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A lack of MHC-II expression results in a severe immunodeficiency syndrome called MHC-II deficiency, or the bare lymphocyte syndrome (BLS\; MIM 209920). Additionally we are shipping RFX5 Antibodies (97) and many more products for this protein.
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Data show arginine methyltransferase PRMT6 (show PRMT6 Proteins) methylates the AT-hook motif of regulatory factor RFX5 and downregulates HLA-DQ expression.
these data have identified as novel pathway whereby SIRT1 (show SIRT1 Proteins) maintains COL1A2 (show COL1A2 Proteins) synthesis in SMCs by modulating RFX5 activity.
RFXAP (show RFXAP Proteins)(C) consists of two alpha-helices that form a V-shaped structure that packs within the RFX5(N)(2) staple.
interaction at COL1A2 (show COL1A2 Proteins) start site and transcription repression
The mutation for the fifth Bbare lymphocyte syndrome complementation group was found in RFX5 and was mapped to one of the arginines in a DNA-binding surface of this protein. Its wild-type counterpart restored function.
RFX5 binds to the collagen transcription start site and represses collagen gene expression
The identification of nuclear import and export sites on RFX molecules provides potential targets to modulate MHC class II expression.
results demonstrate that RFX1 (show RFX1 Proteins) and RFX5 differentially interact with class I HDACs underlying the different pathways when repressing collagen synthesis
PPARgamma (show PPARG Proteins) is within the RFX5.CIITA (show CIITA Proteins) complex as judged by co-immunoprecipitation and DNA affinity precipitation studies
RFXAP (show RFXAP Proteins) and RFXB (show RFXANK Proteins) have roles in relieving autoinhibition of RFX5
TSA (show PRDX2 Proteins) treatment enhances the association of CIITA (show CIITA Proteins) with the transcription factor RFX5, which ameliorates the down-regulation of CIITA (show CIITA Proteins) recruitment to target promoters by HDAC2 (show HDAC2 Proteins).
A lack of MHC-II expression results in a severe immunodeficiency syndrome called MHC-II deficiency, or the bare lymphocyte syndrome (BLS\; MIM 209920). At least 4 complementation groups have been identified in B-cell lines established from patients with BLS. The molecular defects in complementation groups B, C, and D all lead to a deficiency in RFX, a nuclear protein complex that binds to the X box of MHC-II promoters. The lack of RFX binding activity in complementation group C results from mutations in the RFX5 gene encoding the 75-kD subunit of RFX (Steimle et al., 1995). RFX5 is the fifth member of the growing family of DNA-binding proteins sharing a novel and highly characteristic DNA-binding domain called the RFX motif. Multiple alternatively spliced transcript variants have been found but the full-length natures of only two have been determined.
DNA-binding protein RFX5
, regulatory factor X 5
, DNA-binding protein Rfx5
, regulatory factor X, 5
, regulator factor X 5