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Mouse Anti-ARID5B Recombinant Antibody (1C2) (CBMAB-A3561-YC)


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Summary

Host Animal
Mouse
Specificity
Human
Clone
1C2
Antibody Isotype
IgG2a, κ
Application
ELISA

Basic Information

Immunogen
ARID5B (XP_084482, 1483-1582 aa) partial recombinant protein with GST tag.
Specificity
Human
Antibody Isotype
IgG2a, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.

Formulations & Storage [For reference only, actual COA shall prevail!]

Format
Liquid
Buffer
PBS, pH 7.4
Preservative
None
Concentration
Batch dependent
Storage
Store at 4°C short term (1-2 weeks). Aliquot and store at -20°C long term. Avoid repeated freeze/thaw cycles.
Epitope
aa 1483-1582

Target

Full Name
AT rich interactive domain 5B (MRF1-like)
Introduction
ARID5B is 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
Entrez Gene ID
84159
UniProt ID
Q14865
Alternative Names
AT-Rich Interaction Domain 5B; ARID Domain-Containing Protein 5B; MRF1-Like Protein; DESRT; MRF-2; MRF2;
Function
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.
Biological Process
Adipose tissue development Source: UniProtKB
Adrenal gland development Source: Ensembl
Cell development Source: Ensembl
Cellular response to leukemia inhibitory factor Source: Ensembl
Face morphogenesis Source: Ensembl
Fat cell differentiation Source: Ensembl
Fat pad development Source: Ensembl
Female gonad development Source: Ensembl
Fibroblast migration Source: Ensembl
Kidney development Source: Ensembl
Liver development Source: UniProtKB
Male gonad development Source: Ensembl
Multicellular organism growth Source: Ensembl
Muscle organ morphogenesis Source: Ensembl
Negative regulation of transcription, DNA-templated Source: GDB
Negative regulation of transcription by RNA polymerase II Source: NTNU_SB
Nitrogen compound metabolic process Source: Ensembl
Platelet-derived growth factor receptor signaling pathway Source: Ensembl
Positive regulation of DNA-binding transcription factor activity Source: UniProtKB
Post-embryonic development Source: Ensembl
Regulation of transcription by RNA polymerase II Source: GO_Central
Roof of mouth development Source: Ensembl
Skeletal system morphogenesis Source: Ensembl
Cellular Location
Nucleus
Involvement in disease
Defects in ARID5B may be a cause of susceptibility to coronary atherosclerosis in the Japanese population.
Leukemia, acute lymphoblastic (ALL): 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 lymphnodes.
PTM
Methylation at Lys-336 prevents DNA-binding. Demethylation by PHF2 promotes recruitment of the PHF2-ARID5B complex to promoters.
More Infomation

Zhang, X., Nham, G. T. H., Ito, K., & Shinomura, T. (2021). Gene expression of type II collagen is regulated by direct interaction with Kruppel-like factor 4 and AT-rich interactive domain 5B. Gene, 773, 145381.

Okazaki, Y., Murray, J., Ehsani, A., Clark, J., Whitson, R. H., Hirose, L., ... & Itakura, K. (2020). Increased glucose metabolism in Arid5b−/− skeletal muscle is associated with the down-regulation of TBC1 domain family member 1 (TBC1D1). Biological research, 53(1), 1-14.

Wang, P., Deng, Y., Yan, X., Zhu, J., Yin, Y., Shu, Y., ... & Lu, X. (2020). The Role of ARID5B in Acute Lymphoblastic Leukemia and Beyond. Frontiers in Genetics, 11, 598.

Ge, Z., Han, Q., Gu, Y., Ge, Q., Ma, J., Sloane, J., ... & Dovat, S. (2018). Aberrant ARID5B expression and its association with Ikaros dysfunction in acute lymphoblastic leukemia. Oncogenesis, 7(11), 1-10.

Cichocki, F., Wu, C. Y., Zhang, B., Felices, M., Tesi, B., Tuininga, K., ... & Miller, J. S. (2018). ARID5B regulates metabolic programming in human adaptive NK cells. Journal of Experimental Medicine, 215(9), 2379-2395.

Yamakawa, T., Waer, C., & Itakura, K. (2018). AT‐rich interactive domain 5B regulates androgen receptor transcription in human prostate cancer cells. The Prostate, 78(16), 1238-1247.

Sun, L. L., Zhang, S. J., Chen, M. J., Elena, K., & Qiao, H. (2017). Relationship between modulator recognition factor 2/AT-rich interaction domain 5B gene variations and type 2 diabetes mellitus or lipid metabolism in a northern Chinese population. Chinese medical journal, 130(9), 1055.

Hiwatari, M., Seki, M., Akahoshi, S., Yoshida, K., Miyano, S., Shiraishi, Y., ... & Takita, J. (2017). Molecular studies reveal MLL-MLLT10/AF10 and ARID5B-MLL gene fusions displaced in a case of infantile acute lymphoblastic leukemia with complex karyotype. Oncology letters, 14(2), 2295-2299.

Leong, W. Z., Tan, S. H., Ngoc, P. C. T., Amanda, S., Yam, A. W. Y., Liau, W. S., ... & Sanda, T. (2017). ARID5B as a critical downstream target of the TAL1 complex that activates the oncogenic transcriptional program and promotes T-cell leukemogenesis. Genes & development, 31(23-24), 2343-2360.

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For research use only. Not intended for any clinical use.

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