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Mouse Anti-ARID1A Recombinant Antibody (3611) (CBMAB-A3539-YC)


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Summary

Host Animal
Mouse
Specificity
Human, Mouse
Clone
3611
Antibody Isotype
IgG1
Application
WB, IHC, IF, ICC

Basic Information

Immunogen
Recombinant protein encompassing a sequence within the C-terminus region of human ARID1A.
Specificity
Human, Mouse
Antibody Isotype
IgG1
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:500-1:3,000
IF(ICC)1:100-1:1,000
IHC1:100-1:1,000

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

Format
Liquid
Buffer
PBS
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.

Target

Full Name
AT-Rich Interaction Domain 1A
Introduction
ARID1A is a member of the SWI/SNF family, whose members have helicase and ATPase activities and are thought to regulate transcription of certain genes by altering the chromatin structure around those genes. The encoded protein is part of the large ATP-dep
Entrez Gene ID
8289
UniProt ID
O14497
Alternative Names
AT-Rich Interaction Domain 1A; SWI/SNF-Related, Matrix-Associated, Actin-Dependent Regulator Of Chromatin Subfamily F Member 1; AT Rich Interactive Domain 1A (SWI-Like); ARID Domain-Containing Protein 1A; SWI/SNF Complex Protein P270; BRG1-Associated Fact
Function
Involved in transcriptional activation and repression of select genes by chromatin remodeling (alteration of DNA-nucleosome topology). Component of SWI/SNF chromatin remodeling complexes that carry out key enzymatic activities, changing chromatin structure by altering DNA-histone contacts within a nucleosome in an ATP-dependent manner. Binds DNA non-specifically. Belongs to the neural progenitors-specific chromatin remodeling complex (npBAF complex) and the neuron-specific chromatin remodeling complex (nBAF complex). During neural development a switch from a stem/progenitor to a postmitotic chromatin remodeling mechanism occurs as neurons exit the cell cycle and become committed to their adult state. The transition from proliferating neural stem/progenitor cells to postmitotic neurons requires a switch in subunit composition of the npBAF and nBAF complexes. As neural progenitors exit mitosis and differentiate into neurons, npBAF complexes which contain ACTL6A/BAF53A and PHF10/BAF45A, are exchanged for homologous alternative ACTL6B/BAF53B and DPF1/BAF45B or DPF3/BAF45C subunits in neuron-specific complexes (nBAF). The npBAF complex is essential for the self-renewal/proliferative capacity of the multipotent neural stem cells. The nBAF complex along with CREST plays a role regulating the activity of genes essential for dendrite growth (By similarity).
Biological Process
Androgen receptor signaling pathway Source: UniProtKB
ATP-dependent chromatin remodeling Source: GO_Central
Chromatin-mediated maintenance of transcription Source: UniProtKB
Chromatin remodeling Source: BHF-UCL
Glucocorticoid receptor signaling pathway Source: UniProtKB
Intracellular estrogen receptor signaling pathway Source: UniProtKB
Nervous system development Source: UniProtKB-KW
Nucleosome disassembly Source: BHF-UCL
Nucleosome mobilization Source: UniProtKB
Positive regulation of transcription, DNA-templated Source: UniProtKB
Regulation of transcription by RNA polymerase II Source: GO_Central
Cellular Location
Nucleus
Involvement in disease
Coffin-Siris syndrome 2 (CSS2): A form of Coffin-Siris syndrome, a congenital multiple malformation syndrome with broad phenotypic and genetic variability. Cardinal features are intellectual disability, coarse facial features, hypertrichosis, and hypoplastic or absent fifth digit nails or phalanges. Additional features include malformations of the cardiac, gastrointestinal, genitourinary, and/or central nervous systems. Sucking/feeding difficulties, poor growth, ophthalmologic abnormalities, hearing impairment, and spinal anomalies are common findings. Both autosomal dominant and autosomal recessive inheritance patterns have been reported.
More Infomation

Lee, C. G., & Ki, C. S. (2021). A Novel De Novo Heterozygous ARID1A Missense Variant Cluster in cis c.[5954C> G; 6314C> T; 6334C> T; 6843G> C] causes a Coffin–Siris Syndrome. Annals of Laboratory Medicine, 41(3), 350.

Qadir, J., Majid, S., Khan, M. S., Rashid, F., Wani, M. D., Din, I., & Bashir, H. (2020). AT-rich interaction domain 1A gene variations: genetic associations and susceptibility to gastric cancer risk. Pathology & Oncology Research, 26(4), 2237-2246.

Okamura, R., Kato, S., Lee, S., Jimenez, R. E., Sicklick, J. K., & Kurzrock, R. (2020). ARID1A alterations function as a biomarker for longer progression-free survival after anti-PD-1/PD-L1 immunotherapy. Journal for immunotherapy of cancer, 8(1).

Ferri-Borgogno, S., Barui, S., McGee, A. M., Griffiths, T., Singh, P. K., Piett, C. G., ... & Gupta, S. (2020). Paradoxical role of AT-rich interactive domain 1A in restraining pancreatic carcinogenesis. Cancers, 12(9), 2695.

Hu, G., Tu, W., Yang, L., Peng, G., & Yang, L. (2020). ARID1A deficiency and immune checkpoint blockade therapy: From mechanisms to clinical application. Cancer letters, 473, 148-155.

Raffone, A., Travaglino, A., Saccone, G., Cieri, M., Mascolo, M., Mollo, A., ... & Zullo, F. (2019). Diagnostic and prognostic value of ARID1A in endometrial hyperplasia: a novel marker of occult cancer. Apmis, 127(9), 597-606.

Zhou, H., Tan, S., Li, H., & Lin, X. (2019). Expression and significance of EBV, ARID1A and PIK3CA in gastric carcinoma. Molecular medicine reports, 19(3), 2125-2136.

Bui, C. B., Le, H. K., Vu, D. M., Truong, K. D. D., Nguyen, N. M., Ho, M. A. N., & Truong, D. Q. (2019). ARID1A‐SIN3A drives retinoic acid‐induced neuroblastoma differentiation by transcriptional repression of TERT. Molecular carcinogenesis, 58(11), 1998-2007.

Zhang, L., Wang, C., Yu, S., Jia, C., Yan, J., Lu, Z., & Chen, J. (2018). Loss of ARID1A expression correlates with tumor differentiation and tumor progression stage in pancreatic ductal adenocarcinoma. Technology in cancer research & treatment, 17, 1533034618754475.

Hu, C., Li, W., Tian, F., Jiang, K., Liu, X., Cen, J., ... & Hui, L. (2018). Arid1a regulates response to anti-angiogenic therapy in advanced hepatocellular carcinoma. Journal of hepatology, 68(3), 465-475.

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

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