Central (Full Participant titles)
DatabaseTitle	CrossRef PubMed Publicly Available Content Database ProQuest Central Student Technology Research Database ProQuest One Academic Middle East (New) ProQuest Central Essentials Nucleic Acids Abstracts ProQuest Health & Medical Complete (Alumni) ProQuest Central (Alumni Edition) SciTech Premium Collection ProQuest One Community College ProQuest One Health & Nursing ProQuest Natural Science Collection ProQuest Central China ProQuest Central ProQuest One Applied & Life Sciences ProQuest Health & Medical Research Collection Genetics Abstracts Health Research Premium Collection Health and Medicine Complete (Alumni Edition) Natural Science Collection ProQuest Central Korea Health & Medical Research Collection Biological Science Collection ProQuest Central (New) ProQuest Medical Library (Alumni) ProQuest Biological Science Collection ProQuest One Academic Eastern Edition ProQuest Hospital Collection Health Research Premium Collection (Alumni) Biological Science Database ProQuest SciTech Collection ProQuest Hospital Collection (Alumni) Biotechnology and BioEngineering Abstracts ProQuest Health & Medical Complete ProQuest Medical Library ProQuest One Academic UKI Edition Engineering Research Database ProQuest One Academic ProQuest One Academic (New) ProQuest Central (Alumni) MEDLINE - Academic
DatabaseTitleList	PubMed Publicly Available Content Database Genetics Abstracts MEDLINE - Academic
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: PIMPY name: Publicly Available Content Database url: http://search.proquest.com/publiccontent sourceTypes: Aggregation Database
DeliveryMethod	fulltext_linktorsrc
Discipline	Zoology
EISSN	1756-8935
EndPage	28
ExternalDocumentID	PMC3847279 3074164381 A534783528 24004852 10_1186_1756_8935_6_28
Genre	Journal Article
GeographicLocations	United Kingdom
GeographicLocations_xml	– name: United Kingdom
GrantInformation_xml	– fundername: NIGMS NIH HHS grantid: T32 GM080186 – fundername: NCI NIH HHS grantid: R01 CA136705 – fundername: NCI NIH HHS grantid: T32 CA009156 – fundername: NCI NIH HHS grantid: T32 CA009109
GroupedDBID	--- 0R~ 29G 2WC 4.4 53G 5GY 5VS 7X7 88E 8FE 8FH 8FI 8FJ AAFWJ AAJSJ AASML ABDBF ABUWG ACGFS ACIHN ACPRK ACUHS ADBBV ADRAZ ADUKV AEAQA AENEX AFKRA AFPKN AHBYD AHMBA AHSBF AHYZX ALMA_UNASSIGNED_HOLDINGS AMKLP AMTXH AOIJS BAPOH BAWUL BBNVY BCNDV BENPR BFQNJ BHPHI BMC BPHCQ BVXVI C6C CCPQU DIK DU5 E3Z EBD EBLON EBS EJD ESX F5P FYUFA GROUPED_DOAJ GX1 H13 HCIFZ HMCUK HYE IAO IEA IHR INH INR ISR ITC KQ8 LK8 M1P M48 M7P M~E O5R O5S OK1 P2P PGMZT PHGZM PHGZT PIMPY PJZUB PPXIY PQGLB PQQKQ PROAC PSQYO PUEGO RBZ RNS ROL RPM RSV SBL SOJ TR2 TUS UKHRP AAYXX AFFHD CITATION ALIPV NPM 3V. 7TM 7XB 8FD 8FK AZQEC DWQXO FR3 GNUQQ K9. P64 PKEHL PQEST PQUKI PRINS RC3 7X8 5PM
ID	FETCH-LOGICAL-c592t-f7147180fb74934c89dcc87c32deafd741fae19f21429a4eaeaa8fc52b5d09dd3
IEDL.DBID	RSV
ISICitedReferencesCount	34
ISICitedReferencesURI	http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000324521300001&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN	1756-8935
IngestDate	Tue Nov 04 01:53:15 EST 2025 Thu Oct 02 07:06:07 EDT 2025 Sun Nov 09 11:04:36 EST 2025 Tue Oct 14 12:42:15 EDT 2025 Tue Nov 11 10:57:36 EST 2025 Tue Nov 04 18:14:56 EST 2025 Thu Nov 13 16:20:12 EST 2025 Mon Jul 21 06:01:24 EDT 2025 Sat Nov 29 06:22:35 EST 2025 Tue Nov 18 22:53:29 EST 2025 Sat Sep 06 07:27:59 EDT 2025
IsDoiOpenAccess	true
IsOpenAccess	true
IsPeerReviewed	true
IsScholarly	true
Issue	1
Keywords	Epigenetics Chromatin Reprogramming Feedback EMT
Language	English
License	This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
LinkModel	DirectLink
MergedId	FETCHMERGED-LOGICAL-c592t-f7147180fb74934c89dcc87c32deafd741fae19f21429a4eaeaa8fc52b5d09dd3
Notes	ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 ObjectType-Article-2 ObjectType-Feature-1 content type line 23
OpenAccessLink	https://link.springer.com/10.1186/1756-8935-6-28
PMID	24004852
PQID	1433161366
PQPubID	54669
PageCount	1
ParticipantIDs	pubmedcentral_primary_oai_pubmedcentral_nih_gov_3847279 proquest_miscellaneous_1459159714 proquest_miscellaneous_1439220936 proquest_journals_1433161366 gale_infotracmisc_A534783528 gale_infotracacademiconefile_A534783528 gale_incontextgauss_ISR_A534783528 pubmed_primary_24004852 crossref_primary_10_1186_1756_8935_6_28 crossref_citationtrail_10_1186_1756_8935_6_28 springer_journals_10_1186_1756_8935_6_28
PublicationCentury	2000
PublicationDate	2013-09-02
PublicationDateYYYYMMDD	2013-09-02
PublicationDate_xml	– month: 09 year: 2013 text: 2013-09-02 day: 02
PublicationDecade	2010
PublicationPlace	London
PublicationPlace_xml	– name: London – name: England
PublicationTitle	Epigenetics & chromatin
PublicationTitleAbbrev	Epigenetics & Chromatin
PublicationTitleAlternate	Epigenetics Chromatin
PublicationYear	2013
Publisher	BioMed Central BioMed Central Ltd Springer Nature B.V
Publisher_xml	– name: BioMed Central – name: BioMed Central Ltd – name: Springer Nature B.V
References	J Von Burstin (300_CR66) 2009; 137 A Barski (300_CR30) 2007; 129 A Visel (300_CR50) 2009; 457 CY McLean (300_CR52) 2010; 28 R Lambiotte (300_CR91) 2008 EM Mercer (300_CR23) 2011; 35 JM López-Novoa (300_CR60) 2009; 1 C-T Ong (300_CR18) 2011; 12 A Singh (300_CR8) 2010; 29 GK Smyth (300_CR79) 2004; 3 Y Wang (300_CR36) 2009; 37 SJ Arnold (300_CR1) 2009; 10 OG McDonald (300_CR9) 2011; 18 SA Mani (300_CR6) 2008; 133 W Fischle (300_CR13) 2003; 15 DS Johnson (300_CR77) 2007; 316 GE Zentner (300_CR22) 2011; 21 HL Chua (300_CR61) 2007; 26 J Dong (300_CR89) 2007; 1 A Provenzani (300_CR40) 2006; 27 NE Bhola (300_CR49) 2013; 123 SS Hammoud (300_CR21) 2009; 460 S John (300_CR68) 2011; 43 LA Byers (300_CR46) 2012; 19 Z Wang (300_CR35) 2009; 138 T Nakamura (300_CR39) 2007; 67 I Amit (300_CR63) 2007; 39 VD Blondel (300_CR90) 2008 C-Y Wu (300_CR65) 2012; 28 F Jin (300_CR69) 2011; 108 WD Foulkes (300_CR45) 2010; 363 D May (300_CR51) 2012; 44 M Lupien (300_CR70) 2008; 132 H Li (300_CR81) 2010; 26 Y Song (300_CR73) 2010; 70 P Kolasinska-Zwierz (300_CR29) 2009; 41 S Thomson (300_CR67) 2008; 25 JP Thiery (300_CR3) 2003; 15 M Lieber (300_CR26) 1976; 17 P Langfelder (300_CR85) 2008; 9 DS Witherow (300_CR42) 2004; 101 AP Boyle (300_CR20) 2008; 132 Z Li (300_CR72) 2012; 151 S Anders (300_CR83) 2010; 11 RJ Mehta (300_CR76) 2012; 131 SC Stadler (300_CR64) 2012; 22 R Avraham (300_CR41) 2011; 12 A Liberzon (300_CR37) 2011; 27 JJ Kovacs (300_CR43) 2009; 17 J Ernst (300_CR16) 2010; 28 RC Gentleman (300_CR78) 2004; 5 JP Thiery (300_CR5) 2009; 139 D Szklarczyk (300_CR87) 2011; 39 300_CR59 N Dumont (300_CR10) 2008; 105 BD Strahl (300_CR12) 2000; 403 A Newman (300_CR33) 2010; 11 TD Gilmore (300_CR54) 2006; 25 KI Zeller (300_CR57) 2003; 4 C Zang (300_CR84) 2009; 25 KR Rosenbloom (300_CR86) 2012 M Lombaerts (300_CR11) 2006; 94 Z Nie (300_CR55) 2012; 151 E Charafe-Jauffret (300_CR38) 2006; 25 C Granet (300_CR62) 2004; 26 J Yang (300_CR4) 2008; 14 T Sekiya (300_CR71) 2009; 23 RM Kuhn (300_CR80) 2012; 14 SA Hoang (300_CR34) 2011; 4 MP Creyghton (300_CR25) 2010; 107 R Albert (300_CR58) 2000; 406 X Xu (300_CR32) 2010; 11 Y Wu (300_CR48) 2010; 102 I Burtscher (300_CR75) 2009; 136 A-L Barabási (300_CR88) 2004; 5 PV Kharchenko (300_CR19) 2011; 471 I Ben-Porath (300_CR56) 2008; 40 RD Hawkins (300_CR24) 2011; 21 K Hinata (300_CR53) 2003; 22 ND Heintzman (300_CR31) 2009; 459 J Ernst (300_CR17) 2011; 473 LA Borthwick (300_CR27) 2012; 5 H Kasai (300_CR47) 2005; 6 S Thomson (300_CR15) 2011; 28 Z Wu (300_CR44) 2011; 14 JK Pickrell (300_CR82) 2011; 27 S Thomson (300_CR7) 2005; 65 H Wan (300_CR74) 2005; 280 G Wei (300_CR28) 2009; 30 A Bird (300_CR14) 2002; 16 R Kalluri (300_CR2) 2009; 119 21903424 - Immunity. 2011 Sep 23;35(3):413-25 21632746 - Genome Res. 2011 Aug;21(8):1273-83 20049734 - EMBO Mol Med. 2009 Sep;1(6-7):303-14 20979621 - Genome Biol. 2010;11(10):R106 23260146 - Cell. 2012 Dec 21;151(7):1608-16 19339686 - Genes Dev. 2009 Apr 1;23(7):804-9 21194007 - Clin Exp Metastasis. 2011 Feb;28(2):137-55 10935628 - Nature. 2000 Jul 27;406(6794):378-82 15946381 - Respir Res. 2005 Jun 09;6:56 19487818 - J Clin Invest. 2009 Jun;119(6):1420-8 22908213 - Brief Bioinform. 2013 Mar;14(2):144-61 19129791 - Nat Rev Mol Cell Biol. 2009 Feb;10(2):91-103 21402921 - Proc Natl Acad Sci U S A. 2011 Mar 29;108(13):5290-5 19698979 - Cell. 2009 Sep 4;138(5):1019-31 18443585 - Nat Genet. 2008 May;40(5):499-507 22706095 - Semin Cancer Biol. 2012 Oct;22(5-6):404-10 16862183 - Oncogene. 2007 Feb 1;26(5):711-24 21106759 - Proc Natl Acad Sci U S A. 2010 Dec 14;107(50):21931-6 23091115 - Clin Cancer Res. 2013 Jan 1;19(1):279-90 21358745 - Nat Rev Genet. 2011 Apr;12(4):283-93 19661283 - Nucleic Acids Res. 2009 Oct;37(18):5943-58 16230409 - Cancer Res. 2005 Oct 15;65(20):9455-62 21792635 - Cancer Microenviron. 2012 Apr;5(1):45-57 20653935 - BMC Bioinformatics. 2010 Jul 23;11:396 18243105 - Cell. 2008 Jan 25;132(2):311-22 18539112 - Dev Cell. 2008 Jun;14(6):818-29 21252999 - Nat Rev Mol Cell Biol. 2011 Feb;12(2):104-17 17699763 - Cancer Res. 2007 Aug 15;67(16):7597-604 21834981 - BMC Res Notes. 2011 Aug 11;4:288 14735121 - Nat Rev Genet. 2004 Feb;5(2):101-13 17512414 - Cell. 2007 May 18;129(4):823-37 19505939 - Bioinformatics. 2009 Aug 1;25(15):1952-8 12673201 - Oncogene. 2003 Apr 3;22(13):1955-64 20202218 - BMC Bioinformatics. 2010 Mar 04;11:117 14519204 - Genome Biol. 2003;4(10):R69 18696232 - Clin Exp Metastasis. 2008;25(8):843-54 15173580 - Proc Natl Acad Sci U S A. 2004 Jun 8;101(23 ):8603-7 19853559 - Dev Cell. 2009 Oct;17 (4):443-58 15668254 - J Biol Chem. 2005 Apr 8;280(14):13809-16 17072321 - Oncogene. 2006 Oct 30;25(51):6680-4 21067385 - N Engl J Med. 2010 Nov 11;363(20):1938-48 14644200 - Curr Opin Cell Biol. 2003 Dec;15(6):740-6 21045058 - Nucleic Acids Res. 2011 Jan;39(Database issue):D561-8 19362090 - Gastroenterology. 2009 Jul;137(1):361-71, 371.e1-5 16531451 - Carcinogenesis. 2006 Jul;27(7):1323-33 20087353 - Br J Cancer. 2010 Feb 16;102(4):639-44 23021216 - Cell. 2012 Sep 28;151(1):68-79 19144320 - Immunity. 2009 Jan 16;30(1):155-67 21876557 - Cell Res. 2011 Oct;21(10):1393-409 16288205 - Oncogene. 2006 Apr 6;25(15):2273-84 21503684 - Breast Cancer Res Treat. 2012 Feb;131(3):881-90 19114008 - BMC Bioinformatics. 2008 Dec 29;9:559 21441907 - Nature. 2011 May 5;473(7345):43-9 21179089 - Nature. 2011 Mar 24;471(7339):480-5 16646809 - Stat Appl Genet Mol Biol. 2004;3:Article3 175022 - Int J Cancer. 1976 Jan 15;17(1):62-70 22138689 - Nat Genet. 2011 Dec 04;44(1):89-93 19945376 - Cell. 2009 Nov 25;139(5):871-90 21645452 - Zhongguo Fei Ai Za Zhi. 2011 Jun;14 (6):497-501 21546393 - Bioinformatics. 2011 Jun 15;27(12):1739-40 12648673 - Curr Opin Cell Biol. 2003 Apr;15(2):172-83 17547772 - BMC Syst Biol. 2007 Jun 04;1:24 18485877 - Cell. 2008 May 16;133(4):704-15 19234065 - Development. 2009 Mar;136(6):1029-38 16495925 - Br J Cancer. 2006 Mar 13;94(5):661-71 21690102 - Bioinformatics. 2011 Aug 1;27(15):2144-6 17322878 - Nat Genet. 2007 Apr;39(4):503-12 23391723 - J Clin Invest. 2013 Mar;123(3):1348-58 17540862 - Science. 2007 Jun 8;316(5830):1497-502 11782440 - Genes Dev. 2002 Jan 1;16(1):6-21 21258342 - Nat Genet. 2011 Mar;43(3):264-8 10638745 - Nature. 2000 Jan 6;403(6765):41-5 21725293 - Nat Struct Mol Biol. 2011 Jul 03;18(8):867-74 22717049 - Trends Genet. 2012 Sep;28(9):454-63 19182803 - Nat Genet. 2009 Mar;41(3):376-81 23193274 - Nucleic Acids Res. 2013 Jan;41(Database issue):D56-63 15461798 - Genome Biol. 2004;5(10):R80 18358809 - Cell. 2008 Mar 21;132(6):958-70 20436461 - Nat Biotechnol. 2010 May;28(5):495-501 20657582 - Nat Biotechnol. 2010 Aug;28(8):817-25 20160041 - Cancer Res. 2010 Mar 1;70(5):2115-25 19295514 - Nature. 2009 May 7;459(7243):108-12 18806226 - Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):14867-72 19212405 - Nature. 2009 Feb 12;457(7231):854-8 20080505 - Bioinformatics. 2010 Mar 1;26(5):589-95 20531305 - Oncogene. 2010 Aug 26;29(34):4741-51 15149634 - Cytokine. 2004 May 21;26(4):169-77 19525931 - Nature. 2009 Jul 23;460(7254):473-8
References_xml	– volume: 5 start-page: 45 year: 2012 ident: 300_CR27 publication-title: Cancer Microenviron doi: 10.1007/s12307-011-0080-9 – volume: 138 start-page: 1019 year: 2009 ident: 300_CR35 publication-title: Cell doi: 10.1016/j.cell.2009.06.049 – volume: 25 start-page: 843 year: 2008 ident: 300_CR67 publication-title: Clin Exp Metastasis doi: 10.1007/s10585-008-9200-4 – volume: 14 start-page: 818 year: 2008 ident: 300_CR4 publication-title: Dev Cell doi: 10.1016/j.devcel.2008.05.009 – volume: 19 start-page: 279 year: 2012 ident: 300_CR46 publication-title: Clin Cancer Res doi: 10.1158/1078-0432.CCR-12-1558 – volume: 280 start-page: 13809 year: 2005 ident: 300_CR74 publication-title: J Biol Chem doi: 10.1074/jbc.M414122200 – volume: 11 start-page: 396 year: 2010 ident: 300_CR32 publication-title: BMC Bioinforma doi: 10.1186/1471-2105-11-396 – volume: 137 start-page: 361 year: 2009 ident: 300_CR66 publication-title: Gastroenterology doi: 10.1053/j.gastro.2009.04.004 – volume: 5 start-page: R80 year: 2004 ident: 300_CR78 publication-title: Genome Biol doi: 10.1186/gb-2004-5-10-r80 – volume: 14 start-page: 144 year: 2012 ident: 300_CR80 publication-title: Brief Bioinform doi: 10.1093/bib/bbs038 – volume: 457 start-page: 854 year: 2009 ident: 300_CR50 publication-title: Nature doi: 10.1038/nature07730 – volume: 28 start-page: 817 year: 2010 ident: 300_CR16 publication-title: Nat Biotech doi: 10.1038/nbt.1662 – volume: 123 start-page: 1348 year: 2013 ident: 300_CR49 publication-title: J Clin Invest doi: 10.1172/JCI65416 – volume: 67 start-page: 7597 year: 2007 ident: 300_CR39 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-07-0874 – volume: 473 start-page: 43 year: 2011 ident: 300_CR17 publication-title: Nature doi: 10.1038/nature09906 – volume: 107 start-page: 21931 year: 2010 ident: 300_CR25 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.1016071107 – volume: 25 start-page: 6680 year: 2006 ident: 300_CR54 publication-title: Oncogene doi: 10.1038/sj.onc.1209954 – ident: 300_CR59 – volume: 16 start-page: 6 year: 2002 ident: 300_CR14 publication-title: Genes Dev doi: 10.1101/gad.947102 – volume: 102 start-page: 639 year: 2010 ident: 300_CR48 publication-title: Br J Cancer doi: 10.1038/sj.bjc.6605530 – volume: 23 start-page: 804 year: 2009 ident: 300_CR71 publication-title: Genes Dev doi: 10.1101/gad.1775509 – volume: 21 start-page: 1273 year: 2011 ident: 300_CR22 publication-title: Genome Res doi: 10.1101/gr.122382.111 – volume: 5 start-page: 101 year: 2004 ident: 300_CR88 publication-title: Nat Rev Genet doi: 10.1038/nrg1272 – volume: 27 start-page: 2144 year: 2011 ident: 300_CR82 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btr354 – volume: 17 start-page: 62 year: 1976 ident: 300_CR26 publication-title: Int J Cancer J Int Cancer doi: 10.1002/ijc.2910170110 – volume: 101 start-page: 8603 year: 2004 ident: 300_CR42 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0402851101 – volume: 27 start-page: 1739 year: 2011 ident: 300_CR37 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btr260 – volume: 4 start-page: 288 year: 2011 ident: 300_CR34 publication-title: Bmc Res Notes doi: 10.1186/1756-0500-4-288 – volume: 39 start-page: D561 issue: suppl 1 year: 2011 ident: 300_CR87 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkq973 – volume: 15 start-page: 740 year: 2003 ident: 300_CR3 publication-title: Curr Opin Cell Biol doi: 10.1016/j.ceb.2003.10.006 – volume: 151 start-page: 1608 year: 2012 ident: 300_CR72 publication-title: Cell doi: 10.1016/j.cell.2012.11.018 – volume: 65 start-page: 9455 year: 2005 ident: 300_CR7 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-05-1058 – volume: 27 start-page: 1323 year: 2006 ident: 300_CR40 publication-title: Carcinogenesis doi: 10.1093/carcin/bgi377 – volume: 459 start-page: 108 year: 2009 ident: 300_CR31 publication-title: Nature doi: 10.1038/nature07829 – volume: 26 start-page: 169 year: 2004 ident: 300_CR62 publication-title: Cytokine doi: 10.1016/j.cyto.2004.03.002 – volume: 471 start-page: 480 year: 2011 ident: 300_CR19 publication-title: Nature doi: 10.1038/nature09725 – volume: 70 start-page: 2115 year: 2010 ident: 300_CR73 publication-title: Cancer Res doi: 10.1158/0008-5472.CAN-09-2979 – volume: 41 start-page: 376 year: 2009 ident: 300_CR29 publication-title: Nat Genet doi: 10.1038/ng.322 – volume: 136 start-page: 1029 year: 2009 ident: 300_CR75 publication-title: Dev Camb Engl – volume: 132 start-page: 311 year: 2008 ident: 300_CR20 publication-title: Cell doi: 10.1016/j.cell.2007.12.014 – volume-title: Nucleic Acids Res year: 2012 ident: 300_CR86 – volume: 12 start-page: 283 year: 2011 ident: 300_CR18 publication-title: Nat Rev Genet doi: 10.1038/nrg2957 – volume: 105 start-page: 14867 year: 2008 ident: 300_CR10 publication-title: Proc Natl Acad Sci doi: 10.1073/pnas.0807146105 – volume: 108 start-page: 5290 year: 2011 ident: 300_CR69 publication-title: Proc Natl Acad Sci doi: 10.1073/pnas.1017214108 – volume: 30 start-page: 155 year: 2009 ident: 300_CR28 publication-title: Immunity doi: 10.1016/j.immuni.2008.12.009 – volume: 43 start-page: 264 year: 2011 ident: 300_CR68 publication-title: Nat Genet doi: 10.1038/ng.759 – volume: 10 start-page: 91 year: 2009 ident: 300_CR1 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm2618 – volume: 403 start-page: 41 year: 2000 ident: 300_CR12 publication-title: Nature doi: 10.1038/47412 – volume: 139 start-page: 871 year: 2009 ident: 300_CR5 publication-title: Cell doi: 10.1016/j.cell.2009.11.007 – volume: 460 start-page: 473 year: 2009 ident: 300_CR21 publication-title: Nature doi: 10.1038/nature08162 – volume: 37 start-page: 5943 year: 2009 ident: 300_CR36 publication-title: Nucleic Acids Res doi: 10.1093/nar/gkp625 – volume: 3 start-page: Article3 year: 2004 ident: 300_CR79 publication-title: Stat Appl Genet Mol Biol doi: 10.2202/1544-6115.1027 – volume: 151 start-page: 68 year: 2012 ident: 300_CR55 publication-title: Cell doi: 10.1016/j.cell.2012.08.033 – volume: 39 start-page: 503 year: 2007 ident: 300_CR63 publication-title: Nat Genet doi: 10.1038/ng1987 – volume: 316 start-page: 1497 year: 2007 ident: 300_CR77 publication-title: Science doi: 10.1126/science.1141319 – volume: 9 start-page: 559 year: 2008 ident: 300_CR85 publication-title: BMC Bioinforma doi: 10.1186/1471-2105-9-559 – volume: 133 start-page: 704 year: 2008 ident: 300_CR6 publication-title: Cell doi: 10.1016/j.cell.2008.03.027 – volume: 28 start-page: 137 year: 2011 ident: 300_CR15 publication-title: Clin Exp Metastasis doi: 10.1007/s10585-010-9367-3 – volume: 11 start-page: R106 year: 2010 ident: 300_CR83 publication-title: Genome Biol doi: 10.1186/gb-2010-11-10-r106 – volume: 363 start-page: 1938 year: 2010 ident: 300_CR45 publication-title: N Engl J Med doi: 10.1056/NEJMra1001389 – volume: 28 start-page: 454 year: 2012 ident: 300_CR65 publication-title: Trends Genet doi: 10.1016/j.tig.2012.05.005 – volume: 132 start-page: 958 year: 2008 ident: 300_CR70 publication-title: Cell doi: 10.1016/j.cell.2008.01.018 – volume: 29 start-page: 4741 year: 2010 ident: 300_CR8 publication-title: Oncogene doi: 10.1038/onc.2010.215 – volume: 131 start-page: 881 year: 2012 ident: 300_CR76 publication-title: Breast Cancer Res Treat doi: 10.1007/s10549-011-1482-6 – volume: 14 start-page: 497 year: 2011 ident: 300_CR44 publication-title: Zhongguo Fei Ai Za Zhi Chin J Lung Cancer – volume: 21 start-page: 1393 year: 2011 ident: 300_CR24 publication-title: Cell Res doi: 10.1038/cr.2011.146 – volume: 17 start-page: 443 year: 2009 ident: 300_CR43 publication-title: Dev Cell doi: 10.1016/j.devcel.2009.09.011 – volume: 25 start-page: 2273 year: 2006 ident: 300_CR38 publication-title: Oncogene doi: 10.1038/sj.onc.1209254 – volume: 26 start-page: 711 year: 2007 ident: 300_CR61 publication-title: Oncogene doi: 10.1038/sj.onc.1209808 – volume: 26 start-page: 589 year: 2010 ident: 300_CR81 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btp698 – volume: 28 start-page: 495 year: 2010 ident: 300_CR52 publication-title: Nat Biotech doi: 10.1038/nbt.1630 – start-page: 08121770 volume-title: arXiv year: 2008 ident: 300_CR91 – volume: 1 start-page: 303 year: 2009 ident: 300_CR60 publication-title: EMBO Mol Med doi: 10.1002/emmm.200900043 – volume: 11 start-page: 117 year: 2010 ident: 300_CR33 publication-title: BMC Bioinforma doi: 10.1186/1471-2105-11-117 – volume: 25 start-page: 1952 year: 2009 ident: 300_CR84 publication-title: Bioinformatics doi: 10.1093/bioinformatics/btp340 – volume: 40 start-page: 499 year: 2008 ident: 300_CR56 publication-title: Nat Genet doi: 10.1038/ng.127 – volume: 15 start-page: 172 year: 2003 ident: 300_CR13 publication-title: Curr Opin Cell Biol doi: 10.1016/S0955-0674(03)00013-9 – volume: 6 start-page: 56 year: 2005 ident: 300_CR47 publication-title: Respir Res doi: 10.1186/1465-9921-6-56 – volume: 1 start-page: 24 year: 2007 ident: 300_CR89 publication-title: BMC Syst Biol doi: 10.1186/1752-0509-1-24 – volume: 44 start-page: 89 year: 2012 ident: 300_CR51 publication-title: Nat Genet doi: 10.1038/ng.1006 – volume: 22 start-page: 1955 year: 2003 ident: 300_CR53 publication-title: Oncogene doi: 10.1038/sj.onc.1206198 – volume: 22 start-page: 404 year: 2012 ident: 300_CR64 publication-title: Semin Cancer Biol doi: 10.1016/j.semcancer.2012.06.007 – volume: 35 start-page: 413 year: 2011 ident: 300_CR23 publication-title: Immunity doi: 10.1016/j.immuni.2011.06.013 – volume: 18 start-page: 867 year: 2011 ident: 300_CR9 publication-title: Nat Struct Mol Biol doi: 10.1038/nsmb.2084 – volume: 406 start-page: 378 year: 2000 ident: 300_CR58 publication-title: Nature doi: 10.1038/35019019 – volume-title: J Stat Mech Theory Exp year: 2008 ident: 300_CR90 – volume: 119 start-page: 1420 year: 2009 ident: 300_CR2 publication-title: J Clin Invest doi: 10.1172/JCI39104 – volume: 94 start-page: 661 year: 2006 ident: 300_CR11 publication-title: Br J Cancer doi: 10.1038/sj.bjc.6602996 – volume: 12 start-page: 104 year: 2011 ident: 300_CR41 publication-title: Nat Rev Mol Cell Biol doi: 10.1038/nrm3048 – volume: 129 start-page: 823 year: 2007 ident: 300_CR30 publication-title: Cell doi: 10.1016/j.cell.2007.05.009 – volume: 4 start-page: R69 year: 2003 ident: 300_CR57 publication-title: Genome Biol doi: 10.1186/gb-2003-4-10-r69 – reference: 12673201 - Oncogene. 2003 Apr 3;22(13):1955-64 – reference: 15461798 - Genome Biol. 2004;5(10):R80 – reference: 15946381 - Respir Res. 2005 Jun 09;6:56 – reference: 23260146 - Cell. 2012 Dec 21;151(7):1608-16 – reference: 20080505 - Bioinformatics. 2010 Mar 1;26(5):589-95 – reference: 17699763 - Cancer Res. 2007 Aug 15;67(16):7597-604 – reference: 20049734 - EMBO Mol Med. 2009 Sep;1(6-7):303-14 – reference: 19362090 - Gastroenterology. 2009 Jul;137(1):361-71, 371.e1-5 – reference: 21503684 - Breast Cancer Res Treat. 2012 Feb;131(3):881-90 – reference: 17322878 - Nat Genet. 2007 Apr;39(4):503-12 – reference: 175022 - Int J Cancer. 1976 Jan 15;17(1):62-70 – reference: 23021216 - Cell. 2012 Sep 28;151(1):68-79 – reference: 18539112 - Dev Cell. 2008 Jun;14(6):818-29 – reference: 21792635 - Cancer Microenviron. 2012 Apr;5(1):45-57 – reference: 18443585 - Nat Genet. 2008 May;40(5):499-507 – reference: 18243105 - Cell. 2008 Jan 25;132(2):311-22 – reference: 20087353 - Br J Cancer. 2010 Feb 16;102(4):639-44 – reference: 18485877 - Cell. 2008 May 16;133(4):704-15 – reference: 15668254 - J Biol Chem. 2005 Apr 8;280(14):13809-16 – reference: 14519204 - Genome Biol. 2003;4(10):R69 – reference: 21441907 - Nature. 2011 May 5;473(7345):43-9 – reference: 19853559 - Dev Cell. 2009 Oct;17 (4):443-58 – reference: 18358809 - Cell. 2008 Mar 21;132(6):958-70 – reference: 20653935 - BMC Bioinformatics. 2010 Jul 23;11:396 – reference: 22908213 - Brief Bioinform. 2013 Mar;14(2):144-61 – reference: 19182803 - Nat Genet. 2009 Mar;41(3):376-81 – reference: 21045058 - Nucleic Acids Res. 2011 Jan;39(Database issue):D561-8 – reference: 21358745 - Nat Rev Genet. 2011 Apr;12(4):283-93 – reference: 19661283 - Nucleic Acids Res. 2009 Oct;37(18):5943-58 – reference: 17072321 - Oncogene. 2006 Oct 30;25(51):6680-4 – reference: 17540862 - Science. 2007 Jun 8;316(5830):1497-502 – reference: 19487818 - J Clin Invest. 2009 Jun;119(6):1420-8 – reference: 21903424 - Immunity. 2011 Sep 23;35(3):413-25 – reference: 20979621 - Genome Biol. 2010;11(10):R106 – reference: 21194007 - Clin Exp Metastasis. 2011 Feb;28(2):137-55 – reference: 16862183 - Oncogene. 2007 Feb 1;26(5):711-24 – reference: 16531451 - Carcinogenesis. 2006 Jul;27(7):1323-33 – reference: 14644200 - Curr Opin Cell Biol. 2003 Dec;15(6):740-6 – reference: 21690102 - Bioinformatics. 2011 Aug 1;27(15):2144-6 – reference: 10638745 - Nature. 2000 Jan 6;403(6765):41-5 – reference: 21645452 - Zhongguo Fei Ai Za Zhi. 2011 Jun;14 (6):497-501 – reference: 16230409 - Cancer Res. 2005 Oct 15;65(20):9455-62 – reference: 19525931 - Nature. 2009 Jul 23;460(7254):473-8 – reference: 22717049 - Trends Genet. 2012 Sep;28(9):454-63 – reference: 21632746 - Genome Res. 2011 Aug;21(8):1273-83 – reference: 15173580 - Proc Natl Acad Sci U S A. 2004 Jun 8;101(23 ):8603-7 – reference: 22706095 - Semin Cancer Biol. 2012 Oct;22(5-6):404-10 – reference: 19295514 - Nature. 2009 May 7;459(7243):108-12 – reference: 10935628 - Nature. 2000 Jul 27;406(6794):378-82 – reference: 20436461 - Nat Biotechnol. 2010 May;28(5):495-501 – reference: 19114008 - BMC Bioinformatics. 2008 Dec 29;9:559 – reference: 21876557 - Cell Res. 2011 Oct;21(10):1393-409 – reference: 17547772 - BMC Syst Biol. 2007 Jun 04;1:24 – reference: 19212405 - Nature. 2009 Feb 12;457(7231):854-8 – reference: 14735121 - Nat Rev Genet. 2004 Feb;5(2):101-13 – reference: 19945376 - Cell. 2009 Nov 25;139(5):871-90 – reference: 15149634 - Cytokine. 2004 May 21;26(4):169-77 – reference: 16288205 - Oncogene. 2006 Apr 6;25(15):2273-84 – reference: 21258342 - Nat Genet. 2011 Mar;43(3):264-8 – reference: 11782440 - Genes Dev. 2002 Jan 1;16(1):6-21 – reference: 18696232 - Clin Exp Metastasis. 2008;25(8):843-54 – reference: 20657582 - Nat Biotechnol. 2010 Aug;28(8):817-25 – reference: 23193274 - Nucleic Acids Res. 2013 Jan;41(Database issue):D56-63 – reference: 19698979 - Cell. 2009 Sep 4;138(5):1019-31 – reference: 21546393 - Bioinformatics. 2011 Jun 15;27(12):1739-40 – reference: 16495925 - Br J Cancer. 2006 Mar 13;94(5):661-71 – reference: 23391723 - J Clin Invest. 2013 Mar;123(3):1348-58 – reference: 20202218 - BMC Bioinformatics. 2010 Mar 04;11:117 – reference: 21252999 - Nat Rev Mol Cell Biol. 2011 Feb;12(2):104-17 – reference: 20531305 - Oncogene. 2010 Aug 26;29(34):4741-51 – reference: 21179089 - Nature. 2011 Mar 24;471(7339):480-5 – reference: 21067385 - N Engl J Med. 2010 Nov 11;363(20):1938-48 – reference: 20160041 - Cancer Res. 2010 Mar 1;70(5):2115-25 – reference: 19339686 - Genes Dev. 2009 Apr 1;23(7):804-9 – reference: 21402921 - Proc Natl Acad Sci U S A. 2011 Mar 29;108(13):5290-5 – reference: 22138689 - Nat Genet. 2011 Dec 04;44(1):89-93 – reference: 19505939 - Bioinformatics. 2009 Aug 1;25(15):1952-8 – reference: 17512414 - Cell. 2007 May 18;129(4):823-37 – reference: 19129791 - Nat Rev Mol Cell Biol. 2009 Feb;10(2):91-103 – reference: 21725293 - Nat Struct Mol Biol. 2011 Jul 03;18(8):867-74 – reference: 16646809 - Stat Appl Genet Mol Biol. 2004;3:Article3 – reference: 21834981 - BMC Res Notes. 2011 Aug 11;4:288 – reference: 19234065 - Development. 2009 Mar;136(6):1029-38 – reference: 21106759 - Proc Natl Acad Sci U S A. 2010 Dec 14;107(50):21931-6 – reference: 12648673 - Curr Opin Cell Biol. 2003 Apr;15(2):172-83 – reference: 18806226 - Proc Natl Acad Sci U S A. 2008 Sep 30;105(39):14867-72 – reference: 19144320 - Immunity. 2009 Jan 16;30(1):155-67 – reference: 23091115 - Clin Cancer Res. 2013 Jan 1;19(1):279-90
SSID	ssj0062840
Score	2.160873
Snippet	Background The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial... The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial origin aberrant... Background The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial... Doc number: 28 Abstract Background: The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In... Background: The epithelial-mesenchymal transition (EMT) is a de-differentiation process required for wound healing and development. In tumors of epithelial...
SourceID	pubmedcentral proquest gale pubmed crossref springer
SourceType	Open Access Repository Aggregation Database Index Database Enrichment Source Publisher
StartPage	28
SubjectTerms	Activator protein 1 Algorithms Analysis Animal Genetics and Genomics Biomedical and Life Sciences Cancer Cell Biology Cellular signal transduction Chromatin Colleges & universities DNA binding proteins Epigenetic inheritance Epigenetics Gene Expression Gene Function Genes Genetic aspects Genetic transcription Genomes Genotype & phenotype Human Genetics Hypotheses Life Sciences Metastasis Plant Genetics and Genomics Protein-protein interactions Proteins Seeds
SummonAdditionalLinks	– databaseName: ProQuest Central dbid: BENPR link: http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwEB7BFiQuvB-BggJCgotVx87DPqGCtgIJraoCUtWL5XVsulKbLM0uqP8ej-MsuyvohbMnD2cm800mM98AvBbUiswjD7G0MAQJusiUc0Oqwnn88xgjbCBx_VxNJuL4WB7GhFsXyyoHnxgcdd0azJHvZdja47GnLN_NfxCcGoV_V-MIjeuwg0xl-Qh23o8nh0eDLy6986WRqjET5Z7HypJ4hC5ISXD--hoUbTvkNUTarpbc-mUakOjgzv_u4S7cjjFout8bzT24Zpv7cPOkDRn2B3AyniNFJ3Y3pqb1H6ezPmOYti7Fcg-NHewpjjL-pS-7tG90TH0gmdo5dniceZMm59jVZE4vz_2FFoiHoTTsIXw7GH_98JHEEQzEFJItiKsyRC_qplUueW6ErI0RleGsttrVPhxx2mbSIXGb1LnVVmvhTMGmRU1lXfNHMGraxj6BNNec2bLKneTea2g61ZZJSg3TRc6towmQQRvKRH5yHJNxpsJ3iigVak-h9lSpmEjgzUp-3jNz_FPyFSpXId1Fg_U03_Wy69SnL0dqv-A55r7C6aKQa_1ljY7tCf7mkSFrQ3J3Q9K_j2ZzeVC-iv6gU380n8DL1TIeiTVujW2XQUYyRiW_UqaQPgD1WkngcW-Wq82z4I4LlkC1YbArAWQS31xpZqeBUZz7GIVVMoG3g2mv3fpfn-nTq3f5DG6xMDdEEsp2YbS4WNrncMP8XMy6ixfxLf0NK1RGSA priority: 102 providerName: ProQuest
Title	Epigenetic coordination of signaling pathways during the epithelial-mesenchymal transition
URI	https://link.springer.com/article/10.1186/1756-8935-6-28 https://www.ncbi.nlm.nih.gov/pubmed/24004852 https://www.proquest.com/docview/1433161366 https://www.proquest.com/docview/1439220936 https://www.proquest.com/docview/1459159714 https://pubmed.ncbi.nlm.nih.gov/PMC3847279
Volume	6
WOSCitedRecordID	wos000324521300001&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: PRVADU databaseName: BioMedCentral customDbUrl: eissn: 1756-8935 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0062840 issn: 1756-8935 databaseCode: RBZ dateStart: 20080101 isFulltext: true titleUrlDefault: https://www.biomedcentral.com/search/ providerName: BioMedCentral – providerCode: PRVAON databaseName: DOAJ Directory of Open Access Journals customDbUrl: eissn: 1756-8935 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0062840 issn: 1756-8935 databaseCode: DOA dateStart: 20080101 isFulltext: true titleUrlDefault: https://www.doaj.org/ providerName: Directory of Open Access Journals – providerCode: PRVHPJ databaseName: ROAD: Directory of Open Access Scholarly Resources customDbUrl: eissn: 1756-8935 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0062840 issn: 1756-8935 databaseCode: M~E dateStart: 20080101 isFulltext: true titleUrlDefault: https://road.issn.org providerName: ISSN International Centre – providerCode: PRVPQU databaseName: Biological Science Database customDbUrl: eissn: 1756-8935 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0062840 issn: 1756-8935 databaseCode: M7P dateStart: 20090101 isFulltext: true titleUrlDefault: http://search.proquest.com/biologicalscijournals providerName: ProQuest – providerCode: PRVPQU databaseName: Health & Medical Collection customDbUrl: eissn: 1756-8935 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0062840 issn: 1756-8935 databaseCode: 7X7 dateStart: 20090101 isFulltext: true titleUrlDefault: https://search.proquest.com/healthcomplete providerName: ProQuest – providerCode: PRVPQU databaseName: ProQuest Central customDbUrl: eissn: 1756-8935 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0062840 issn: 1756-8935 databaseCode: BENPR dateStart: 20090101 isFulltext: true titleUrlDefault: https://www.proquest.com/central providerName: ProQuest – providerCode: PRVPQU databaseName: Publicly Available Content Database customDbUrl: eissn: 1756-8935 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0062840 issn: 1756-8935 databaseCode: PIMPY dateStart: 20090101 isFulltext: true titleUrlDefault: http://search.proquest.com/publiccontent providerName: ProQuest – providerCode: PRVAVX databaseName: Springer Nature - Connect here FIRST to enable access customDbUrl: eissn: 1756-8935 dateEnd: 99991231 omitProxy: false ssIdentifier: ssj0062840 issn: 1756-8935 databaseCode: RSV dateStart: 20081201 isFulltext: true titleUrlDefault: https://link.springer.com/search?facet-content-type=%22Journal%22 providerName: Springer Nature
link	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwlV3db9MwED_tAyRe-P4IjCogJHix5tr5sB8H6sQkqKoO0NhL5Do2q7Ql1dqC9t9z5ybVUj4EL3mIL4nj3N3v7Nz9DPBKcaf6iDzM8dQyIuhiEykty1OP-IcYo1wgcf2QD4fq5ESPtoC3tTAh2739JRk8dTBrle0jzmUM0TVlGRNqG3YR6hSZ4vj4S-t7M3S2vKFm_PWaDvRsOuBrCLSZHbnxizQgz-Gd_-_zXbjdRJnxwUot7sGWq-7DzdM6rKE_gNPBjEg4qX4xtjVOP6erNcG49jEldBiqUY9ps-If5moer0oZYwwVYzejGo5zVFp2QXVL9uzqAh-0IMQLyV8P4fPh4NO796zZZIHZVIsF83mf8In7SZ5omVilS2tVbqUonfElBhzeuL72RM2mTeKMM0Z5m4pJWnJdlvIR7FR15Z5AnBgpXJYnXkv0C4ZPjBOacytMmkjneQSsHf_CNgzktBHGeRFmIioraLwKGq8iK4SK4PVafrbi3vij5Ev6nAURWlSUMfPNLOfz4uh4XBykMqHVrXC7RsjX-FhrmgIE7DxxYHUk9zqSaHG229xqTdFY_BynUFJi9CyzLIIX62a6krLYKlcvg4wWgmv5V5lUY4iJXyWCxytFXL-8CA43FRHkHRVdCxBXeLelmp4FznCJUYjIdQRvWkW91vXfjunTfxd9BrdE2CVEMy72YGdxuXTP4Yb9vpjOL3uwnZ_k4ah6sPt2MByNe2Hpo0eJtiM8Nzr6OPraC5b8EyNZP0Q
linkProvider	Springer Nature
linkToHtml	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMw1V1LbxMxELZKAZUL78JCgQWB4GLVsfflA0IVtGrUECEoUtSLcbw2jdTuhm5ClT_Fb2TGuxuSCHrrgbNnd-31zHx-zHxDyMuM2awDyEMtiw1Fgi46FMLQNHaAf4AxmfUkrr20388GA_lpjfxqc2EwrLL1id5R56XBM_LtDqb2APYkybvxD4pVo_B2tS2hUavFgZ2dw5atetv9APP7ivO93cP3-7SpKkBNLPmEurSDDpm5YRpJEZlM5sZkqRE8t9rlgLBO2450yEUmdWS11TpzJubDOGcyzwW89wq5Co0phpClg_kGLwFXzxpiyE6WbAMyJxTWAzFNKFZ7XwC-Vfe_gH-rsZkrF7Qe9_Zu_W9_7Da52ayww53aJO6QNVvcJdePSn9_cI8c7Y6RgBRzN0NTQq9G9XloWLoQg1k05ueHWKj5XM-qsE7jDGGZHNox5q-cgMHSU8zZMsezU_jQBNHeB77dJ18vZWCbZL0oC_uQhJEW3CZp5KQAn6jZUFsuGTNcx5GwjgWEtrOvTMO-jkVATpTfhWWJQm1RqC0qUTwLyOu5_LjmHfmn5AtUJoVkHgVGC33X06pS3S-f1U4sIjzZ869rhFwJnzW6Sb6AziP_15Lk1pIkeBuz3Nwqm2q8XaX-aFpAns-b8UmM4CtsOfUyknMmxYUysYTlNcxKQB7UZjAfPPdgE_OApEsGMhdAnvTllmJ07PnSBazAeCoD8qY1pYWu__WfPrp4lM_Ixv7hx57qdfsHj8kN7iukSMr4FlmfnE3tE3LN_JyMqrOn3j-E5Ntlm9dvtRakfw
linkToPdf	http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwEB6V8hAX3rSBAgEh0YtVr52HLXGpoCsqqlVFAVW9WF7Hpiu1yarJgvrv8TjJqlkeQuLsSeLY4_nG9sw3AK8FtWLkkYdYmhqCBF1kyrkheeo8_nmMETaQuB7kk4k4PpaHa_C2z4UJ0e79lWSb04AsTWWzMy9cu8RFtuMxLyMeaVOSESauwfUECwbhXv3oa2-HM294aUfT-OszAxhaNcZX0Gg1UnLlujSg0Pju__X_HtzpvM94t1WX-7Bmywdw86QKZ-sP4WRvjuScmNcYm8pvS2ftWWFcuRgDPTTmrsdYxPiHvqzjNsUx9i5kbOeY23HmlZmcYz6TOb089x9qEAlDUNgj-DLe-_zuA-mKLxCTStYQl48Qt6ib5onkiRGyMEbkhrPCald4R8RpO5IOKdukTqy2WgtnUjZNCyqLgj-G9bIq7SbEiebMZnniJPf2QtOptkxSaphOE24djYD0c6FMx0yOBTLOVNihiEzheCkcL5UpJiJ4s5Sft5wcf5R8hVOrkOiixEiab3pR12r_6JPaTXmCp17hdZ2Qq_xnje4SE3znkRtrILk1kPQr0Qybew1SnSWo_daKc-9V8yyL4OWyGZ_E6LbSVosgIxmjkv9VJpXe9fSzEsFGq5TLn2fBEKcsgnygrksB5BAftpSz08Alzr13wnIZwXavtFe6_tsxffLvoi_g1uH7sTrYn3x8CrdZKCQiCWVbsN5cLOwzuGG-N7P64nlYuD8B5FtEBw
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=Epigenetic+coordination+of+signaling+pathways+during+the+epithelial-mesenchymal+transition&rft.jtitle=Epigenetics+%26+chromatin&rft.au=Cie%C5%9Blik%2C+Marcin&rft.au=Hoang%2C+Stephen+A&rft.au=Baranova%2C+Natalya&rft.au=Chodaparambil%2C+Sanjay&rft.date=2013-09-02&rft.issn=1756-8935&rft.eissn=1756-8935&rft.volume=6&rft.issue=1&rft_id=info:doi/10.1186%2F1756-8935-6-28&rft.externalDBID=n%2Fa&rft.externalDocID=10_1186_1756_8935_6_28
thumbnail_l	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=1756-8935&client=summon
thumbnail_m	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=1756-8935&client=summon
thumbnail_s	http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=1756-8935&client=summon