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Over-expression of the transcription factor ARID3A (Bright)

ABSTRACT: Retroviral contructs containing the full-length murine ARID3A (aka Bright) gene and a GFP gene or the GFP gene alone were used to electroporate the human RAJI B cell line. GFP positive cells were sorted and expanded in vitro. Differences in gene expression between the constructs were identified.

ORGANISM(S): Homo sapiens

PROVIDER: GSE33777 | GEO | 2013/11/15

SECONDARY ACCESSION(S): PRJNA148597

REPOSITORIES: GEO

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Over-expression of the transcription factor ARID3A (Bright)

Project description:Retroviral contructs containing the full-length murine ARID3A (aka Bright) gene and a GFP gene or the GFP gene alone were used to electroporate the human RAJI B cell line. GFP positive cells were sorted and expanded in vitro. Differences in gene expression between the constructs were identified. Total RNA was isolated from 4 independent cell culture replicates of each retroviral construct.

2013-11-15 | E-GEOD-33777 | biostudies-arrayexpress

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Loss of Bright/Arid3A reprograms MEFs to a pluripotent state

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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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