Human Gene Set: ZHENG_FOXP3_TARGETS_IN_THYMUS_UP

For the Mouse gene set with the same name, see ZHENG_FOXP3_TARGETS_IN_THYMUS_UP

Standard name ZHENG_FOXP3_TARGETS_IN_THYMUS_UP
Systematic name M1746
Brief description Genes with promoters bound by FOXP3 [GeneID=50943] and which are up-regulated only in developing (located in the thymus) regulatory CD4+ [GeneID=920] T lymphocytes.
Full description or abstract Transcription factor Foxp3 (forkhead box P3), restricted in its expression to a specialized regulatory CD4+ T-cell subset (T(R)) with a dedicated suppressor function, controls T(R) lineage development. In humans and mice, Foxp3 deficiency results in a paucity of T(R) cells and a fatal breach in immunological tolerance, causing highly aggressive multi-organ autoimmune pathology. Here, through genome-wide analysis combining chromatin immunoprecipitation with mouse genome tiling array profiling, we identify Foxp3 binding regions for approximately 700 genes and for an intergenically encoded microRNA. We find that a large number of Foxp3-bound genes are up- or downregulated in Foxp3+ T cells, suggesting that Foxp3 acts as both a transcriptional activator and repressor. Foxp3-mediated regulation unique to the thymus affects, among others, genes encoding nuclear factors that control gene expression and chromatin remodelling. In contrast, Foxp3 target genes shared by the thymic and peripheral T(R) cells encode primarily plasma membrane proteins, as well as cell signalling proteins. Together, our studies suggest that distinct transcriptional sub-programmes implemented by Foxp3 establish T(R) lineage during differentiation and its proliferative and functional competence in the periphery.
Collection C2: Curated
      CGP: Chemical and Genetic Perturbations
Source publication Pubmed 17237761   Authors: Zheng Y,Josefowicz SZ,Kas A,Chu TT,Gavin MA,Rudensky AY
Exact source Table 3S: thymus only
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Source species Mus musculus
Contributed by Jessica Robertson (MSigDB Team)
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identifier namespace		 MOUSE_GENE_SYMBOL
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Version history 3.1: First introduced

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