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231225s2018 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2017.12.001
|2 doi
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|a pubmed25n0929.xml
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|a (NLM)29223407
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|a (PII)S1521-6616(17)30875-6
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|a DE-627
|b ger
|c DE-627
|e rakwb
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| 041 |
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|a eng
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| 100 |
1 |
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|a Hou, Can
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a STAT3-mediated epigenetic silencing of FOXP3 in LADA T cells is regulated through HDAC5 and DNMT1
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| 264 |
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|c 2018
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| 336 |
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|a Text
|b txt
|2 rdacontent
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| 337 |
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|a ƒaComputermedien
|b c
|2 rdamedia
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| 338 |
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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| 500 |
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|a Date Completed 05.07.2019
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|a Date Revised 31.03.2022
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2017. Published by Elsevier Inc.
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|a In LADA patients, Tregs are reduced and FOXP3 is downregulated in CD4+ T cells, but the etiology remains unclear. Our study included in 20 LADA patients and 20 healthy control patients. qRT-PCR results showed that STAT3, HDAC3, HDAC5, SIRT1, DNMT1 and DNMT3b mRNAs were significantly upregulated in LADA CD4+ T cells than controls, while FOXP3 mRNA significantly decreased. p-STAT3, STAT3, DNMT1 and DNMT3b expressions were increased demonstrated by western blot. ChIP-PCR suggested that p-STAT3 binds to the Foxp3 promoter, meanwhile, histone H3 acetylation at K9 and K14 of FOXP3 promoter were significantly lower than controls. Luciferase reporter assay showed that ectopic STAT3 expression significantly reduced FOXP3 promoter activities. The Foxp3 promoter was significantly hypermethylated in LADA than controls. LADA patients showed stronger binding of p-STAT3, HDAC5 and DNMT1 than controls using CHIP. These findings reveal a crucial role of STAT3 in regulating the epigenetic status of T cells in LADA
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|a Journal Article
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| 650 |
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|a Research Support, Non-U.S. Gov't
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| 650 |
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|a DNMT1
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| 650 |
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|a FOXP3
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| 650 |
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|a HDAC5
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| 650 |
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|a LADA
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|a STAT3
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| 650 |
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|a FOXP3 protein, human
|2 NLM
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| 650 |
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|a Forkhead Transcription Factors
|2 NLM
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| 650 |
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|a STAT3 Transcription Factor
|2 NLM
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| 650 |
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|a STAT3 protein, human
|2 NLM
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| 650 |
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7 |
|a DNA (Cytosine-5-)-Methyltransferase 1
|2 NLM
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| 650 |
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7 |
|a EC 2.1.1.37
|2 NLM
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| 650 |
|
7 |
|a DNMT1 protein, human
|2 NLM
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| 650 |
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7 |
|a EC 2.1.1.37
|2 NLM
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| 650 |
|
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|a HDAC5 protein, human
|2 NLM
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| 650 |
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7 |
|a EC 3.5.1.98
|2 NLM
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| 650 |
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7 |
|a Histone Deacetylases
|2 NLM
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| 650 |
|
7 |
|a EC 3.5.1.98
|2 NLM
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| 700 |
1 |
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|a Zhong, Yanjun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Zhen
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ming, Zhao
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Huang, Gan
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ouyang, Lin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Li, Yijun
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lu, Qianjin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhou, Zhiguang
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 191(2018) vom: 14. Juni, Seite 116-125
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
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|g volume:191
|g year:2018
|g day:14
|g month:06
|g pages:116-125
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| 856 |
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|u http://dx.doi.org/10.1016/j.clim.2017.12.001
|3 Volltext
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