BAZ1B Antibody (N-term)
Affinity Purified Rabbit Polyclonal Antibody (Pab)
- SPECIFICATION
- CITATIONS
- PROTOCOLS
- BACKGROUND
Application
| WB, E |
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Primary Accession | Q9UIG0 |
Other Accession | NP_115784.1 |
Reactivity | Human |
Host | Rabbit |
Clonality | Polyclonal |
Isotype | Rabbit IgG |
Calculated MW | 170903 Da |
Antigen Region | 157-186 aa |
Gene ID | 9031 |
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Other Names | Tyrosine-protein kinase BAZ1B, Bromodomain adjacent to zinc finger domain protein 1B, Williams syndrome transcription factor, Williams-Beuren syndrome chromosomal region 10 protein, Williams-Beuren syndrome chromosomal region 9 protein, hWALp2, BAZ1B, WBSC10, WBSCR10, WBSCR9, WSTF |
Target/Specificity | This BAZ1B antibody is generated from rabbits immunized with a KLH conjugated synthetic peptide between 157-186 amino acids from the N-terminal region of human BAZ1B. |
Dilution | WB~~1:1000 |
Format | Purified polyclonal antibody supplied in PBS with 0.09% (W/V) sodium azide. This antibody is purified through a protein A column, followed by peptide affinity purification. |
Storage | Maintain refrigerated at 2-8°C for up to 2 weeks. For long term storage store at -20°C in small aliquots to prevent freeze-thaw cycles. |
Precautions | BAZ1B Antibody (N-term) is for research use only and not for use in diagnostic or therapeutic procedures. |
Name | BAZ1B |
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Synonyms | WBSC10, WBSCR10, WBSCR9, WSTF |
Function | Atypical tyrosine-protein kinase that plays a central role in chromatin remodeling and acts as a transcription regulator (PubMed:19092802). Involved in DNA damage response by phosphorylating 'Tyr-142' of histone H2AX (H2AXY142ph) (PubMed:19092802, PubMed:19234442). H2AXY142ph plays a central role in DNA repair and acts as a mark that distinguishes between apoptotic and repair responses to genotoxic stress (PubMed:19092802, PubMed:19234442). Regulatory subunit of the ATP-dependent WICH-1 and WICH-5 ISWI chromatin remodeling complexes, which form ordered nucleosome arrays on chromatin and facilitate access to DNA during DNA-templated processes such as DNA replication, transcription, and repair (PubMed:11980720, PubMed:28801535). Both complexes regulate the spacing of nucleosomes along the chromatin and have the ability to slide mononucleosomes to the center of a DNA template (PubMed:28801535). The WICH-1 ISWI chromatin remodeling complex has a lower ATP hydrolysis rate than the WICH-5 ISWI chromatin remodeling complex (PubMed:28801535). The WICH-5 ISWI chromatin-remodeling complex regulates the transcription of various genes, has a role in RNA polymerase I transcription (By similarity). Within the B-WICH complex has a role in RNA polymerase III transcription (PubMed:16603771). Mediates the recruitment of the WICH-5 ISWI chromatin remodeling complex to replication foci during DNA replication (PubMed:15543136). |
Cellular Location | Nucleus {ECO:0000255|PROSITE-ProRule:PRU00063, ECO:0000255|PROSITE-ProRule:PRU00475, ECO:0000269|PubMed:11980720, ECO:0000269|PubMed:15543136, ECO:0000269|PubMed:16603771, ECO:0000269|PubMed:25593309}. Note=Accumulates in pericentromeric heterochromatin during replication (PubMed:15543136). Co-localizes with PCNA at replication foci during S phase (PubMed:15543136). Co-localizes with SMARCA5/SNF2H at replication foci during late-S phase (PubMed:15543136). Also localizes to replication foci independently of SMARCA5/SNF2H and PCNA (PubMed:15543136). Localizes to sites of DNA damage (PubMed:25593309). |
Tissue Location | Ubiquitously expressed with high levels of expression in heart, brain, placenta, skeletal muscle and ovary |
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Background
This gene encodes a member of the bromodomain protein family. The bromodomain is a structural motif characteristic of proteins involved in chromatin-dependent regulation of transcription. This gene is deleted in Williams-Beuren syndrome, a developmental disorder caused by deletion of multiple genes at 7q11.23.
References
Bailey, S.D., et al. Diabetes Care 33(10):2250-2253(2010)
Johansen, C.T., et al. Nat. Genet. 42(8):684-687(2010)
Chidambaram, M., et al. Metab. Clin. Exp. (2010) In press :
Oya, H., et al. J. Biol. Chem. 284(47):32472-32482(2009)
Talmud, P.J., et al. Am. J. Hum. Genet. 85(5):628-642(2009)
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