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ATF2 and ATF7 mediation of intestinal repair in murine colitis model

ABSTRACT: ATF2 and ATF7 mediation of intestinal repair in murine colitis model

PROVIDER: PRJNA595848 | ENA |

REPOSITORIES: ENA

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ATF2 and ATF7 mediation of intestinal repair in murine colitis model

Project description:AP1 transcription factor family members: activating transcription factor 2 (ATF2) and activating transcription factor 7 (ATF7) have highly redundant functions due to homology and hence overlapping DNA-binding sites. The role of these transcription factors in intestinal epithelial homeostasis and repair has not been critically examined. Here, by using an intestine-specific deletion of ATF2 combined with body wide deletion of ATF7 in mice we assess the role of these proteins during intestinal homeostasis and repair after inflammation.

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ATF2 and ATF7 Are Critical Mediators of Intestinal Epithelial Repair.

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ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (ChIP)

Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe 3,811 ATF7 binding sites in mouse peritoneal macrophages, and 95% of the ATF7 signals in wild-type macrophages are lost in ATF7 knockout macrophages. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory. This series contains one set of whole genome ChIP-chip data and 2 sets of promoter array ChIP-chip data. For all sample, we use three IP .CEL files and three WCE .CEL files (they are triplicated experiments) to make one profile.

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Project description:Activation transcription factor 2 (ATF2), a member of the ATF/CREB family of transcription factors, is implicated in a broad spectrum of cancer-related biological functions, such as cell proliferation, apoptosis and DNA repair. Growing evidence indicates ATF2 act as an oncogene or a tumor suppressor in different cancer types depending on its expression level and subcellular localization. In this study, RNA-seq and ChIP-seq were performed for identification of genome-wide DNA binding sites and potential transcription targets for ATF2.

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ATF7 mediates lipopolysaccharide-induced epigenetic changes in macrophages involved in innate immunological memory (expression)

Project description:Immunological memory is generally thought to be mediated exclusively by lymphocytes such as memory T and B cells. However, enhanced innate immune responses caused by a previous infection increase protection against reinfection suggesting the presence of innate immunological memory. Here, we describe expression profile of peritoneal macrophages from wild-type mice pre-administrated with TLR ligands or from ATF7 knockout mice. ATF7 suppresses a group of innate-immunity genes in macrophage by recruiting H3K9 dimethyltransferase G9a. TLR ligands induce ATF7 phosphorylation, leading to release of ATF7 from chromatin and reduction in H3K9me2 level. Partially disrupted chromatin structure and increased basal expression on target genes are maintained for a long period, increasing resistance pathogens. Therefore we speculate ATF7 is important factor in controlling innate immunological memory. This series contains seven sets of exression array data. For all sample, we use four CEL files generated by four biological-independent experiments.

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