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

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

PROVIDER: PRJNA475908 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7305540_1.fastq.gz	Fastqsanger.gz
	SRR7305540_2.fastq.gz	Fastqsanger.gz
	SRR7305541_1.fastq.gz	Fastqsanger.gz
	SRR7305541_2.fastq.gz	Fastqsanger.gz
	SRR7305542_1.fastq.gz	Fastqsanger.gz

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

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

| PRJNA475906 | 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-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 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 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

RNA-Seq of sorted E10.5 and E11.5 AGM cell populations from Gata3-GFP embryos

Project description:The aim of this study was to examine the whole transcriptome of pools of 20 cells of Gata3-expressing AGM subpopulations (haematopoietic [HC], mesenchymal [MC], sympathetic nervous system [SNS], and endothelial [EC]) and compare them to their non-Gata3 expressing counterparts

2020-05-25 | GSE114926 | GEO

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

GATA3 mutation disrupts functional network governed by Estrogen receptor, FOXA1 and GATA3

Project description:Estrogen Receptor (ER) is a steroid hormone receptor that regulates epithelial genes in breast cancer. ER forms a regulatory network with the other transcription factors, FOXA1 and GATA3. GATA3 is known to be capable of specifying chromatin localization of FOXA1 and ER. GATA3 has been identified as one of the most frequently mutated genes in breast cancer. However, how GATA3 mutations impact this transcriptional network is unknown. Here we investigate the function of one of the recurrent patient-derived GATA3 mutations (R330fs) for this regulatory network. Genomic analysis indicates that the R330fs mutant can disrupt the cooperative action of ER, FOXA1, and GATA3, and induce chromatin relocalization of these factors. Relocalizations of ER and FOXA1 are associated with altered chromatin architectures leading to differential gene expression in the GATA3 mutant cells. These results suggest the active role of GATA3 mutants in ER positive breast tumors.

2020-02-27 | GSE130703 | GEO

GATA3 siRNA in utricle sensory epithelia

Project description:The inner ear utilizes sensory hair cells as mechano-electric transducers for sensing sound and balance. In mammals, these hair cells lack the capacity for regeneration. Unlike mammals, hair cells from non-mammalian vertebrates, such as birds, can be regenerated throughout the life of the organism making them a useful model for studying inner ear genetics pathways. The zinc finger transcription factor GATA3 is required for inner ear development and mutations cause sensory neural deafness in humans. In the avian cochlea GATA3 is expressed throughout the sensory epithelia; however, expression is limited to the striola of the utricle. The striola corresponds to an abrupt change in morphologically distinct hair cell types and a 180Â° shift in hair cell orientation. We used 3 complimentary approaches to identify potential downstream targets of GATA3 in the avian utricle. Specifically we used microarray expression profiling of GATA3 knockdown by siRNA and GATA3 over-expression treatments as well as direct comparisons of GATA3 expressing cells from the striola and non GATA3 expressing cells from the extra-striola. Whole utricle specimens were treated with streptomycin for 24 hrs, rinsed and allowed to recover for an additional 24 hrs. Whole utricles were transfected with either GATA3 or GFP 21mer synthetic siRNAs for an additional 48 hrs and pure sensory epithelia were isolated. There are 2 biological samples and experiments include technical replicates as well as dye-switches for a total of 8 microarrays.

2010-06-24 | E-GEOD-14785 | biostudies-arrayexpress

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