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GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3 overexpression]

ABSTRACT: GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3 overexpression]

PROVIDER: PRJNA475906 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7305530_1.fastq.gz	Fastqsanger.gz
	SRR7305530_2.fastq.gz	Fastqsanger.gz
	SRR7305531_1.fastq.gz	Fastqsanger.gz
	SRR7305531_2.fastq.gz	Fastqsanger.gz
	SRR7305532_1.fastq.gz	Fastqsanger.gz

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GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3-GFP]

Project description:GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3-GFP]

| PRJNA475908 | ENA

GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion

Project description:GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion

| PRJNA475904 | ENA

GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3 overexpression]

Project description:RNA-seq in DN3a stage thymocytes isolated from wild type and GATA3 overexpression Tg mouse

2018-06-14 | GSE115743 | GEO

GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion [GATA3-GFP]

Project description:RNA-seq in GFP-positive and GFP-negative DN4 stage thymocytes isolated from GATA3-GFP fusion protein knock-in mouse

2018-06-14 | GSE115740 | GEO

GATA3 Abundance Is a Critical Determinant of T Cell Receptor β Allelic Exclusion.

Project description:Allelic exclusion describes the essential immunological process by which feedback repression of sequential DNA rearrangements ensures that only one autosome expresses a functional T or B cell receptor. In wild-type mammals, approximately 60% of cells have recombined the DNA of one T cell receptor β (TCRβ) V-to-DJ-joined allele in a functional configuration, while the second allele has recombined only the DJ sequences; the other 40% of cells have recombined the V to the DJ segments on both alleles, with only one of the two alleles predicting a functional TCRβ protein. Here we report that the transgenic overexpression of GATA3 leads predominantly to biallelic TCRβ gene (Tcrb) recombination. We also found that wild-type immature thymocytes can be separated into distinct populations based on intracellular GATA3 expression and that GATA3LO cells had almost exclusively recombined only one Tcrb locus (that predicted a functional receptor sequence), while GATA3HI cells had uniformly recombined both Tcrb alleles (one predicting a functional and the other predicting a nonfunctional rearrangement). These data show that GATA3 abundance regulates the recombination propensity at the Tcrb locus and provide new mechanistic insight into the historic immunological conundrum for how Tcrb allelic exclusion is mediated.

| S-EPMC5452726 | biostudies-literature

GATA3 abundance is a critical determinant of T cell receptor beta allelic exclusion

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

2018-06-14 | GSE115745 | GEO

The master male sex determinant Gdf6Y of the turquoise killifish arose through allelic neofunctionalization

Project description:The master male sex determinant Gdf6Y of the turquoise killifish arose through allelic neofunctionalization

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The master male sex determinant Gdf6Y of the turquoise killifish arose through allelic neofunctionalization [Human]

Project description:The master male sex determinant Gdf6Y of the turquoise killifish arose through allelic neofunctionalization [Human]

| PRJNA979165 | ENA

The master male sex determinant Gdf6Y of the turquoise killifish arose through allelic neofunctionalization [Mouse]

Project description:The master male sex determinant Gdf6Y of the turquoise killifish arose through allelic neofunctionalization [Mouse]

| PRJNA979170 | ENA

The¬¬¬ androgen receptor interacts with GATA3 to transcriptionally regulate a luminal epithelial cell phenotype in breast cancer

Project description:Background: The androgen receptor (AR) is a tumor suppressor in estrogen receptor (ER) positive breast cancer, a role sustained in some ER negative breast cancers. Key factors dictating AR genomic activity in a breast context are largely unknown. Herein, we employed an unbiased chromatin immunoprecipitation-based proteomic technique to identify endogenous AR interacting co-regulatory proteins in ER positive and negative models of breast cancer to gain new insight into mechanisms of AR signaling in this disease. Results: The DNA-binding factor GATA3 is identified and validated as a novel AR interacting protein in breast cancer cells irrespective of ER status. AR activation by the natural ligand 5α-dihydrotestosterone (DHT) increases nuclear AR-GATA3 interactions, resulting in AR-dependent enrichment of GATA3 chromatin binding at a sub-set of genomic loci. Silencing GATA3 reduces but does not prevent AR DNA binding and transactivation of genes associated with AR/GATA3 co-occupied loci, indicating a co-regulatory role for GATA3 in AR signaling. DHT-induced AR/GATA3 binding coincides with upregulation of luminal differentiation genes, including EHF and KDM4B, established master regulators of a breast epithelial cell lineage. These findings are validated in a patient-derived xenograft model of breast cancer. Interaction between AR and GATA3 is also associated with AR-mediated growth inhibition in ER positive and ER negative breast cancer.

2024-01-30 | PXD047997 | Pride

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