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ARID3a is Required for Erythrocyte Lineage Differentiation of Hemin Stimulated Human K562 Cells

ABSTRACT: ARID3a is Required for Erythrocyte Lineage Differentiation of Hemin Stimulated Human K562 Cells

PROVIDER: PRJNA544276 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9109410_1.fastq.gz	Fastqsanger.gz
	SRR9109410_2.fastq.gz	Fastqsanger.gz
	SRR9109420_1.fastq.gz	Fastqsanger.gz
	SRR9109420_2.fastq.gz	Fastqsanger.gz
	SRR9109430_1.fastq.gz	Fastqsanger.gz

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ARID3a is Required for Erythrocyte Lineage Differentiation of Hemin Stimulated Human K562 Cells

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ChIP-chip from 48h hemin induced K562 cells with GATA-1, EKLF, and NF-E2 antibodies

Project description:The transcription factor GATA-1, EKLF and NF-E2 promotes erythroid differentition by regulating their target genes, however, the intricate interplays between these key TFs and microRNA genes are largely unknown. Chromatin immunoprecipitation (ChIP) of GATA-1, EKLF and NF-E2 together with microRNA genomic promoter profiling by ChIP-on-chip analysis demonstrated that GATA-1, EKLF and NF-E2 collaborately regulate a series of microRNA genes. Comparison of microRNA promoter arrays of GATA-1 VS EKLF VS NF-E2 in K562 cells suffering with hemin induced erythroid differentiation

2011-12-31 | E-GEOD-30808 | biostudies-arrayexpress

Expression profile of hemin induced erythroid differentiation, over-expressing and knocking-down GATA-1, EKLF and NF-E2 in K562s

Project description:we profiled miRNA gene expression with the Illumina hybridization system in K562 cells induced by hemin and K562 cells with over-expressing or knocking-down GATA-1, EKLF or NF-E2 treatments. To find differential expression miRNAs, we profiled miRNA gene expression with the Illumina hybridization system in untreated, hemin-treated 48h and 72h K562 cells. To define GATA-1, EKLF or NF-E2 directly targeted miRNA genes, a comprehensive analysis of TF induced miRNA gene expression changes was performed using over-expressing or knocking-down TFs in K562 cells and illumina miRNA profiling Beadchip system.

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Hemin timecourse 0-72h

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CMK LC-MS/MS after CoIP of ARID3A

Project description:In order to determine proteins interacting with ARID3A in the ML-DS cell line CMK, we performed CoIP of endogenous ARID3A followed by LC-MS/MS

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Arid3a is required for mammalian placenta development

Project description:Previous studies in the mouse indicated that Arid3a plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that Arid3a is widely expressed during mouse and human placentation and essential for early embryonic viability. Arid3a is located within trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with sever defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in inflammatory response-related genes, cytokines and chemokines. We provide evidence that BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent (iPS) stem cells results in ARID3A upregulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in human iPS and BMP4-mediated TS-like cells up-regulated TE markers, whereas pluripotent markers were down-regulated. Our results indicate that the roles of Arid3a are conserved and essential for mammalian placental development through regulation of both intrinsic and extrinsic developmental programs. Placentas of E10.5 and E11.5 wild type (WT) and Arid3a-/- mice were generated by deep sequencing, using Illumina

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