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Article: A possible role of HMGB1 in DNA demethylation in CD4+ T Cells from patients with systemic lupus erythematosus

TitleA possible role of HMGB1 in DNA demethylation in CD4+ T Cells from patients with systemic lupus erythematosus
Authors
Issue Date2013
PublisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/cdi/
Citation
Clinical & Developmental Immunology, 2013, v. 2013, article no. 206298 How to Cite?
AbstractThe aberrant activity of CD4(+) T cells in patients with systemic lupus erythematosus (SLE) is associated with DNA hypomethylation of the regulatory regions in CD11a and CD70 genes. Our previous studies demonstrated that Gadd45a contributes to the development of SLE by promoting DNA demethylation in CD4(+) T cells. In this study, we identified proteins that bind to Gadd45a in CD4(+) T cells during SLE flare by using the method of co-immunoprecipitation and mass spectrometry, High mobility group box protein 1 (HMGB1) is one of identified proteins. Furthermore, gene and protein expression of HMGB1 was significantly increased in SLE CD4(+) T cells compared to controls, and HMGB1 mRNA was correlated with CD11a and CD70 mRNA. A significant, positive correlation was found between HMGB1 mRNA and SLEDAI for SLE patients. Our data demonstrate that HMGB1 binds to Gadd45a and may be involved in DNA demethylation in CD4(+) T cells during lupus flare.
Persistent Identifierhttp://hdl.handle.net/10722/203150
ISSN
2015 Impact Factor: 3.603
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLi, Yen_US
dc.contributor.authorHuang, Cen_US
dc.contributor.authorZhao, Men_US
dc.contributor.authorLiang, Gen_US
dc.contributor.authorXiao, Ren_US
dc.contributor.authorYung, SSYen_US
dc.contributor.authorChan, DTMen_US
dc.contributor.authorLu, Qen_US
dc.date.accessioned2014-09-19T11:33:39Z-
dc.date.available2014-09-19T11:33:39Z-
dc.date.issued2013en_US
dc.identifier.citationClinical & Developmental Immunology, 2013, v. 2013, article no. 206298en_US
dc.identifier.issn1740-2522-
dc.identifier.urihttp://hdl.handle.net/10722/203150-
dc.description.abstractThe aberrant activity of CD4(+) T cells in patients with systemic lupus erythematosus (SLE) is associated with DNA hypomethylation of the regulatory regions in CD11a and CD70 genes. Our previous studies demonstrated that Gadd45a contributes to the development of SLE by promoting DNA demethylation in CD4(+) T cells. In this study, we identified proteins that bind to Gadd45a in CD4(+) T cells during SLE flare by using the method of co-immunoprecipitation and mass spectrometry, High mobility group box protein 1 (HMGB1) is one of identified proteins. Furthermore, gene and protein expression of HMGB1 was significantly increased in SLE CD4(+) T cells compared to controls, and HMGB1 mRNA was correlated with CD11a and CD70 mRNA. A significant, positive correlation was found between HMGB1 mRNA and SLEDAI for SLE patients. Our data demonstrate that HMGB1 binds to Gadd45a and may be involved in DNA demethylation in CD4(+) T cells during lupus flare.-
dc.languageengen_US
dc.publisherHindawi Publishing Corporation. The Journal's web site is located at http://www.hindawi.com/journals/cdi/-
dc.relation.ispartofClinical & Developmental Immunologyen_US
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCD4-Positive T-Lymphocytes - immunology - metabolism-
dc.subject.meshDNA Methylation-
dc.subject.meshGene Expression Regulation-
dc.subject.meshHMGB1 Protein - genetics - metabolism-
dc.subject.meshLupus Erythematosus, Systemic - genetics - immunology - metabolism-
dc.titleA possible role of HMGB1 in DNA demethylation in CD4+ T Cells from patients with systemic lupus erythematosusen_US
dc.typeArticleen_US
dc.identifier.emailYung, SSY: ssyyung@hku.hken_US
dc.identifier.emailChan, DTM: dtmchan@hku.hken_US
dc.identifier.authorityYung, SSY=rp00455en_US
dc.identifier.authorityChan, DTM=rp00394en_US
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1155/2013/206298en_US
dc.identifier.pmid24082908-
dc.identifier.pmcidPMC3776363-
dc.identifier.hkuros239890en_US
dc.identifier.volume2013en_US
dc.identifier.isiWOS:000324422300001-
dc.publisher.placeUnited States-

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