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RORα is critical for mTORC1 activity in T cell-mediated colitis.

ABSTRACT: RORα is critical for mTORC1 activity in T cell-mediated colitis.

PROVIDER: PRJNA706568 | ENA |

REPOSITORIES: ENA

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RORα is critical for mTORC1 activity in T cell-mediated colitis [ChIP-seq]

Project description:Inflammatory bowel disease (IBD) is multi-factorial chronic intestinal inflammation driven by pathogenic T cells. The mechanisms underlying colitis pathogenicity and anti-TNF therapy resistance are not fully understood. Here we demonstrate that RORα is highly expressed in active UC patients, particularly in those non-responsive to anti-TNF treatment. Rorα deficient CD4+ T cells could not induce severe gut inflammation in a T cell transfer colitis model. Mechanistically, RORα regulated T cell infiltration in colon by promoting T cell migration and inhibiting T cell apoptosis. Meanwhile, genome-wide occupancy and transcriptome analysis revealed that RORα promoted mTORC1 activation. mTORC1 signaling, also hyperactivated in active UC patients, was necessary for T cell-mediated colitis.

2021-07-28 | GSE168217 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [RNA-seq]

2021-07-28 | GSE168216 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [16S rRNA-seq]

2021-07-28 | GSE168218 | GEO

RORα is critical for mTORC1 activity in T cell-mediated colitis [ChIP-seq]

Project description:RORα is critical for mTORC1 activity in T cell-mediated colitis [ChIP-seq]

| PRJNA706572 | ENA

RORα is critical for mTORC1 activity in T cell-mediated colitis [RNA-seq]

Project description:RORα is critical for mTORC1 activity in T cell-mediated colitis [RNA-seq]

| PRJNA706573 | ENA

RORα is critical for mTORC1 activity in T cell-mediated colitis [16S rRNA-seq]

Project description:RORα is critical for mTORC1 activity in T cell-mediated colitis [16S rRNA-seq]

| PRJNA706571 | ENA

RORα is critical for mTORC1 activity in T cell-mediated colitis.

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-07-28 | GSE168219 | GEO

Screen mRNAs specifically regulated by mTORC1 in colon epithelial cells from mice with dextran sulfate sodium (DSS)-induced experimental colitis

Project description:To screen mRNAs specifically regulated by mTORC1, a global mRNA expression profile in colon epithelial cells (CECs) from mice with or without CECs-specific TSC1 knockout (KO) was developed using microarray. Wile-type or CECs-specific TSC1 KO mice with experimental colitis were sacrificed, with CECs harvested and subjected to total RNA extraction.

2015-11-05 | E-GEOD-74674 | biostudies-arrayexpress

Transcription profiling by array of mouse immortalized embryonic fibroblasts to identify genes regulated by mTORC1

Project description:Mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a critical regulator of cell growth by integrating multiple signals (nutrients, growth factors, energy and stress) and is frequently deregulated in many types of cancer. We used a robust experimental paradigm involving the combination of two interventions, one genetic and one pharmacologic to identify genes regulated transcriptionally by mTORC1. In Tsc2+/+, but not Tsc2-/- immortalized mouse embryo fibroblasts (MEFs), serum deprivation downregulates mTORC1 activity. In Tsc2-/- cells, abnormal mTORC1 activity can be downregulated by treatment with rapamycin (sirolimus). By contrast, rapamycin has little effect on mTORC1 in Tsc2+/+ cells in which mTORC1 is already inhibited by low serum. Thus, under serum deprived conditions, mTORC1 activity is low in Tsc2+/+ cells (untreated or rapamycin treated), high in Tsc2-/- cells, but lowered by rapamycin; a pattern referred to as a M-^Slow/low/high/lowM-^T or M-^SLLHLM-^T, which allowed the identification of genes regulated by mTORC1 by performing the appropriate comparisons

2011-08-02 | E-GEOD-27982 | biostudies-arrayexpress

Identification of Tfeb-dependent genes downstream of mTORC1 in MEFs

Project description:Mammalian target of rapamycin (mTOR) complex 1 (mTORC1) is a critical regulator of cell growth by integrating multiple signals (nutrients, growth factors, energy and stress) and is frequently deregulated in many types of cancer. We used a robust experimental paradigm involving the combination of two interventions, one genetic and one pharmacologic to identify genes regulated transcriptionally by mTORC1. In Tsc2+/+, but not Tsc2-/- immortalized mouse embryo fibroblasts (MEFs), serum deprivation downregulates mTORC1 activity. In Tsc2-/- cells, abnormal mTORC1 activity can be downregulated by treatment with rapamycin (sirolimus). By contrast, rapamycin has little effect on mTORC1 in Tsc2+/+ cells in which mTORC1 is already inhibited by low serum. Thus, under serum deprived conditions, mTORC1 activity is low in Tsc2+/+ cells (untreated or rapamycin treated), high in Tsc2-/- cells, but lowered by rapamycin; a pattern referred to as a M-bM-^@M-^\low/low/high/lowM-bM-^@M-^] or M-bM-^@M-^\LLHLM-bM-^@M-^]. We found that mTORC1 regulated the expression of, among other lysosomal genes, V-ATPases through the transcription factor EB (TFEB, Tcfeb in the mouse). The knockdown of Tfeb resulted in the 'flattening' of the LLHL pattern and allowed the identification of genes regulated by mTORC1 through Tfeb Mouse embryo fibroblasts (MEFs) wild type or deficient in Tsc2 expressing a Tfeb shRNA or scrambled shRNA vector were treated with 25 nM rapamycin or vehicle (methanol) for 24 h under low serum conditions (0.1% FBS)

2011-08-02 | E-GEOD-28021 | biostudies-arrayexpress

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