Expression data of overexpression of ABF-1 in SKW cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE26583 | GEO | 2014/01/15
SECONDARY ACCESSION(S): PRJNA136473
REPOSITORIES: GEO
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Project description:ABF-1, a bHLH trancriptional repressor expresses in human activated B cells. Overexpression of ABF-1 in a SKW lymphoblastoid cells suppressed IgM production. We used cDNA microarray to identify genes under ABF-1 regulation. SKW cells ectopically expressed ABF-1-GFP or GFP were harvested for RNA extraction and array hybridization.
2014-01-15 | E-GEOD-26583 | biostudies-arrayexpress
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Project description:Cell-fate specification relies on a close cooperation of distinct transcription factors and their crosstalk with the epigenetic landscape during embryonic development. NeuroD1 is known to be essential for eliciting neurogenesis and is able to reprogram other cell types into neurons. Despite progress, its global impact on the epigenome and cooperativity with other transcription factors during neurogenesis remains unknown. Here we show that despite NeuroD1 binding and a gain of active chromatin, only sites that show high local density of adjacent bHLH motifs, higher minor groove width and propeller twist as well as enrichment of another novel bHLH motif were able to get transcriptionally induced. Transcription factor activity analysis on the epigenome timecourse following NeuroD1 induction further identified this bHLH factor among top factors that gained activity during this process. Importantly, this bHLH factor was induced simultaneously to NeuroD1 as cells transit from an apical to a basal progenitor state during cortical development. Moreover, this bHLH factor interacts with NeuroD1 and co-occupies NeuroD1 target distinct genomic regions. We further show that the loss of this bHLH factor during cortical development severely impairs neurogenesis. Our study not only reveals the mechanistic basis underlying a productive transcriptional response of NeuroD1 during neurogenesis but also identified a novel bHLH transcription factor that partners with NeuroD1 and plays a critical role during cortical development.
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Project description:Characteristic extinguishing of B-cell phenotype in cHL is believed to be a result of transcription factor network deregulation due to the overexpression of repressor proteins ID2 and ABF-1. KLF4 is a versatile transcription factor, participating in regulation of differentiation processes in various tissues. Epigenetic silencing of KLF4 in cHL hints that KLF4 is involved in the complex mechanism of extinguishing of B-cell phenotype in cHL. To clarify this issue we investigated transcriptome changes, induced by KLF4 activation in two cHL cell lines KM-H2 and L428.
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Project description:To determine the effect of the deletion of the trancriptional repressor Hypermethylated in cancer 1 (Hic1) on quiescence, adult mesenchymal progenitors (MPs) were isolated from skeletal muscle of both wild type mice and those conditionally deleted for Hic1 and profiled by RNA sequencing. Comparison to MPs activated by using a muscle injury model of the tibialis anterior muscle revealed similar pathways affected under both conditions, highlighting the role for Hic1 in maintaining the quiescent state of MPs
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Project description:Background: Setleis Syndrome (SS) is a rare focal facial dermal dysplasia frequently found in Puerto Ricans, presenting with bilateral temporal skin lesions, eyelash abnormalities and absent meibomian glands. SS is caused by homozygous mutations in the TWIST2 gene, which codes for a transcription factor of the bHLH family known to be involved in skin and facial development. Methods: We obtained gene expression profiles by microarray analyses from control and Setleis Syndrome patient primary skin fibroblast and lymphoblastoid cell lines. Results: Out of 983 differentially regulated genes in fibroblasts, 479 were down-regulated and 504 were up-regulated, while in lymphoblasts a greater number of differentially regulated genes (1248 down-regulated and 73 up-regulated) were found after microarray analysis. Real time PCR reactions confirmed altered expression of several differentially regulated genes. Conclusion: TWIST2 is described as a repressor, but expression profiling indicates it has a role in gene activation, as evidenced by the much higher proportion of down-regulated genes in cells from SS patients, including cytokine genes, in fibroblasts, the top three networks involved genes that function in Cancer, Nervous System Development and Function, Lipid Metabolism, Molecular Transport and Organismal Injury and Abnormalities. In Lymphoblastoid cells, the top three networks involved genes in Endocrine System Disorders, Cell Cycle, Cellular Assembly and Organization, Cardiovascular Disease and Developmental Disorders
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Project description:The mechanisms that activate some genes while silencing others are critical to ensure precision in lineage specification as multipotent progenitors become restricted in cell fate. During neurodevelopment, these mechanisms are required to generate the wide variety of neuronal subtypes found in the nervous system. Here we report interactions between basic helix-loop-helix (bHLH) transcriptional activators and the transcriptional repressor PRDM13 that are critical for these processes during specification of dorsal spinal cord neurons. PRDM13 inhibits gene expression programs for the excitatory neuronal lineages in the dorsal neural tube while also suppressing a battery of genes that determine ventral neural tube fates including Olig1, Olig2 and Prdm12. PRDM13 does this via recruitment to chromatin by multiple neural bHLH factors to restrict gene expression in specific neuronal lineages. Together these findings highlight the function of PRDM13 in repressing bHLH transcriptional activators that together are required to achieve precise neuronal specification during development.
2017-08-04 | GSE90936 | GEO
Project description:The mechanisms that activate some genes while silencing others are critical to ensure precision in lineage specification as multipotent progenitors become restricted in cell fate. During neurodevelopment, these mechanisms are required to generate the wide variety of neuronal subtypes found in the nervous system. Here we report interactions between basic helix-loop-helix (bHLH) transcriptional activators and the transcriptional repressor PRDM13 that are critical for these processes during specification of dorsal spinal cord neurons. PRDM13 inhibits gene expression programs for the excitatory neuronal lineages in the dorsal neural tube while also suppressing a battery of genes that determine ventral neural tube fates including Olig1, Olig2 and Prdm12. PRDM13 does this via recruitment to chromatin by multiple neural bHLH factors to restrict gene expression in specific neuronal lineages. Together these findings highlight the function of PRDM13 in repressing bHLH transcriptional activators that together are required to achieve precise neuronal specification during development.
2017-08-04 | GSE90937 | GEO
Project description:Analysis of IgM+CD27+ B cells in individuals with hepatitis C virus (HCV)-associated mixed cryoglobulinemia (MC). We have previously shown that HCV+MC+ individuals have clonal expansions of IgM+ memory B cells. This study aims to characterize differentially expressed genes in peripheral IgM+CD27+ B cells in HCV RNA+MC+ individuals, compared to HCV RNA+MC- subjects and HCV RNA- healthy controls. IgM+ B cells were isolated form donor PBMCs by immunomagnetic negative selection, and the CD27+ subset was further purified by positive selection. 2ng RNA was isolated from cells and amplified using the Nugen WT-Ovation Amplification Kit. cDNA was synthesized, biotin labeled, and hybridized to Illumina human v2 microarrays. Data were collected and analyzed with Illumina Genome Studio. Raw data were normalized by transforming measurements less than 0.01 to 0.01, normalizing per chip to the 50th percentile, and normalizing per gene to the median. Normalized data were then filtered to remove genes with control signals <170. Genes that were significantly upregulated in HCV RNA+MC+ vs HCV RNA+MC- subjects' IgM+CD27+ B cells were identified using a Welch t-test with p-calue cutoff 0.05 and Benjamini-Hochberg false discovery rate of 0.05. The resulting gene list was then filtered for genes showing >2-fold differential expression.
2009-10-01 | GSE18084 | GEO
Project description:The inhibitor of DNA-binding 3 (ID3) is a transcriptional repressor protein that limits the binding of basic helixÂÂloop-helix (bHLH) transcription factors to DNA. Preliminary results from our lab confirm that cellular depletion of ID3 is associated with an impaired DNA damage response. we hypothesize that ID3 has the potential to epigenetically affect DNA repair. This is based on our observation that upon cellular ID3 knockdown, a reduction of chromatin-bound H4K16ac and H3K36me3.
| EGAS00001004478 | EGA