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Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function [ATAC-seq]

ABSTRACT: Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function [ATAC-seq]

PROVIDER: PRJNA713901 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13945360.fastq.gz	Fastqsanger.gz
	SRR13945360_1.fastq.gz	Fastqsanger.gz
	SRR13945360_2.fastq.gz	Fastqsanger.gz
	SRR13945361_1.fastq.gz	Fastqsanger.gz
	SRR13945361_2.fastq.gz	Fastqsanger.gz

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Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function [RNA-seq]

Project description:The transcription factor ThPOK is critical for homeostasis and differentiation of mature T helper cells. Overall goal of this experiment is to show divergent gene expression profiles of ThPOK-dependent autoregulatory loop disrupted in CD4 T cells.

2021-04-05 | GSE168770 | GEO

Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function [ATAC-seq]

Project description:The transcription factor ThPOK is critical for homeostasis and differentiation of mature T helper cells. Overall goal of this experiment is to show divergent Chromatin pattern of ThPOK-dependent autoregulatory loop disrupted in CD4 T cells compared to WT.

2021-04-05 | GSE168771 | GEO

Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function

Project description:Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function

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Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function [RNA-seq]

Project description:Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function [RNA-seq]

| PRJNA713902 | ENA

Essential role of a ThPOK autoregulatory loop in the maintenance of mature CD4<sup>+</sup> T cell identity and function.

Project description:The transcription factor ThPOK (encoded by the Zbtb7b gene) controls homeostasis and differentiation of mature helper T cells, while opposing their differentiation to CD4+ intraepithelial lymphocytes (IELs) in the intestinal mucosa. Thus CD4 IEL differentiation requires ThPOK transcriptional repression via reactivation of the ThPOK transcriptional silencer element (SilThPOK). In the present study, we describe a new autoregulatory loop whereby ThPOK binds to the SilThPOK to maintain its own long-term expression in CD4 T cells. Disruption of this loop in vivo prevents persistent ThPOK expression, leads to genome-wide changes in chromatin accessibility and derepresses the colonic regulatory T (Treg) cell gene expression signature. This promotes selective differentiation of naive CD4 T cells into GITRloPD-1loCD25lo (Triplelo) Treg cells and conversion to CD4+ IELs in the gut, thereby providing dominant protection from colitis. Hence, the ThPOK autoregulatory loop represents a key mechanism to physiologically control ThPOK expression and T cell differentiation in the gut, with potential therapeutic relevance.

| S-EPMC8887595 | biostudies-literature

Essential role of ThPOK autoregulatory loop in maintenance of mature CD4 T cell identity and function

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

2021-04-05 | GSE168772 | GEO

Gene Expression in Effector T cells, wildtype of Thpok-deficient

Project description:The transcription factor Thpok is essential for CD4 T cell development in the thymus and remains expressed in post-thymic CD4 T cells. We post-thymically inactivated Thpok and compared microarray gene expression in Thpok-deficient CD4 T cells to that in their wildtype CD4 or CD8 counterparts We show that Thpok constrains the transcriptional circuitry to maintain CD4+-lineage integrity in naM-CM-/ve cells and to couple effector differentiation to environmental cues after antigenic stimulation. Redundantly with the related factor LRF, Thpok is continuously needed to prevent the trans-differentiation of mature CD4+ into -CD8+ T cells. We activated naM-CM-/ve CD4 T cells (either wild-type or Thpok-deficient) and CD8 T cells (wild-type) in vitro under Th1 conditions. Differentiated effectors were sorted 4 days after activation into CD4+CD8- and CD4-CD8+ (wild-type) and CD4+CD8- and CD4+CD8+ (Thpok-deficient) subsets. Total RNA was extracted from sorted subsets and processed for microarray analyses (Affymetrix Mouse Exon 1.0 ST array) at the NCI microarray facility, following the manufacturerM-bM-^@M-^Ys recommendation. Data is from 3 replicates (except wild-type CD4-CD8+ cells, for which two samples only were processed), generated from two distinct cell preparations.

2014-08-15 | E-GEOD-57846 | biostudies-arrayexpress

Gene expression in MHCII restricted mature thymocytes from Thpok-RKF- or Thpok-RKF+ Thpokfl/flRunx3fl/dYFPCd4-Cre+ mixed Bone marrow chimera.

Project description:Thpok-RKF which harbors a mutation in the BTB domain and disrupts the interaction between NuRD complex could not repress CD8 and CD8 lineage genes expression in Thpokfl/flRunx3fl/dYFPCd4-Cre+ from B2m-/- host. However, Thpok-RKF upregulates CD4 expression in these mice.

2022-06-10 | GSE185217 | GEO

Gene Expression in Effector T cells, wildtype of Thpok-deficient

2014-08-15 | GSE57846 | GEO

Genome wide screen of estrogen receptor Î± regulated microRNAs reveals a negative autoregulatory feedback loop

Project description:Estrogen receptor alpha (ERÎ±) is a nuclear receptor linked to progression of the majority of human breast cancers. Following activation ERÎ± regulates the transcription of target genes via DNA binding. Through a genome wide approach we have identified a subset of microRNAs (miRNAs or miRs) modulated by ERÎ±. Among them, miRNAs encoded from 2 paralogous clusters, miR-17-92 and miR-106a-363, were up-regulated. In addition, increased expression of miR-424, miR-542-3p and miR-450, located within the same genomic region and down-regulation of miR-181 family members were observed during the estrogenic response. We observed that ERÎ± alone is sufficient for sustained transcription of miR-17-92 and we show that levels of this cluster increase earlier than miRNAs encoded by it, implicating post-transcriptional regulation. Since miR-17-92 a pri-miRNA, is immediately cleaved by DROSHA to pre-miR-18a, this regulation occurs during the formation of the mature molecule from the precursor. Moreover, pre-miR-18a was significantly up-regulated in ERÎ±-positive breast cancers compared to ERÎ±-negative breast cancers. We also demonstrate that the miRNAs belonging to these paralogous clusters target and down-regulate ERÎ±, while a subset of cluster-derived miRNAs inhibit protein translation of its major oncogenic transcriptional p160 co-activator by targeting AIB1 revealing a negative autoregulatory feedback loop. This pathway adds to the highly regulated cellular response to estrogen that fine tunes ERÎ± transcriptional activity and cell proliferation. 4 time points (0hr,3hr,6hr,12hr) and 4 treatments (TO,JP,TO+TET,JP13+TET) x 3 biological replicates of each condition = 24 arrays

2010-06-25 | E-GEOD-14685 | biostudies-arrayexpress

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