Chromatin function of IkBa: ChIP-on-chip of IkBa
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE24011 | GEO | 2013/08/28
SECONDARY ACCESSION(S): PRJNA130365
REPOSITORIES: GEO
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Project description:The Inhibitor of the NFkB, IkBa, is the main regulator of the NFkB pathway. Our data has demonstrated that there is an alternative function for IkBa in the chromatin that affects HOX and other developmental genes. Keywords: CHIP-chip Chip-on-chip analysis has demonstrated that IkBa associates to the promoters of several genes. Chromatin fragments were obtained from NIH-3T3 cells and precipitated with 3 different IkBa comercial antibodies (raised in mouse, goat and rabbit), and fold enrichment was compared to input.
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Project description:The activation of NFkB pathway is commonly observed in many neurodegenerative disease and contributes to the disease pathogenesis. However, with hundreds of target genes expressed in the brain, the mechanism of NFkB signaling transduction pathway is bearly understood. We were interested in revealing the downstream mediators of NFkB in the brain and chose the IkBa-dificient model as our tool. IkBa is the essential negative regulator of NFkB activity and deletioon of IkBa induced NFkB hyperactivation. We used Nestin-Cre to conditionally knockout IkBa in the brain cells of neural lineage and performed the microarray to give us candidate genes.
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Project description:The activation of NFkB pathway is commonly observed in many neurodegenerative disease and contributes to the disease pathogenesis. However, with hundreds of target genes expressed in the brain, the mechanism of NFkB signaling transduction pathway is bearly understood. We were interested in revealing the downstream mediators of NFkB in the brain and chose the IkBa-dificient model as our tool. IkBa is the essential negative regulator of NFkB activity and deletioon of IkBa induced NFkB hyperactivation. We used Nestin-Cre to conditionally knockout IkBa in the brain cells of neural lineage and performed the microarray to give us candidate genes. Mouse hippocampi were dissected from 3 pairs of 2-3 month old IkBa brain-specific knockout animals and their littermate controls and used for RNA extraction and subsequent microarray assay
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Project description:In human, the 39 coding HOX genes and 18 referenced non-coding antisense transcripts are arranged in four genomic clusters named HOXA, B, C, and D. This highly conserved family belongs to the homeobox class of genes that encode transcription factors required for normal development. Therefore, HOX gene deregulation might contribute to the development of many cancer types. Here, we study HOX gene deregulation in adult glioma, a common type of primary brain tumor. We performed extensive molecular analysis of tumor samples, classified according to their isocitrate dehydrogenase (IDH1) gene mutation status, and of glioma stem cells. We found widespread expression of sense and antisense HOX transcripts only in aggressive (IDHwt) glioma samples, although the four HOX clusters displayed DNA hypermethylation. Integrative analysis of expression-, DNA methylation- and histone modification signatures along the clusters revealed that HOX gene upregulation relies on canonical and alternative bivalent CpG island promoters that escape hypermethylation. H3K27me3 loss at these promoters emerges as the main cause of widespread HOX gene upregulation in IDHwt glioma cell lines and tumors. Our study provides the first comprehensive description of the epigenetic changes at HOX clusters and their contribution to the transcriptional changes observed in adult glioma. It also identified putative "master" HOX proteins that might contribute to the tumorigenic potential of glioma stem cells.
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Project description:Here, we demonstrate that IkBa displays a predominant and unique nuclear localization in normal basal keratinocytes. This nuclear IkBa binds the chromatin through direct interaction of the ankyrin repeats with histone H2A and associates with the promoter and regulatory regions of several developmental-related genes including HOXA10, HOXB2 and HOXB9. Most importantly, IkBa dictates the competence of these HOX genes to be activated upon TNFa stimulation.
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Project description:Chromatin function of IkBa: ChIP-on-chip of IkBa
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Project description:Here, we demonstrate that IkBa displays a predominant and unique nuclear localization in normal basal keratinocytes. This nuclear IkBa binds the chromatin through direct interaction of the ankyrin repeats with histone H2A and associates with the promoter and regulatory regions of several developmental-related genes including HOXA10, HOXB2 and HOXB9. Most importantly, IkBa dictates the competence of these HOX genes to be activated upon TNFa stimulation. Examination of IkBalpha location in keratinocyte cells
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