Anti-ARID5B monoclonal antibody (DCABH-707)

Mouse anti-Human ARID5B monoclonal antibody for ELISA, sELISA Datasheet

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Specifications


Host Species
Mouse
Antibody Isotype
IgG2a
Species Reactivity
Human
Immunogen
Recombinant fragment, corresponding to amino acids 1483-1583 of Human ARID5B with a proprietary tag (XP_084482.3).
Conjugate
Unconjugated

Applications


Application Notes
Sandwich ELISA: 10 μg/ml.
*Suggested working dilutions are given as a guide only. It is recommended that the user titrates the product for use in their own experiment using appropriate negative and positive controls.

Target


Alternative Names
ARID5B; AT rich interactive domain 5B (MRF1-like); AT-rich interactive domain-containing protein 5B; FLJ21150; MRF2; MRF1-like protein
Entrez Gene ID
UniProt ID

Product Background


Gene summary
ARID5B (AT-Rich Interaction Domain 5B) is a Protein Coding gene. Diseases associated with ARID5B include lymphoblastic leukemia and childhood leukemia. Among its related pathways are Chromatin organization and Activated PKN1 stimulates transcription of AR (androgen receptor) regulated genes KLK2 and KLK3. 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 ARID5A. 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.
Antigen Description
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. Leukemia, acute lymphoblastic (ALL) [MIM:613065]: A subtype of acute leukemia, a cancer of the white blood cells. ALL is a malignant disease of bone marrow and the most common malignancy diagnosed in children. The malignant cells are lymphoid precursor cells (lymphoblasts) that are arrested in an early stage of development. The lymphoblasts replace the normal marrow elements, resulting in a marked decrease in the production of normal blood cells. Consequently, anemia, thrombocytopenia, and neutropenia occur to varying degrees. The lymphoblasts also proliferate in organs other than the marrow, particularly the liver, spleen, and lymphonodes. Note=Disease susceptibility is associated with variations affecting the gene represented in this entry. Note=Defects in ARID5B may be a cause of susceptibility to coronary atherosclerosis in the Japanese population. AT-rich interactive domain-containing protein 5B is a protein that in humans is encoded by the ARID5B gene. 0The function about ARID5B antigen include DNA binding; protein binding; contributes_to transcription coactivator activity; transcription regulatory region DNA binding.

Citations


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References


Suzuki, T; Ikari, K; et al. PADI4 and HLA-DRB1 Are Genetic Risks for Radiographic Progression in RA Patients, Independent of ACPA Status: Results from the IORRA Cohort Study. PLOS ONE 8:-(2013).

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