Global gene expression reveals an increase of HMGB1 and APEX1 proteins and their involvement in oxidative stress, apoptosis and inflammation pathways among beta‐thalassaemia intermedia and major phenotypes

Summary Beta‐thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form, requiring regular transfusions while transfusion need is only occasional in BTI. Differential gene expression between patients has n...

Full description

Saved in:
Bibliographic Details
Published in:British journal of haematology Vol. 186; no. 4; pp. 608 - 619
Main Authors: Maia de Oliveira da Silva, João Pedro, Brugnerotto, Ana Flávia, S. Romanello, Karen, K. L. Teixeira, Karina, Lanaro, Carolina, S. Duarte, Adriana, G. L. Costa, Gustavo, da Silva Araújo, Aderson, C. Bezerra, Marcos André, de Farias Domingos, Igor, Pereira Martins, Diego A., Malavazi, Iran, F. Costa, Fernando, Cunha, Anderson F.
Format: Journal Article
Language:English
Published: England Blackwell Publishing Ltd 01.08.2019
Subjects:
APEX1
Apoptosis
Beta‐thalassaemia
Blood diseases
Blood transfusion
Cell differentiation
Erythroid cells
Gene expression
haemolytic anaemia
Hematology
HMGB1
HMGB1 protein
Metabolic pathways
Mutation
Oxidative stress
Phenotypes
Reactive oxygen species
Thalassemia
Transcription
haemolytic anaemia
HMGB1
APEX1
Beta-thalassaemia
oxidative stress
ISSN:0007-1048, 1365-2141, 1365-2141
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Abstract Summary Beta‐thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form, requiring regular transfusions while transfusion need is only occasional in BTI. Differential gene expression between patients has not been assessed so far. Here, we evaluated the global gene expression profiles during differentiation of human erythroid cells of two patients carrying the same mutation [CD39, (C → T)], though displaying different phenotypes (BTI and BTM). Considering the role of reactive oxygen species (ROS) in the pathophysiology of thalassaemia, we focused on differentially expressed genes involved in metabolic pathways triggered by ROS, such as inflammation and apoptosis, and, from these, we selected the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) and High Mobility Group Box1 (HMGB1) genes, whose role in BT is not well established. An in‐depth expression analysis of transcriptional and protein levels in patients carrying a range of mutations associated with BT phenotypes indicated that APEX1 was increased in both BTI and BTM. Furthermore, higher amounts of HMGB1 was found in the plasma of BTI patients. Our findings suggest that these proteins have important roles in BT and could represent new targets for further studies aiming to improve the management of the disease.
AbstractList Beta-thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form, requiring regular transfusions while transfusion need is only occasional in BTI. Differential gene expression between patients has not been assessed so far. Here, we evaluated the global gene expression profiles during differentiation of human erythroid cells of two patients carrying the same mutation [CD39, (C → T)], though displaying different phenotypes (BTI and BTM). Considering the role of reactive oxygen species (ROS) in the pathophysiology of thalassaemia, we focused on differentially expressed genes involved in metabolic pathways triggered by ROS, such as inflammation and apoptosis, and, from these, we selected the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) and High Mobility Group Box1 (HMGB1) genes, whose role in BT is not well established. An in-depth expression analysis of transcriptional and protein levels in patients carrying a range of mutations associated with BT phenotypes indicated that APEX1 was increased in both BTI and BTM. Furthermore, higher amounts of HMGB1 was found in the plasma of BTI patients. Our findings suggest that these proteins have important roles in BT and could represent new targets for further studies aiming to improve the management of the disease.
Beta‐thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form, requiring regular transfusions while transfusion need is only occasional in BTI. Differential gene expression between patients has not been assessed so far. Here, we evaluated the global gene expression profiles during differentiation of human erythroid cells of two patients carrying the same mutation [CD39, (C → T)], though displaying different phenotypes (BTI and BTM). Considering the role of reactive oxygen species (ROS) in the pathophysiology of thalassaemia, we focused on differentially expressed genes involved in metabolic pathways triggered by ROS, such as inflammation and apoptosis, and, from these, we selected the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) and High Mobility Group Box1 (HMGB1) genes, whose role in BT is not well established. An in‐depth expression analysis of transcriptional and protein levels in patients carrying a range of mutations associated with BT phenotypes indicated that APEX1 was increased in both BTI and BTM. Furthermore, higher amounts of HMGB1 was found in the plasma of BTI patients. Our findings suggest that these proteins have important roles in BT and could represent new targets for further studies aiming to improve the management of the disease.
Summary Beta‐thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form, requiring regular transfusions while transfusion need is only occasional in BTI. Differential gene expression between patients has not been assessed so far. Here, we evaluated the global gene expression profiles during differentiation of human erythroid cells of two patients carrying the same mutation [CD39, (C → T)], though displaying different phenotypes (BTI and BTM). Considering the role of reactive oxygen species (ROS) in the pathophysiology of thalassaemia, we focused on differentially expressed genes involved in metabolic pathways triggered by ROS, such as inflammation and apoptosis, and, from these, we selected the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) and High Mobility Group Box1 (HMGB1) genes, whose role in BT is not well established. An in‐depth expression analysis of transcriptional and protein levels in patients carrying a range of mutations associated with BT phenotypes indicated that APEX1 was increased in both BTI and BTM. Furthermore, higher amounts of HMGB1 was found in the plasma of BTI patients. Our findings suggest that these proteins have important roles in BT and could represent new targets for further studies aiming to improve the management of the disease.
Beta‐thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form, requiring regular transfusions while transfusion need is only occasional in BTI. Differential gene expression between patients has not been assessed so far. Here, we evaluated the global gene expression profiles during differentiation of human erythroid cells of two patients carrying the same mutation [ CD39 , (C → T)], though displaying different phenotypes (BTI and BTM). Considering the role of reactive oxygen species (ROS) in the pathophysiology of thalassaemia, we focused on differentially expressed genes involved in metabolic pathways triggered by ROS, such as inflammation and apoptosis, and, from these, we selected the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 ( APEX1 ) and High Mobility Group Box1 ( HMGB1 ) genes, whose role in BT is not well established. An in‐depth expression analysis of transcriptional and protein levels in patients carrying a range of mutations associated with BT phenotypes indicated that APEX1 was increased in both BTI and BTM. Furthermore, higher amounts of HMGB1 was found in the plasma of BTI patients. Our findings suggest that these proteins have important roles in BT and could represent new targets for further studies aiming to improve the management of the disease.
Beta-thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form, requiring regular transfusions while transfusion need is only occasional in BTI. Differential gene expression between patients has not been assessed so far. Here, we evaluated the global gene expression profiles during differentiation of human erythroid cells of two patients carrying the same mutation [CD39, (C → T)], though displaying different phenotypes (BTI and BTM). Considering the role of reactive oxygen species (ROS) in the pathophysiology of thalassaemia, we focused on differentially expressed genes involved in metabolic pathways triggered by ROS, such as inflammation and apoptosis, and, from these, we selected the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) and High Mobility Group Box1 (HMGB1) genes, whose role in BT is not well established. An in-depth expression analysis of transcriptional and protein levels in patients carrying a range of mutations associated with BT phenotypes indicated that APEX1 was increased in both BTI and BTM. Furthermore, higher amounts of HMGB1 was found in the plasma of BTI patients. Our findings suggest that these proteins have important roles in BT and could represent new targets for further studies aiming to improve the management of the disease.Beta-thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form, requiring regular transfusions while transfusion need is only occasional in BTI. Differential gene expression between patients has not been assessed so far. Here, we evaluated the global gene expression profiles during differentiation of human erythroid cells of two patients carrying the same mutation [CD39, (C → T)], though displaying different phenotypes (BTI and BTM). Considering the role of reactive oxygen species (ROS) in the pathophysiology of thalassaemia, we focused on differentially expressed genes involved in metabolic pathways triggered by ROS, such as inflammation and apoptosis, and, from these, we selected the Apurinic/Apyrimidinic Endodeoxyribonuclease 1 (APEX1) and High Mobility Group Box1 (HMGB1) genes, whose role in BT is not well established. An in-depth expression analysis of transcriptional and protein levels in patients carrying a range of mutations associated with BT phenotypes indicated that APEX1 was increased in both BTI and BTM. Furthermore, higher amounts of HMGB1 was found in the plasma of BTI patients. Our findings suggest that these proteins have important roles in BT and could represent new targets for further studies aiming to improve the management of the disease.
Author Maia de Oliveira da Silva, João Pedro
S. Romanello, Karen
da Silva Araújo, Aderson
S. Duarte, Adriana
Pereira Martins, Diego A.
C. Bezerra, Marcos André
K. L. Teixeira, Karina
de Farias Domingos, Igor
G. L. Costa, Gustavo
Malavazi, Iran
Cunha, Anderson F.
F. Costa, Fernando
Lanaro, Carolina
Brugnerotto, Ana Flávia
Author_xml – sequence: 1
  givenname: João Pedro
  surname: Maia de Oliveira da Silva
  fullname: Maia de Oliveira da Silva, João Pedro
  organization: Universidade Federal de São Carlos
– sequence: 2
  givenname: Ana Flávia
  surname: Brugnerotto
  fullname: Brugnerotto, Ana Flávia
  organization: Universidade Estadual de Campinas
– sequence: 3
  givenname: Karen
  surname: S. Romanello
  fullname: S. Romanello, Karen
  organization: Universidade Federal de São Carlos
– sequence: 4
  givenname: Karina
  surname: K. L. Teixeira
  fullname: K. L. Teixeira, Karina
  organization: Universidade Federal de São Carlos
– sequence: 5
  givenname: Carolina
  surname: Lanaro
  fullname: Lanaro, Carolina
  organization: Universidade Estadual de Campinas
– sequence: 6
  givenname: Adriana
  surname: S. Duarte
  fullname: S. Duarte, Adriana
  organization: Universidade Estadual de Campinas
– sequence: 7
  givenname: Gustavo
  surname: G. L. Costa
  fullname: G. L. Costa, Gustavo
  organization: Centro Nacional de Processamento de Alto Desempenho em São Paulo. CENAPAD‐SP
– sequence: 8
  givenname: Aderson
  surname: da Silva Araújo
  fullname: da Silva Araújo, Aderson
  organization: Fundação de Hematologia e Hemoterapia de Pernambuco. HEMOPE
– sequence: 9
  givenname: Marcos André
  surname: C. Bezerra
  fullname: C. Bezerra, Marcos André
  organization: Universidade Federal de Pernambuco
– sequence: 10
  givenname: Igor
  surname: de Farias Domingos
  fullname: de Farias Domingos, Igor
  organization: Universidade Federal de Pernambuco
– sequence: 11
  givenname: Diego A.
  surname: Pereira Martins
  fullname: Pereira Martins, Diego A.
  organization: Universidade Federal de Pernambuco
– sequence: 12
  givenname: Iran
  surname: Malavazi
  fullname: Malavazi, Iran
  organization: Universidade Federal de São Carlos
– sequence: 13
  givenname: Fernando
  surname: F. Costa
  fullname: F. Costa, Fernando
  organization: Universidade Estadual de Campinas
– sequence: 14
  givenname: Anderson F.
  orcidid: 0000-0003-3485-5659
  surname: Cunha
  fullname: Cunha, Anderson F.
  email: anderf2611@gmail.com
  organization: Universidade Federal de São Carlos
BackLink https://www.ncbi.nlm.nih.gov/pubmed/31218684$$D View this record in MEDLINE/PubMed
BookMark eNp1ks9uEzEQxi1URNPCgRdAlriARFqP1-vdHNuqJKAiOIDEbTW7mW0c7dqL7aTNjUfgzXgHngTnTy8V-DLW-Pd9Ho_nhB1ZZ4mxlyDOIK3zerk4Ay20fMJGkOl8LEHBERsJIYoxCFUes5MQlkJAJnJ4xo4zkFDqUo3Y72nnauz4LVnidD94CsE4yz2tCbvA0XJjG08YiLuWzz5NLyEl5_ziy_V34IN3kYwNu1RckPEJX7tuTT3ZmPbc3Zs5RrMmHuLW_B3HwQ3RBbMXGdt22PcJSbcOGBd3uEknvbO3vKaIf37-igvsMASk3mDiI_me5mm7lfe4dJ4PC7IubgYKz9nTNtVNLw7xlH17f_31aja--Tz9cHVxM26yPJNjLXKZS4FKFYCaSDZlowFa3Qidi4loQcwxK8qilRMSRV3DPAVoSJUZlIqyU_Zm75s68GNFIVa9CQ11HVpyq1BJqRQoOREioa8foUu38jZVlyhd6EyqTCfq1YFa1el51eBNj35TPXxVAs73QONdCJ7aqjFx17bo0XQViGo7DFUahmo3DEnx9pHiwfRf7MH9znS0-T9YXX6c7RV_AcT2xqU
CitedBy_id crossref_primary_10_1016_j_intimp_2020_106912
crossref_primary_10_3389_fphar_2025_1615269
crossref_primary_10_1038_s41467_023_41961_9
crossref_primary_10_1007_s00109_023_02368_7
crossref_primary_10_3390_hematolrep14040045
Cites_doi 10.1093/bioinformatics/16.7.650
10.1038/nrrheum.2011.222
10.4161/oxim.3.1.10476
10.1016/j.bcmd.2006.04.005
10.2174/156652408786241384
10.3324/haematol.2010.027698
10.1111/j.1365-2141.2005.05463.x
10.1128/MCB.05772-11
10.1093/hmg/ddp401
10.1093/nar/gkq537
10.1111/j.1365-2141.2008.07084.x
10.1038/srep29389
10.1097/GIM.0b013e3181cd68ed
10.1089/ars.2008.2218
10.1073/pnas.0803181105
10.1186/1471-213X-8-118
10.1160/TH04-04-0234
10.1182/asheducation-2005.1.31
10.1038/emm.2014.42
10.1093/emboj/19.11.2492
10.3324/haematol.2014.106567
10.1038/nrm.2016.132
10.1186/1750-1172-5-11
10.1083/jcb.201107050
10.1111/j.1600-0609.2010.01528.x
10.1016/j.molcel.2011.11.027
10.1126/science.285.5425.248
10.1093/emboj/18.7.1905
10.1053/j.gastro.2013.12.015
10.1111/j.1365-2141.2009.07650.x
10.1371/journal.pone.0208316
10.1016/j.cell.2016.05.006
10.1093/nar/gkw1138
10.1101/gr.1239303
10.1006/meth.2001.1262
10.1016/j.str.2012.09.004
10.1006/bbrc.1998.9548
10.1002/j.1460-2075.1992.tb05411.x
10.1089/ars.2016.6806
10.1016/S0021-9258(19)52451-6
10.1093/nar/gks1118
10.1161/CIRCULATIONAHA.110.003418
10.1146/annurev-immunol-030409-101323
10.1073/pnas.95.9.5061
10.1155/2010/964630
10.1007/s11010-013-1680-0
10.1073/pnas.91.1.23
10.1111/joim.12309
10.1002/hep.26976
10.1093/emboj/18.20.5609
10.5114/ceji.2015.56973
10.1111/bjh.13530
10.1002/ptr.3116
10.1158/1541-7786.MCR-12-0086
10.1089/ars.2017.7214
10.1093/nar/gkt533
10.1034/j.1600-0609.2000.90032.x
10.1016/j.redox.2015.07.018
10.1016/S0039-6060(99)70182-0
10.1111/j.1365-2184.2010.00679.x
10.1016/j.jdermsci.2010.03.003
ContentType Journal Article
Copyright 2019 British Society for Haematology and John Wiley & Sons Ltd
2019 British Society for Haematology and John Wiley & Sons Ltd.
Copyright © 2019 John Wiley & Sons Ltd
Copyright_xml – notice: 2019 British Society for Haematology and John Wiley & Sons Ltd
– notice: 2019 British Society for Haematology and John Wiley & Sons Ltd.
– notice: Copyright © 2019 John Wiley & Sons Ltd
DBID AAYXX
CITATION
NPM
7T5
H94
K9.
7X8
DOI 10.1111/bjh.16062
DatabaseName CrossRef
PubMed
Immunology Abstracts
AIDS and Cancer Research Abstracts
ProQuest Health & Medical Complete (Alumni)
MEDLINE - Academic
DatabaseTitle CrossRef
PubMed
AIDS and Cancer Research Abstracts
ProQuest Health & Medical Complete (Alumni)
Immunology Abstracts
MEDLINE - Academic
DatabaseTitleList PubMed
AIDS and Cancer Research Abstracts

CrossRef
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: 7X8
  name: MEDLINE - Academic
  url: https://search.proquest.com/medline
  sourceTypes: Aggregation Database
DeliveryMethod fulltext_linktorsrc
Discipline Medicine
EISSN 1365-2141
EndPage 619
ExternalDocumentID 31218684
10_1111_bjh_16062
BJH16062
Genre article
Research Support, Non-U.S. Gov't
Journal Article
GrantInformation_xml – fundername: São Paulo Research Foundation
  funderid: 2011/50358-3
– fundername: Brazilian National Council for Scientific and Technological Development‐CNPq
– fundername: Coordination for the Improvement of Higher Education Personnel‐CAPES
GroupedDBID ---
.3N
.55
.GA
.GJ
.Y3
05W
0R~
10A
1KJ
1OB
1OC
23N
24P
31~
33P
36B
3O-
3SF
4.4
50Y
50Z
51W
51X
52M
52N
52O
52P
52R
52S
52T
52U
52V
52W
52X
53G
5GY
5HH
5LA
5RE
5VS
66C
6J9
6P2
702
7PT
8-0
8-1
8-3
8-4
8-5
8F7
8UM
930
A01
A03
AAESR
AAEVG
AAHHS
AAHQN
AAIPD
AAKAS
AAMNL
AANHP
AANLZ
AAONW
AASGY
AAXRX
AAYCA
AAYEP
AAZKR
ABCQN
ABCUV
ABEML
ABJNI
ABLJU
ABOCM
ABPVW
ABQWH
ABXGK
ACAHQ
ACBWZ
ACCFJ
ACCZN
ACFBH
ACGFO
ACGFS
ACGOF
ACMXC
ACPOU
ACPRK
ACRPL
ACSCC
ACXBN
ACXQS
ACYXJ
ADBBV
ADBTR
ADEOM
ADIZJ
ADKYN
ADMGS
ADNMO
ADOZA
ADXAS
ADZCM
ADZMN
ADZOD
AEEZP
AEGXH
AEIGN
AEIMD
AENEX
AEQDE
AEUQT
AEUYR
AFBPY
AFEBI
AFFNX
AFFPM
AFGKR
AFPWT
AFRAH
AFWVQ
AFZJQ
AHBTC
AHEFC
AI.
AIACR
AIAGR
AITYG
AIURR
AIWBW
AJBDE
ALAGY
ALMA_UNASSIGNED_HOLDINGS
ALUQN
ALVPJ
AMBMR
AMYDB
ASPBG
ATUGU
AVWKF
AZBYB
AZFZN
AZVAB
BAFTC
BDRZF
BFHJK
BHBCM
BMXJE
BROTX
BRXPI
BY8
C45
CAG
COF
CS3
D-6
D-7
D-E
D-F
DCZOG
DPXWK
DR2
DRFUL
DRMAN
DRSTM
DU5
EBS
EGARE
EJD
EMOBN
ESX
EX3
F00
F01
F04
F5P
FEDTE
FUBAC
FZ0
G-S
G.N
GODZA
H.X
HF~
HGLYW
HVGLF
HZI
HZ~
IH2
IHE
IX1
J0M
J5H
K48
KBYEO
L7B
LATKE
LC2
LC3
LEEKS
LH4
LITHE
LOXES
LP6
LP7
LUTES
LW6
LYRES
MEWTI
MK4
MRFUL
MRMAN
MRSTM
MSFUL
MSMAN
MSSTM
MXFUL
MXMAN
MXSTM
N04
N05
N4W
N9A
NF~
O66
O9-
OIG
OK1
OVD
P2P
P2W
P2X
P2Z
P4B
P4D
PALCI
Q.N
Q11
QB0
R.K
RIWAO
RJQFR
ROL
RX1
SAMSI
SUPJJ
TEORI
UB1
V8K
V9Y
VH1
W8V
W99
WBKPD
WHWMO
WIH
WIJ
WIK
WIN
WOHZO
WOW
WQJ
WRC
WUP
WVDHM
WXI
WXSBR
X7M
XG1
YFH
YOC
YUY
ZGI
ZXP
ZZTAW
~IA
~WT
AAMMB
AAYXX
AEFGJ
AEYWJ
AGHNM
AGQPQ
AGXDD
AGYGG
AIDQK
AIDYY
AIQQE
CITATION
O8X
NPM
7T5
H94
K9.
7X8
ID FETCH-LOGICAL-c3532-6052520a4471a6ee2c8c611f6c065090f10da3787f29e07bb1de071ce483184e3
IEDL.DBID WIN
ISICitedReferencesCount 7
ISICitedReferencesURI http://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=Summon&SrcAuth=ProQuest&DestLinkType=CitingArticles&DestApp=WOS_CPL&KeyUT=000478608100029&url=https%3A%2F%2Fcvtisr.summon.serialssolutions.com%2F%23%21%2Fsearch%3Fho%3Df%26include.ft.matches%3Dt%26l%3Dnull%26q%3D
ISSN 0007-1048
1365-2141
IngestDate Thu Oct 02 11:49:52 EDT 2025
Mon Oct 06 17:26:34 EDT 2025
Thu Apr 03 06:59:39 EDT 2025
Tue Nov 18 22:38:16 EST 2025
Sat Nov 29 02:02:40 EST 2025
Wed Jan 22 16:39:37 EST 2025
IsPeerReviewed true
IsScholarly true
Issue 4
Keywords haemolytic anaemia
HMGB1
APEX1
Beta-thalassaemia
oxidative stress
Language English
License 2019 British Society for Haematology and John Wiley & Sons Ltd.
LinkModel DirectLink
MergedId FETCHMERGED-LOGICAL-c3532-6052520a4471a6ee2c8c611f6c065090f10da3787f29e07bb1de071ce483184e3
Notes This work was supported by the São Paulo Research Foundation (FAPESP, grant number 2011/50358‐3). Fellowships were granted to KSR and JPMOS (from Coordination for the Improvement of Higher Education Personnel‐CAPES), to KKLT (from the Brazilian National Council for Scientific and Technological Development‐CNPq).
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 14
content type line 23
ORCID 0000-0003-3485-5659
PMID 31218684
PQID 2267632436
PQPubID 36395
PageCount 12
ParticipantIDs proquest_miscellaneous_2244142900
proquest_journals_2267632436
pubmed_primary_31218684
crossref_citationtrail_10_1111_bjh_16062
crossref_primary_10_1111_bjh_16062
wiley_primary_10_1111_bjh_16062_BJH16062
PublicationCentury 2000
PublicationDate August 2019
PublicationDateYYYYMMDD 2019-08-01
PublicationDate_xml – month: 08
  year: 2019
  text: August 2019
PublicationDecade 2010
PublicationPlace England
PublicationPlace_xml – name: England
– name: Oxford
PublicationTitle British journal of haematology
PublicationTitleAlternate Br J Haematol
PublicationYear 2019
Publisher Blackwell Publishing Ltd
Publisher_xml – name: Blackwell Publishing Ltd
References 2010; 12
2010; 58
2009; 80
2004; 69
2017; 45
2006; 37
2003; 13
2011; 96
2008; 8
2008; 105
1992; 11
2012; 10
2005; 2005
2008; 141
2009; 11
2015; 171
2011; 124
2000; 19
2000; 16
2010; 24
2010; 29
1999; 18
1951; 193
2014; 59
2016; 41
2010; 3
1998; 95
2010; 5
2011; 29
2012; 20
2014; 99
2009; 18
2018; 28
2015; 6
2010; 38
2017; 26
1999b; 285
2013; 41
2000; 64
1999a; 126
2016; 166
2014; 46
2014; 276
2001; 25
2013; 380
2010; 85
1998; 252
2012; 196
2010; 43
2017; 53
2016; 6
2004; 92
2013; 33
2005; 129
2009; 145
2017; 18
1994; 91
2012; 45
2012; 8
2014; 146
2018; 13
e_1_2_7_5_1
e_1_2_7_3_1
e_1_2_7_9_1
e_1_2_7_7_1
e_1_2_7_19_1
e_1_2_7_60_1
e_1_2_7_17_1
e_1_2_7_62_1
e_1_2_7_15_1
e_1_2_7_41_1
e_1_2_7_64_1
e_1_2_7_13_1
e_1_2_7_43_1
e_1_2_7_11_1
e_1_2_7_45_1
e_1_2_7_47_1
e_1_2_7_26_1
e_1_2_7_49_1
e_1_2_7_28_1
e_1_2_7_50_1
e_1_2_7_25_1
e_1_2_7_31_1
e_1_2_7_52_1
e_1_2_7_23_1
e_1_2_7_33_1
e_1_2_7_54_1
e_1_2_7_56_1
e_1_2_7_37_1
e_1_2_7_58_1
e_1_2_7_39_1
e_1_2_7_6_1
Gomes W.R. (e_1_2_7_21_1) 2017; 53
e_1_2_7_4_1
e_1_2_7_8_1
e_1_2_7_18_1
e_1_2_7_16_1
e_1_2_7_40_1
e_1_2_7_61_1
e_1_2_7_2_1
e_1_2_7_42_1
e_1_2_7_63_1
e_1_2_7_12_1
Muncie H.L. (e_1_2_7_35_1) 2009; 80
e_1_2_7_44_1
e_1_2_7_65_1
e_1_2_7_10_1
e_1_2_7_46_1
e_1_2_7_48_1
e_1_2_7_27_1
e_1_2_7_29_1
e_1_2_7_51_1
e_1_2_7_30_1
e_1_2_7_53_1
e_1_2_7_24_1
e_1_2_7_32_1
e_1_2_7_55_1
e_1_2_7_22_1
e_1_2_7_34_1
e_1_2_7_57_1
e_1_2_7_20_1
e_1_2_7_36_1
e_1_2_7_59_1
e_1_2_7_38_1
Dhaliwal G. (e_1_2_7_14_1) 2004; 69
References_xml – volume: 91
  start-page: 23
  year: 1994
  end-page: 27
  article-title: The redox and DNA‐repair activities of ref‐1 are encoded by nonoverlapping domains
  publication-title: Proceedings of the National Academy of Sciences of United States of America
– volume: 16
  start-page: 650
  year: 2000
  end-page: 651
  article-title: Esage: managing and analysing data generated with serial analysis of gene expression (sage)
  publication-title: Bioinformatics
– volume: 6
  start-page: 29389
  year: 2016
  article-title: Peroxiredoxin 1 interacts with and blocks the redox factor ape1 from activating interleukin‐8 expression
  publication-title: Scientific Reports
– volume: 85
  start-page: 529
  year: 2010
  end-page: 537
  article-title: Oxidative stress status, clinical outcome, and beta‐globin gene cluster haplotypes in pediatric patients with sickle cell disease
  publication-title: European Journal of Haematology
– volume: 59
  start-page: 1984
  year: 2014
  end-page: 1997
  article-title: Hepatocyte‐specific high‐mobility group box 1 deletion worsens the injury in liver ischemia/reperfusion: a role for intracellular high‐mobility group box 1 in cellular protection
  publication-title: Hepatology
– volume: 8
  start-page: 195
  year: 2012
  end-page: 202
  article-title: Hmgb1: A multifunctional alarmin driving autoimmune and inflammatory disease
  publication-title: Nature Reviews Rheumatology
– volume: 2005
  start-page: 31
  year: 2005
  end-page: 37
  article-title: Pathophysiology of β thalassemia—a guide to molecular therapies
  publication-title: ASH Education Program Book
– volume: 105
  start-page: 10320
  year: 2008
  end-page: 10325
  article-title: High mobility group protein B1 enhances DNA repair and chromatin modification after DNA damage
  publication-title: Proceedings of the National Academy of Sciences of United States of America
– volume: 41
  start-page: D377
  year: 2013
  end-page: D386
  article-title: Panther in 2013: Modeling the evolution of gene function, and other gene attributes, in the context of phylogenetic trees
  publication-title: Nucleic Acids Research
– volume: 33
  start-page: 3879
  year: 2013
  end-page: 3892
  article-title: Erythropoietic defect associated with reduced cell proliferation in mice lacking the 26s proteasome shuttling factor rad23b
  publication-title: Molecular and cellular biology
– volume: 124
  start-page: 806
  year: 2011
  end-page: 813
  article-title: Mitochondrial transporter atp binding cassette mitochondrial erythroid is a novel gene required for cardiac recovery after ischemia/reperfusion
  publication-title: Circulation
– volume: 166
  start-page: 140
  year: 2016
  end-page: 151
  article-title: Lifespan control by redox‐dependent recruitment of chaperones to misfolded proteins
  publication-title: Cell
– volume: 3
  start-page: 2
  year: 2010
  end-page: 619
  article-title: Markers of oxidative stress in erythrocytes and plasma during aging in humans
  publication-title: Oxidative Medicine and Cellular Longevity
– volume: 64
  start-page: 292
  year: 2000
  end-page: 303
  article-title: Two‐phase liquid culture system models normal human adult erythropoiesis at the molecular level
  publication-title: European Journal of Haematology
– volume: 38
  start-page: W214
  year: 2010
  end-page: W220
  article-title: The genemania prediction server: biological network integration for gene prioritization and predicting gene function
  publication-title: Nucleic Acids Research
– volume: 19
  start-page: 2492
  year: 2000
  end-page: 2502
  article-title: Abc‐me: a novel mitochondrial transporter induced by gata‐1 during erythroid differentiation
  publication-title: EMBO Journal
– volume: 43
  start-page: 297
  year: 2010
  end-page: 309
  article-title: Global gene expression reveals a set of new genes involved in the modification of cells during erythroid differentiation
  publication-title: Cell Proliferation
– volume: 45
  start-page: D183
  year: 2017
  end-page: D189
  article-title: Panther version 11: Expanded annotation data from gene ontology and reactome pathways, and data analysis tool enhancements
  publication-title: Nucleic Acids Research
– volume: 6
  start-page: 226
  year: 2015
  end-page: 239
  article-title: Oxidative stress in beta‐thalassaemia and sickle cell disease
  publication-title: Redox Biology
– volume: 193
  start-page: 265
  year: 1951
  end-page: 275
  article-title: Protein measurement with the folin phenol reagent
  publication-title: Journal of Biological Chemistry
– volume: 37
  start-page: 12
  year: 2006
  end-page: 20
  article-title: Thalassemia intermedia: revisited
  publication-title: Blood Cells, Molecules, & Diseases
– volume: 141
  start-page: 357
  year: 2008
  end-page: 366
  article-title: Genetic modifiers of the beta‐haemoglobinopathies
  publication-title: British Journal of Haematology
– volume: 13
  start-page: 2498
  year: 2003
  end-page: 2504
  article-title: Cytoscape: a software environment for integrated models of biomolecular interaction networks
  publication-title: Genome Research
– volume: 24
  start-page: 1334
  year: 2010
  end-page: 1338
  article-title: Amelioration of oxidative stress in red blood cells from patients with beta‐thalassemia major and intermedia and e‐beta‐thalassemia following administration of a fermented papaya preparation
  publication-title: Phytotherapy Research
– volume: 41
  start-page: 116
  year: 2016
  end-page: 124
  article-title: Oxidative stress and age‐related changes in t cells: is thalassemia a model of accelerated immune system aging?
  publication-title: Central European Journal of Immunology
– volume: 252
  start-page: 178
  year: 1998
  end-page: 183
  article-title: Ref‐1 controls pax‐8 DNA‐binding activity
  publication-title: Biochemical and Biophysical Research Communications
– volume: 26
  start-page: 794
  year: 2017
  end-page: 813
  article-title: Hbe/β‐thalassemia and oxidative stress: the key to pathophysiological mechanisms and novel therapeutics
  publication-title: Antioxidants & Redox Signaling
– volume: 126
  start-page: 389
  year: 1999a
  end-page: 392
  article-title: Proinflammatory cytokines (tumor necrosis factor and interleukin 1) stimulate release of high mobility group protein‐1 by pituicytes
  publication-title: Surgery
– volume: 10
  start-page: 1098
  year: 2012
  end-page: 1108
  article-title: Ews/fli1 regulates eya3 in ewing sarcoma via modulation of mirna‐708, resulting in increased cell survival and chemoresistance
  publication-title: Molecular Cancer Research
– volume: 129
  start-page: 435
  year: 2005
  end-page: 441
  article-title: Chronic oxidative stress reduces the respiratory burst response of neutrophils from beta‐thalassaemia patients
  publication-title: British Journal of Haematology
– volume: 11
  start-page: 651
  year: 2009
  end-page: 668
  article-title: Going ape as an approach to cancer therapeutics
  publication-title: Antioxidants & Redox Signaling
– volume: 20
  start-page: 2014
  year: 2012
  end-page: 2024
  article-title: Hmgb1‐facilitated p53 DNA binding occurs via hmg‐box/p53 transactivation domain interaction, regulated by the acidic tail
  publication-title: Structure
– volume: 92
  start-page: 1052
  year: 2004
  end-page: 1059
  article-title: Oxidative status of platelets in normal and thalassemic blood
  publication-title: Thrombosis and Haemostasis
– volume: 46
  start-page: e106
  year: 2014
  article-title: Ape1/ref‐1 as an emerging therapeutic target for various human diseases: phytochemical modulation of its functions
  publication-title: Experimental & Molecular Medicine
– volume: 146
  start-page: 1097
  year: 2014
  end-page: 1107
  article-title: Intracellular hmgb1 inhibits inflammatory nucleosome release and limits acute pancreatitis in mice
  publication-title: Gastroenterology
– volume: 276
  start-page: 420
  year: 2014
  end-page: 424
  article-title: The functions of hmgb1 depend on molecular localization and post‐translational modifications
  publication-title: Journal of Internal Medicine
– volume: 5
  start-page: 11
  year: 2010
  article-title: Beta‐thalassemia
  publication-title: Orphanet Journal of Rare Diseases
– volume: 171
  start-page: 130
  year: 2015
  end-page: 136
  article-title: Thalassaemia major and infectious risk: high mobility group box‐1 represents a novel diagnostic and prognostic biomarker
  publication-title: British Journal of Haematology
– volume: 8
  start-page: 609
  year: 2008
  end-page: 619
  article-title: The role of oxidative stress in hemolytic anemia
  publication-title: Current Molecular Medicine
– volume: 99
  start-page: 1555
  year: 2014
  end-page: 1564
  article-title: Meis1 regulates early erythroid and megakaryocytic cell fate
  publication-title: Haematologica
– volume: 13
  start-page: e0208316
  year: 2018
  article-title: Global analysis of erythroid cells redox status reveals the involvement of prdx1 and prdx2 in the severity of beta thalassemia
  publication-title: PLoS ONE
– volume: 145
  start-page: 455
  year: 2009
  end-page: 467
  article-title: Discovering the genetics underlying foetal haemoglobin production in adults
  publication-title: British Journal of Haematology
– volume: 18
  start-page: 1905
  year: 1999
  end-page: 1914
  article-title: Molecular mechanisms of transcription activation by hlf and hif1alpha in response to hypoxia: their stabilization and redox signal‐induced interaction with cbp/p300
  publication-title: EMBO Journal
– volume: 380
  start-page: 249
  year: 2013
  end-page: 257
  article-title: The activation of hmgb1 as a progression factor on inflammation response in normal human bronchial epithelial cells through rage/jnk/nf‐kappab pathway
  publication-title: Molecular and Cellular Biochemistry
– volume: 45
  start-page: 398
  year: 2012
  end-page: 408
  article-title: Inactivation of a peroxiredoxin by hydrogen peroxide is critical for thioredoxin‐mediated repair of oxidized proteins and cell survival
  publication-title: Molecular Cell
– volume: 95
  start-page: 5061
  year: 1998
  end-page: 5066
  article-title: Activation of apurinic/apyrimidinic endonuclease in human cells by reactive oxygen species and its correlation with their adaptive response to genotoxicity of free radicals
  publication-title: Proceedings of the National Academy of Sciences of United States of America
– volume: 11
  start-page: 3323
  year: 1992
  end-page: 3335
  article-title: Redox activation of fos‐jun DNA binding activity is mediated by a DNA repair enzyme
  publication-title: EMBO Journal
– volume: 69
  start-page: 2599
  year: 2004
  end-page: 2606
  article-title: Hemolytic anemia
  publication-title: American Family Physician
– volume: 41
  start-page: W115
  year: 2013
  end-page: W122
  article-title: Genemania prediction server 2013 update
  publication-title: Nucleic Acids Research
– volume: 28
  start-page: 574
  year: 2018
  end-page: 590
  article-title: Hyperoxidation of peroxiredoxins: gain or loss of function?
  publication-title: Antioxidants & Redox Signaling
– volume: 18
  start-page: R216
  year: 2009
  end-page: R223
  article-title: Control of fetal hemoglobin: new insights emerging from genomics and clinical implications
  publication-title: Human Molecular Genetics
– volume: 285
  start-page: 248
  year: 1999b
  end-page: 251
  article-title: Hmg‐1 as a late mediator of endotoxin lethality in mice
  publication-title: Science
– volume: 80
  start-page: 339
  year: 2009
  end-page: 344
  article-title: Alpha and beta thalassemia
  publication-title: American Family Physician
– volume: 29
  start-page: 139
  year: 2011
  end-page: 162
  article-title: Hmgb1 is a therapeutic target for sterile inflammation and infection
  publication-title: Annual Review of Immunology
– volume: 58
  start-page: 85
  year: 2010
  end-page: 90
  article-title: Role of antioxidants in the skin: anti‐aging effects
  publication-title: Journal of Dermatological Science
– volume: 29
  start-page: 31
  year: 2010
  end-page: 36
  article-title: Plasma protein oxidation and its correlation with antioxidant potential during human aging
  publication-title: Disease Markers
– volume: 196
  start-page: 681
  year: 2012
  end-page: 688
  article-title: Recognition of DNA damage by xpc coincides with disruption of the xpc‐rad23 complex
  publication-title: Journal of Cell Biology
– volume: 12
  start-page: 61
  year: 2010
  end-page: 76
  article-title: Beta‐thalassemia
  publication-title: Genetics in Medicine
– volume: 96
  start-page: 190
  year: 2011
  end-page: 198
  article-title: The role of meis1 in primitive and definitive hematopoiesis during zebrafish development
  publication-title: Haematologica
– volume: 18
  start-page: 31
  year: 2017
  end-page: 42
  article-title: Post‐transcriptional gene regulation by mrna modifications
  publication-title: Nature reviews. Molecular cell biology
– volume: 18
  start-page: 5609
  year: 1999
  end-page: 5621
  article-title: Ref‐1 regulates the transactivation and pro‐apoptotic functions of p53 in vivo
  publication-title: EMBO Journal
– volume: 25
  start-page: 402
  year: 2001
  end-page: 408
  article-title: Analysis of relative gene expression data using real‐time quantitative pcr and the 2(‐delta delta c(t)) method
  publication-title: Methods
– volume: 53
  start-page: 362
  year: 2017
  end-page: 367
  article-title: Frequencies of cd39, ivs1‐1, ivs1‐6 and ivs1‐110 mutations in beta‐thalassemia carriers and their influence on hematimetric indices
  publication-title: Journal Brasileiro de Patologia e Medicina Laboratorial
– volume: 8
  start-page: 118
  year: 2008
  article-title: Pleiotropic effects in eya3knockout mice
  publication-title: BMC Developmental Biology
– ident: e_1_2_7_31_1
  doi: 10.1093/bioinformatics/16.7.650
– volume: 80
  start-page: 339
  year: 2009
  ident: e_1_2_7_35_1
  article-title: Alpha and beta thalassemia
  publication-title: American Family Physician
– volume: 53
  start-page: 362
  year: 2017
  ident: e_1_2_7_21_1
  article-title: Frequencies of cd39, ivs1‐1, ivs1‐6 and ivs1‐110 mutations in beta‐thalassemia carriers and their influence on hematimetric indices
  publication-title: Journal Brasileiro de Patologia e Medicina Laboratorial
– ident: e_1_2_7_23_1
  doi: 10.1038/nrrheum.2011.222
– ident: e_1_2_7_37_1
  doi: 10.4161/oxim.3.1.10476
– ident: e_1_2_7_48_1
  doi: 10.1016/j.bcmd.2006.04.005
– ident: e_1_2_7_16_1
  doi: 10.2174/156652408786241384
– ident: e_1_2_7_12_1
  doi: 10.3324/haematol.2010.027698
– ident: e_1_2_7_3_1
  doi: 10.1111/j.1365-2141.2005.05463.x
– ident: e_1_2_7_8_1
  doi: 10.1128/MCB.05772-11
– ident: e_1_2_7_54_1
  doi: 10.1093/hmg/ddp401
– ident: e_1_2_7_59_1
  doi: 10.1093/nar/gkq537
– ident: e_1_2_7_52_1
  doi: 10.1111/j.1365-2141.2008.07084.x
– ident: e_1_2_7_36_1
  doi: 10.1038/srep29389
– ident: e_1_2_7_9_1
  doi: 10.1097/GIM.0b013e3181cd68ed
– ident: e_1_2_7_6_1
  doi: 10.1089/ars.2008.2218
– ident: e_1_2_7_27_1
  doi: 10.1073/pnas.0803181105
– ident: e_1_2_7_47_1
  doi: 10.1186/1471-213X-8-118
– ident: e_1_2_7_2_1
  doi: 10.1160/TH04-04-0234
– ident: e_1_2_7_51_1
  doi: 10.1182/asheducation-2005.1.31
– ident: e_1_2_7_50_1
  doi: 10.1038/emm.2014.42
– ident: e_1_2_7_46_1
  doi: 10.1093/emboj/19.11.2492
– ident: e_1_2_7_63_1
  doi: 10.3324/haematol.2014.106567
– ident: e_1_2_7_64_1
  doi: 10.1038/nrm.2016.132
– ident: e_1_2_7_19_1
  doi: 10.1186/1750-1172-5-11
– ident: e_1_2_7_7_1
  doi: 10.1083/jcb.201107050
– ident: e_1_2_7_44_1
  doi: 10.1111/j.1600-0609.2010.01528.x
– ident: e_1_2_7_13_1
  doi: 10.1016/j.molcel.2011.11.027
– volume: 69
  start-page: 2599
  year: 2004
  ident: e_1_2_7_14_1
  article-title: Hemolytic anemia
  publication-title: American Family Physician
– ident: e_1_2_7_58_1
  doi: 10.1126/science.285.5425.248
– ident: e_1_2_7_15_1
  doi: 10.1093/emboj/18.7.1905
– ident: e_1_2_7_26_1
  doi: 10.1053/j.gastro.2013.12.015
– ident: e_1_2_7_53_1
  doi: 10.1111/j.1365-2141.2009.07650.x
– ident: e_1_2_7_42_1
  doi: 10.1371/journal.pone.0208316
– ident: e_1_2_7_22_1
  doi: 10.1016/j.cell.2016.05.006
– ident: e_1_2_7_34_1
  doi: 10.1093/nar/gkw1138
– ident: e_1_2_7_45_1
  doi: 10.1101/gr.1239303
– ident: e_1_2_7_29_1
  doi: 10.1006/meth.2001.1262
– ident: e_1_2_7_43_1
  doi: 10.1016/j.str.2012.09.004
– ident: e_1_2_7_49_1
  doi: 10.1006/bbrc.1998.9548
– ident: e_1_2_7_61_1
  doi: 10.1002/j.1460-2075.1992.tb05411.x
– ident: e_1_2_7_24_1
  doi: 10.1089/ars.2016.6806
– ident: e_1_2_7_30_1
  doi: 10.1016/S0021-9258(19)52451-6
– ident: e_1_2_7_33_1
  doi: 10.1093/nar/gks1118
– ident: e_1_2_7_28_1
  doi: 10.1161/CIRCULATIONAHA.110.003418
– ident: e_1_2_7_4_1
  doi: 10.1146/annurev-immunol-030409-101323
– ident: e_1_2_7_40_1
  doi: 10.1073/pnas.95.9.5061
– ident: e_1_2_7_38_1
  doi: 10.1155/2010/964630
– ident: e_1_2_7_60_1
  doi: 10.1007/s11010-013-1680-0
– ident: e_1_2_7_62_1
  doi: 10.1073/pnas.91.1.23
– ident: e_1_2_7_5_1
  doi: 10.1111/joim.12309
– ident: e_1_2_7_25_1
  doi: 10.1002/hep.26976
– ident: e_1_2_7_18_1
  doi: 10.1093/emboj/18.20.5609
– ident: e_1_2_7_20_1
  doi: 10.5114/ceji.2015.56973
– ident: e_1_2_7_10_1
  doi: 10.1111/bjh.13530
– ident: e_1_2_7_17_1
  doi: 10.1002/ptr.3116
– ident: e_1_2_7_41_1
  doi: 10.1158/1541-7786.MCR-12-0086
– ident: e_1_2_7_55_1
  doi: 10.1089/ars.2017.7214
– ident: e_1_2_7_65_1
  doi: 10.1093/nar/gkt533
– ident: e_1_2_7_39_1
  doi: 10.1034/j.1600-0609.2000.90032.x
– ident: e_1_2_7_56_1
  doi: 10.1016/j.redox.2015.07.018
– ident: e_1_2_7_57_1
  doi: 10.1016/S0039-6060(99)70182-0
– ident: e_1_2_7_11_1
  doi: 10.1111/j.1365-2184.2010.00679.x
– ident: e_1_2_7_32_1
  doi: 10.1016/j.jdermsci.2010.03.003
SSID ssj0013051
Score 2.3386738
Snippet Summary Beta‐thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most...
Beta‐thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form,...
Beta-thalassaemia (BT) is classified according to blood transfusion requirement as minor (BTMi), intermedia (BTI) and major (BTM). BTM is the most severe form,...
SourceID proquest
pubmed
crossref
wiley
SourceType Aggregation Database
Index Database
Enrichment Source
Publisher
StartPage 608
SubjectTerms APEX1
Apoptosis
Beta‐thalassaemia
Blood diseases
Blood transfusion
Cell differentiation
Erythroid cells
Gene expression
haemolytic anaemia
Hematology
HMGB1
HMGB1 protein
Metabolic pathways
Mutation
Oxidative stress
Phenotypes
Reactive oxygen species
Thalassemia
Transcription
Title Global gene expression reveals an increase of HMGB1 and APEX1 proteins and their involvement in oxidative stress, apoptosis and inflammation pathways among beta‐thalassaemia intermedia and major phenotypes
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fbjh.16062
https://www.ncbi.nlm.nih.gov/pubmed/31218684
https://www.proquest.com/docview/2267632436
https://www.proquest.com/docview/2244142900
Volume 186
WOSCitedRecordID wos000478608100029&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: PRVWIB
  databaseName: Wiley Online Library Full Collection 2020
  customDbUrl:
  eissn: 1365-2141
  dateEnd: 99991231
  omitProxy: false
  ssIdentifier: ssj0013051
  issn: 0007-1048
  databaseCode: DRFUL
  dateStart: 19970101
  isFulltext: true
  titleUrlDefault: https://onlinelibrary.wiley.com
  providerName: Wiley-Blackwell
– providerCode: PRVWIB
  databaseName: Wiley Online Library Open Access
  customDbUrl:
  eissn: 1365-2141
  dateEnd: 20241209
  omitProxy: false
  ssIdentifier: ssj0013051
  issn: 0007-1048
  databaseCode: WIN
  dateStart: 19970101
  isFulltext: true
  titleUrlDefault: https://onlinelibrary.wiley.com
  providerName: Wiley-Blackwell
link http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3NbtQwEB6VghAX_ksXysogDhyIFCdufsSphS4LoqsKUbG3yHEmaqo2WW1SKDcegTfjHXgSZuxsoAIkJHJJ5IzjSJ4Zf_6ZbwCe6ABpFFKlp8pCeSpOIk-T0_N0II2OylKmcWmTTcSzWTKfpwdr8HwVC-P4IYYFN7YM66_ZwHXe_mLk-fERL41Y_yuVNcoPr2c_dxD87T5bXkyuRiU9qxCf4hlqXhyLfgOYF_GqHXAmN_7rV2_C9R5nih2nGLdgDevbcHW_30m_A98c2b8g_UGB5_1x2FowoxNppNC1qGpGlC2KphTT_Ve7kgoLsXOwN5fC0jtUdWuL7GYDiZOns-zjHT2L5rwqLKm4cOEoz4ReNIuuaStXiTSblNEFTgrOi_xJf6Y3nPtI5Njp71--dkcc5NlqPK20YF6LpY1zsdVP9XGzFHxAreFV5PYuHE723r-Yen1yB8-E22HgRZxAL_C1otFRR4iBSUwkZRkZS-rnl9IvdEjupAxS9OM8lwXdpEGVkBtSGG7Aet3UuAnCEMwxBSHbECOafxmtaBpGl8E0R_rkCJ6uujkzPfM5J-A4yVYzIOqgzHbQCB4PogtH9_Enoa2VrmS9xbcZwdiYqe_DaASPhtdkq7wBo2tszliGwCcBAN8fwT2nY0MroeTsYImin7Wq9Pfms903U_tw_99FH8A1QnqpO7m4Bevd8gwfwhXzsava5RguxfNkDJdfvpscvh1bO_oBVVYgxg
linkProvider Wiley-Blackwell
linkToHtml http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV3NbtQwEB5VWwRcyj9dKGAQBw5EihNvfiQuLXRZYHdVoVbaW-Q4tpqKJqtNCuXGI_BmvANPwozjDVSAhEQuieJxYskz488_8w3AUxloHIWE8YQphCfiJPIkOj1PBlzJyBiexsYmm4jn82SxSA824MU6Fqbjh-gX3MgyrL8mA6cF6V-sPD85prURcsCbAtVoNIDNV-_HR9Ofuwj-yGXMi9HdiMQxC9FJnr7yxfHoN5B5EbPaQWd87f-aex22HNhku5123IANXd2EyzO3nX4LvnWM_wyVSDN97s7EVoxonVAtmaxYWRGsbDSrDZvMXu9xfFmw3YP9BWeW46GsGvvK7jigOLo7S0He4jOrz8vCMouzLiblOZPLetnWTdlVQvVGjeyiJxklR_4kP2MJJUBiuW7l9y9f22OK9GykPi0lI3KLlQ12sdVP5Um9YnRKraal5OY2HI33D19OPJfhwVPhKAy8iLLoBb4UOETKSOtAJSri3ETKMvv5hvuFDNGnmCDVfpznvMAbV1ok6IuEDu_AoKorvQ1MIdZRBcLbUEc4CVNS4FwML6XTXOMnh_Bs3c-ZcvTnlIXjQ7aeBmEHZbaDhvCkF112nB9_EtpZK0vmzL7JEMvGxH8fRkN43BejwdIujKx0fUYyiEARBfj-EO52Stb_JeSUIiwR2FirS3__fbb3dmIf7v276CO4MjmcTbPpm_m7-3AVoV_aHWXcgUG7OtMP4JL62JbN6qEzpB_1-iOK
linkToPdf http://cvtisr.summon.serialssolutions.com/2.0.0/link/0/eLvHCXMwpV1Lb9QwELaqFlVcWt5sKWAQBw5EihNvHhKXlnZZoF2tEJX2FjnOWE3VJqtN-uDGT-Cf8R_4Jcw43kAFSEjkksgZx5E8M_78mG8Ye6ECwFFIGk-aQnoyTiJPodPzVCC0iowRaWxssol4Mklms3S6wl4vY2E6foh-wY0sw_prMnCYF-YXK89PjmlthBzwmhymEZrl2t7H0dHBz10Ef-gy5sXobmTimIXoJE9f-fp49BvIvI5Z7aAz2vy_373FNhzY5DuddtxmK1DdYeuHbjv9LvvWMf5zVCLgcOXOxFacaJ1QLbmqeFkRrGyA14aPD9_uCiws-M50fya45Xgoq8YW2R0HFEd3ZynIW3zm9VVZWGZx3sWkvOJqXs_buim7SqjeqJFd9CSn5MiX6jO-oQRIPIdWff_ytT2mSM9GwVmpOJFbLGywi61-pk7qBadTajUtJTf32NFo_9ObsecyPHg6HIaBF1EWvcBXEodIFQEEOtGRECbSltnPN8IvVIg-xQQp-HGeiwJvQoNM0BdJCO-z1aqu4CHjGrGOLhDehhDhJEwriXMxvDSkOeAnB-zlsp8z7ejPKQvHabacBmEHZbaDBux5LzrvOD_-JLS9VJbMmX2TIZaNif8-jAbsWf8aDZZ2YVQF9TnJIAJFFOD7A_agU7K-lVBQirBE4s9aXfp789nu-7F92Pp30adsfbo3yg7eTT48YjcR-aXdScZtttouzuExu6Ev2rJZPHF29ANOVCMF
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=Global+gene+expression+reveals+an+increase+of+HMGB1+and+APEX1+proteins+and+their+involvement+in+oxidative+stress%2C+apoptosis+and+inflammation+pathways+among+beta%E2%80%90thalassaemia+intermedia+and+major+phenotypes&rft.jtitle=British+journal+of+haematology&rft.au=Maia+de+Oliveira+da+Silva%2C+Jo%C3%A3o+Pedro&rft.au=Brugnerotto%2C+Ana+Fl%C3%A1via&rft.au=S.+Romanello%2C+Karen&rft.au=K.+L.+Teixeira%2C+Karina&rft.date=2019-08-01&rft.issn=0007-1048&rft.eissn=1365-2141&rft.volume=186&rft.issue=4&rft.spage=608&rft.epage=619&rft_id=info:doi/10.1111%2Fbjh.16062&rft.externalDBID=n%2Fa&rft.externalDocID=10_1111_bjh_16062
thumbnail_l http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/lc.gif&issn=0007-1048&client=summon
thumbnail_m http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/mc.gif&issn=0007-1048&client=summon
thumbnail_s http://covers-cdn.summon.serialssolutions.com/index.aspx?isbn=/sc.gif&issn=0007-1048&client=summon