Aliases for ARID5B Gene
External Ids for ARID5B Gene
Previous GeneCards Identifiers for ARID5B Gene
This gene encodes a member of the AT-rich interaction domain (ARID) family of DNA binding proteins. The encoded protein forms a histone H3K9Me2 demethylase complex with PHD finger protein 2 and regulates the transcription of target genes involved in adipogenesis and liver development. This gene also plays a role in cell growth and differentiation of B-lymphocyte progenitors, and single nucleotide polymorphisms in this gene are associated with acute lymphoblastic leukemia. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Sep 2011]
GeneCards Summary for ARID5B Gene
ARID5B (AT Rich Interactive Domain 5B (MRF1-Like)) is a Protein Coding gene. Diseases associated with ARID5B include childhood leukemia and lymphoblastic leukemia. Among its related pathways are Chromatin organization and RNA Polymerase I Promoter Opening. GO annotations related to this gene include transcription coactivator activity and RNA polymerase II regulatory region sequence-specific DNA binding. An important paralog of this gene is ARID4A.
UniProtKB/Swiss-Prot for ARID5B Gene
Transcription coactivator that binds to the 5-AATA[CT]-3 core sequence and plays a key role in adipogenesis and liver development. Acts by forming a complex with phosphorylated PHF2, which mediates demethylation at Lys-336, leading to target the PHF2-ARID5B complex to target promoters, where PHF2 mediates demethylation of dimethylated Lys-9 of histone H3 (H3K9me2), followed by transcription activation of target genes. The PHF2-ARID5B complex acts as a coactivator of HNF4A in liver. Required for adipogenesis: regulates triglyceride metabolism in adipocytes by regulating expression of adipogenic genes. Overexpression leads to induction of smooth muscle marker genes, suggesting that it may also act as a regulator of smooth muscle cell differentiation and proliferation. Represses the cytomegalovirus enhancer.