Mouse Gene Set: ZHENG_FOXP3_TARGETS_IN_T_LYMPHOCYTE_DN

For the Human gene set with the same name, see ZHENG_FOXP3_TARGETS_IN_T_LYMPHOCYTE_DN

Standard name ZHENG_FOXP3_TARGETS_IN_T_LYMPHOCYTE_DN
Systematic name MM733
Brief description Genes with promoters bound by FOXP3 [GeneID=50943] and which are down-regulated only in mature (peripheral blood) 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 M2: 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: periphery only
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Source species Mus musculus
Contributed by Jessica Robertson (MSigDB Team)
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Version history 2022.1.Mm: First Introduced.

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