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Mouse Anti-ARID1B Recombinant Antibody (KMN1) (CBMAB-A3546-YC)


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Published Data
Mouse Anti-ARID1B Recombinant Antibody (KMN1) CBMAB-A3546-YC in IP and WB
Western blots of ARID1B-containing BAF complex in FLAG-tagged FGF13A immunoprecipitations in 293T cell lysates. ...View More
Yang, Q. Q., Zhai, Y. Q., Wang, H. F., Cai, Y. C., Ma, X. Y., Yin, Y. Q., ... & Zhou, J. W. (2021). Nuclear isoform of FGF13 regulates post-natal neurogenesis in the hippocampus through an epigenomic mechanism. Cell Reports, 35(7).
Mouse Anti-ARID1B Recombinant Antibody (KMN1) CBMAB-A3546-YC in Immunoblot
Time-course immunoblot conducted using Control Line-1 during CNCC differentiation shows that ARID1B is active in the first 7 days of the differentiation, with a peak of activity between day 5 and day 7. The ARID1B protein level strongly decreases after day 7. The experiment was repeated twice (the second replicate is shown in Fig. 7). Marker bars display kDa. ...View More
Pagliaroli, L., Porazzi, P., Curtis, A. T., Scopa, C., Mikkers, H. M., Freund, C., ... & Trizzino, M. (2021). Inability to switch from ARID1A-BAF to ARID1B-BAF impairs exit from pluripotency and commitment towards neural crest formation in ARID1B-related neurodevelopmental disorders. Nature Communications, 12(1), 6469.
Mouse Anti-ARID1B Recombinant Antibody (KMN1) CBMAB-A3546-YC in WB
Expression of ARID1A, ARID1B, SNF5 and β-actin in the ARID1A wildtype control and ARID1A knockout mouse ovarian ID8-Defb29/Vegf cells. ...View More
Fukumoto, T., Fatkhutdinov, N., Zundell, J. A., Tcyganov, E. N., Nacarelli, T., Karakashev, S., ... & Zhang, R. (2019). HDAC6 inhibition synergizes with anti-PD-L1 therapy in ARID1A-inactivated ovarian cancer. Cancer research, 79(21), 5482-5489.

Summary

Host Animal
Mouse
Specificity
Human, Mouse, Rat
Clone
KMN1
Antibody Isotype
IgG1, κ
Application
WB, IP

Basic Information

Immunogen
Amino acids 1-422 of ARID1B of human origin.
Specificity
Human, Mouse, Rat
Antibody Isotype
IgG1, κ
Clonality
Monoclonal
Application Notes
The COA includes recommended starting dilutions, optimal dilutions should be determined by the end user.
ApplicationNote
WB1:100-1:1,000
IP1-2 µg per 100-500 µg of total protein (1 ml of cell lysate)

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

Format
Liquid
Buffer
PBS, 0.1% gelatin
Preservative
< 0.1% sodium azide
Concentration
0.2 mg/ml
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 1B
Introduction
ARID1B is an AT-rich DNA interacting domain-containing protein. ARID1B is a component of the SWI/SNF chromatin remodeling complex and may play a role in cell-cycle activation. The protein encoded by this locus is similar to AT-rich interactive domain-cont
Entrez Gene ID
Human57492
Mouse239985
Rat282546
UniProt ID
HumanQ8NFD5
MouseE9Q4N7
RatF1LNP1
Alternative Names
AT-Rich Interaction Domain 1B; AT Rich Interactive Domain 1B (SWI1-Like); ARID Domain-Containing Protein 1B; BRG1-Associated Factor 250b; BAF250B; P250R; DAN15; OSA2; AT-Rich Interactive Domain-Containing Protein 1B; BRG1-Binding Protein HELD/OSA1; BRG1-B
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. 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).
Binds DNA non-specifically (PubMed:14982958, PubMed:15170388).
Biological Process
ATP-dependent chromatin remodeling Source: GO_Central
Cellular response to angiotensin Source: Ensembl
Chromatin-mediated maintenance of transcription Source: UniProtKB
Nervous system development Source: UniProtKB-KW
Positive regulation of transcription, DNA-templated Source: GO_Central
Regulation of transcription by RNA polymerase II Source: GO_Central
Response to ischemia Source: Ensembl
Cellular Location
Nucleus
Involvement in disease
Coffin-Siris syndrome 1 (CSS1): 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

Ellegood, J., Petkova, S. P., Kinman, A., Qiu, L. R., Adhikari, A., Wade, A. A., ... & Lerch, J. P. (2021). Neuroanatomy and behavior in mice with a haploinsufficiency of AT-rich interactive domain 1B (ARID1B) throughout development. Molecular autism, 12(1), 1-24.

Min, Z., Qian, C., & Ying, D. (2021). Novel ARID1B variant inherited from somatogonadal mosaic mother in siblings with Coffin‑Siris syndrome 1. Experimental and Therapeutic Medicine, 21(6), 1-6.

Liu, X., Hu, G., Ye, J., Ye, B., Shen, N., Tao, Y., ... & Yu, Y. (2020). De Novo ARID1B mutations cause growth delay associated with aberrant Wnt/β–catenin signaling. Human mutation, 41(5), 1012-1024.

Fujita, T., Ihara, Y., Hayashi, H., Ishii, A., Ideguchi, H., Inoue, T., ... & Hirose, S. (2020). Coffin‐Siris syndrome with bilateral macular dysplasia caused by a novel exonic deletion in ARID1B. Congenital Anomalies, 60(6), 189-193.

Boerstler, T., Wend, H., Krumbiegel, M., Kavyanifar, A., Reis, A., Lie, D. C., ... & Turan, S. (2020). CRISPR/Cas9 mediated generation of human ARID1B heterozygous knockout hESC lines to model Coffin-Siris syndrome. Stem Cell Research, 47, 101889.

Pascolini, G., Valiante, M., Bottillo, I., Laino, L., Fleischer, N., Ferraris, A., & Grammatico, P. (2020). Striking phenotypic overlap between Nicolaides-Baraitser and Coffin-Siris syndromes in monozygotic twins with ARID1B intragenic deletion. European journal of medical genetics, 63(3), 103739.

Cui, Y., Bai, X., Niu, M., Qin, Y., Zhang, X., & Pang, D. (2019). Upregulated expression of AT‑rich interactive domain‑containing protein 1B predicts poor prognosis in patients with triple‑negative breast cancer. Oncology letters, 17(3), 3289-3295.

Lin, J. (2018). ARID1B: From the Garden of Eden to the Sahara. The Journal of thoracic and cardiovascular surgery, 155(6), e193-e194.

Sato, E., Nakayama, K., Razia, S., Nakamura, K., Ishikawa, M., Minamoto, T., ... & Kyo, S. (2018). ARID1B as a potential therapeutic target for ARID1A-mutant ovarian clear cell carcinoma. International journal of molecular sciences, 19(6), 1710.

Jung, E. M., Moffat, J. J., Liu, J., Dravid, S. M., Gurumurthy, C. B., & Kim, W. Y. (2017). Arid1b haploinsufficiency disrupts cortical interneuron development and mouse behavior. Nature neuroscience, 20(12), 1694-1707.

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

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