ag-490 and Purpura--Thrombocytopenic--Idiopathic

The CD3. However, the molecular mechanisms mediating STAT5b-dependent Treg genes expression and Treg cell phenotype and function in autoimmune diseases are not well defined. Here, we report that the MKL-1 is a coactivator for the major Treg genes transcription factor STAT5b, which is required for human Treg cell phenotype and function. The N terminus of STAT5b, which contains a basic coiled-coil protein-protein interaction domain, binds the C-terminal activation domain of MKL-1 and enhances MKL-1 mediated transcriptional activation of Treg-specific, CArG containing promoters, including the Treg-specific genes Foxp3. Suppression of endogenous STAT5b expression by specific small interfering RNA attenuates MKL-1 transcriptional activation in cultured human cells. The STAT5b-MKL-1 interaction identifies a role of Treg-specific gene regulation and regulated mouse Treg cell development and function and suggests a possible mechanism for the protective effects of autoimmune disease Idiopathic Thrombocytopenic Purpura (ITP).. Our studies demonstrate for the first time that MKL-1 is a coactivator for STAT5b, the regulator of Treg cell development and function. Video abstract.

Topics: Amides; Base Sequence; Biomarkers; CD3 Complex; Cell Nucleus; Forkhead Transcription Factors; Humans; Interleukin-2; Interleukin-2 Receptor alpha Subunit; Janus Kinase 3; Lymphocyte Count; Phosphorylation; Promoter Regions, Genetic; Protein Binding; Protein Domains; Purpura, Thrombocytopenic, Idiopathic; Pyridines; rhoA GTP-Binding Protein; Serum Response Factor; Signal Transduction; STAT5 Transcription Factor; T-Lymphocytes, Regulatory; Trans-Activators; Tyrphostins