Over-expression of the transcription factor ARID3A (Bright)
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Bart Frank
PROVIDER: E-GEOD-33777 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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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.
2013-11-15 | GSE33777 | GEO
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Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a ChIP was performed using bioChIP-sequencing. Control ChIP-sequencing was performed using BirA cells. HDAC1 ChIP was performed as native antibody ChIP-sequencing.
2014-10-16 | E-GEOD-56876 | biostudies-arrayexpress
Project description:Arid3a, a transcription factor known for its requirement in B-lymphocyte development, has been recently identified as a member of ES cell pluripotency network. Arid3a is moderately expressed in ES cells, and its expression is gradually increased during differentiation. Since Arid3a shows the highest expression in placenta, we hypothesized that Arid3a may play important roles in TE development. We report that Arid3a is a central regulator of both TE-specific and pluripotency-associated gene expression during ES cell differentiation. While dispensable for self-renewal, we observed that knockdown of Arid3a delays differentiation of ES cells. Induction of Arid3a leads ES cells to promote differentiation, specifically towards TE lineage. Moreover, these Arid3a-overexpressing cells maintained in TE culture media are sufficient to generate functional trophoblast stem-like cells, suggesting roles of Arid3a in TE differentiation. By integrative analyses using the chromosomal targets of Arid3a with expression profiling, we revealed the dual roles of Arid3a, as a direct activator of TE-specific genes and a repressor of pluripotency-associated genes. We further revealed the repressive roles of Arid3a are mediated by histone deacetylases (HDACs). Taken together, our results demonstrate that Arid3a is a critical novel regulator in TE lineage specification. Arid3a overexpression and Arid3a knockdown Total RNA was isolated from cultured cells using RNeasy plus mini kit (Qiagen). cDNA were synthesized and labelled, followed by hybridization on Affymetrix GeneChip mouse genome 430A 2.0 arrays.
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Project description:Transcriptomic characterization of ABCD2 KO mice to fibrate treatment in liver tissue, 3 months of age ABCD2 KO and age-matched WT mice were administered fenofibrate (100 mg/kg/day) for 14 days.
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Project description:Methyl-seq data was obtained from total peripheral blood mononuclear cells of two patients with systemic lupus erythematosus who were characterized as having>2 standard deviations more ARID3a-expressing B lymphocytes than healthy controls. Similarly, methyl-seq data was also obtained from two SLE patient samples with normal (low) numbers of ARID3-expressing B lymphocytes. Our previous studies showed that increased ARID3a expression in B lymphocytes was associated increased disease activity. Data were generated on an Illumina Hiseq 2000 with paired-end 100bp reads and quality control metrics were assessed with Picard tools. Methylation profiles of genomic DNA from four SLE patient PBMC samples, two with high numbers of ARID3a expressing B cells (ARID3aH) versus two with normal numbers of ARID3a+ B cells (ARID3aN), were generated on an Illumina Hiseq 2000 with paired-end 100bp reads.
2016-08-19 | E-GEOD-84965 | biostudies-arrayexpress
Project description:Eight different types of sample (three samples each) were used in this study of cardiac cell migration in the tunicate Ciona intestinalis. The B7.5 lineage cells were isolated by Fluorescent Activated Cell Sorting (FACS) at the tailbud stage, when the cardiac precursors (anterior B7.5 lineage cells) are migrating into the trunk, while their sister cells (posterior 7.5 lineage cells) remain in the tail, where they form muscle cells. Cells were sorted at the late gastrula stage, prior to migration induction and after manipulation of the FGF-MAPK-Ets signaling pathway (targeted expression of dominant negative FGF receptor and Ets:VP16 fusion protein, targeted expression was achieved using the Mesp cis-regulatory DNA), FoxF function (a direct target of FGF-MAPK-Ets signaling, required primarily for cell migration) by targeted expression of FoxF:VP16 (constitutive activator) or FoxF:WRPW (constitutive repressor, dominant negative), Mesp function (over-expression of Mesp:VP16 inhibits primarily cell migration). Finally, the "whole embryo" samples were collected from dissociated whole tailbud embryos, without FACS. in summary the eight conditions are: "wt (files LC-wt-1,-2,-3)": wild_type B7.5 lineage cells, expressing GFP, sorted at the tailbud stage "Ets:VP16 (files LC-EV-1,-2,-3)": B7.5 lineage cells, expressing GFP and Ets:VP16, sorted at the tailbud stage "DnFGFR (files LC-dnFGFR-1,-2,-3)": B7.5 lineage cells, expressing GFP and dominant-negative FGF receptor, sorted at the tailbud stage. "FoxF:VP16 (files LC-FV-1,-2,-3)": B7.5 lineage cells, expressing GFP and FoxF:VP16, sorted at the tailbud stage. "FoxF:WRPW (files LC-FW-1,-2,-3)": B7.5 lineage cells, expressing GFP and FoxF:WRPW, sorted at the tailbud stage". "Mesp:VP16 (files LC-MV-1,-2,-3)": B7.5 lineage cells, expressing GFP and Mesp:VP16, sorted at the tailbud stage. "Late Gastrula (files LC-LG-1,-2,-3)": wild_type B7.5 lineage cells, expressing GFP, sorted at the late gastrula stage "whole embryo (files LC-whole-1,-2,-3": whole embryos, dissociated at the tailbud stage, not sorted.
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2014-04-16 | E-GEOD-37473 | biostudies-arrayexpress
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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