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231229s2024 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2023.109883
|2 doi
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|a pubmed24n1371.xml
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|a (DE-627)NLM366386107
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|a (NLM)38147957
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|a (PII)S1521-6616(23)00647-2
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Wang, Fang
|e verfasserin
|4 aut
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| 245 |
1 |
0 |
|a Peptidase inhibitor 16 promotes inflammatory arthritis by suppressing Foxp3 expression via regulating K48-linked ubiquitin degradation Bmi-1 in regulatory T cells
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|c 2024
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| 336 |
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 01.02.2024
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|a Date Revised 10.04.2024
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2023. Published by Elsevier Inc.
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|a Abnormalities of regulatory T cells (Tregs) has been suggested in rheumatoid arthritis (RA), and Forkhead box P3 (Foxp3) is the key transcriptional factor of Tregs expression. However, the underlying molecular mechanism remains unclear. Here, we demonstrated peptidase inhibitor 16 (PI16) was significantly increased in the peripheral blood, synovial fluid, and synovial tissue from RA patients. PI16 transgenic mice (PI16Tg) aggravated arthritis severity partly through suppressing Foxp3 expression. Mechanistically, PI16 could interact with and stabilize Bmi-1 in Tregs via inhibiting K48-linked polyubiquitin of Bmi-1, which promotes the enrichment of repressive histone mark in Foxp3 promoter. Furthermore, Bmi-1 specific inhibitor PTC209 could restore Foxp3 expression and alleviate arthritis progression in PI16Tg mice, accompanied by increased recruitment of active histone mark in the promoter of Tregs. Our results suggest that PI16-Bmi-1 axis plays an important role in RA and other autoimmune diseases by suppressing Foxp3 expression in Tregs via Bmi-1-mediated histone modification
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4 |
|a Journal Article
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| 650 |
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4 |
|a Research Support, Non-U.S. Gov't
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| 650 |
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4 |
|a Bmi-1
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| 650 |
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4 |
|a Foxp3
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| 650 |
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4 |
|a PI16
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4 |
|a Regulatory T cells
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| 650 |
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4 |
|a Rheumatoid arthritis
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| 650 |
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|a Forkhead Transcription Factors
|2 NLM
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| 650 |
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7 |
|a Foxp3 protein, mouse
|2 NLM
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| 650 |
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7 |
|a Protease Inhibitors
|2 NLM
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| 650 |
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7 |
|a Ubiquitin
|2 NLM
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| 650 |
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7 |
|a PI16 protein, human
|2 NLM
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| 650 |
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7 |
|a protease inhibitor 16, mouse
|2 NLM
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| 650 |
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7 |
|a FOXP3 protein, human
|2 NLM
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| 650 |
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7 |
|a Bmi1 protein, mouse
|2 NLM
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| 650 |
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7 |
|a BMI1 protein, human
|2 NLM
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| 700 |
1 |
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|a Gu, Xin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Lin, Shiyu
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wu, Qin
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sun, Yuankai
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Zhang, Qian
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Luo, Aishu
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Feng, Xiaoke
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Lei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Xu, Lingxiao
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Sun, Wei
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Tan, Wenfeng
|e verfasserin
|4 aut
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| 773 |
0 |
8 |
|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 259(2024) vom: 01. Feb., Seite 109883
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
1 |
8 |
|g volume:259
|g year:2024
|g day:01
|g month:02
|g pages:109883
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| 856 |
4 |
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|u http://dx.doi.org/10.1016/j.clim.2023.109883
|3 Volltext
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|a GBV_ILN_11
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|a GBV_ILN_24
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|a GBV_ILN_350
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|a AR
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| 952 |
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|d 259
|j 2024
|b 01
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|h 109883
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