An LKB1-mitochondria axis controls Th17 effector function
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2022-10-21
相关数据集
Global gene-regulatory targets of FOSL1, FOSL2 and BATF in human Th17 cells [RNA-seq]. Global gene-regulatory targets of FOSL1, FOSL2 and BATF in human Th17 cells [RNA-seq]
The aim of this study was to investigate the transciptional mechanisms governed by FOSL1, FOSL2 and BATF for regulation of human Th17 cell-function. FOSL factors were transiently perturbed using RNAi
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Data_Sheet_4_Lnc-ITSN1-2, Derived From RNA Sequencing, Correlates With Increased Disease Risk, Activity and Promotes CD4+ T Cell Activation, Proliferation and Th1/Th17 Cell Differentiation by Serving as a ceRNA for IL-23R via Sponging miR-125a in Inflammatory Bowel Disease.zip
Background: This study aimed to investigate long-non-coding RNA (lncRNA) expression profiles and the correlation of lnc-ITSN1-2 expression with disease risk, activity and inflammation, and its influen
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Data_Sheet_3_Lnc-ITSN1-2, Derived From RNA Sequencing, Correlates With Increased Disease Risk, Activity and Promotes CD4+ T Cell Activation, Proliferation and Th1/Th17 Cell Differentiation by Serving as a ceRNA for IL-23R via Sponging miR-125a in Inflammatory Bowel Disease.zip
Background: This study aimed to investigate long-non-coding RNA (lncRNA) expression profiles and the correlation of lnc-ITSN1-2 expression with disease risk, activity and inflammation, and its influen
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Transcription factor TCF1 binds Rorgt and orchestrates a regulatory network that determines homeostatic Th17 cell state [ATAC-seq]. Transcription factor TCF1 binds Rorgt and orchestrates a regulatory network that determines homeostatic Th17 cell state [ATAC-seq]
CD4+ T helper 17 (Th17) cells encompass a spectrum of cell states including homeostatic cells that maintain physiological functions such as barrier integrity and pathogenic cells that drive autoimmune
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Distinctive CD39+CD9+ lung interstitial macrophages suppress IL-23/Th17-mediated neutrophilic asthma by inhibiting NETosis [bulk RNA-Seq]
IL-23-Th17 signaling axis is responsible for neutrophilic inflammation in various barrier tissues. However, mechanistic links between IL-23 and Th17 activation remain unclear, despite of their critica
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