BAP1 (D7W7O) Rabbit mAb #13271
- WB
- IP
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 95 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
Storage
Protocol
Specificity / Sensitivity
BAP1 (D7W7O) Rabbit mAb recognizes endogenous levels of total BAP1 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Leu709 within the BRCA1 interaction region of human BAP1 protein.
Background
BRCA1-Associated Protein 1 (BAP1) was originally identified as a BRCA1 associated, nuclear localized ubiquitin hydrolase that suppresses cell growth (1). The protein belongs to the UCH family of deubiquitinases, with a UCH domain in its amino-terminal segment and a BRCA1 interaction domain as well as a nuclear localization signal in its carboxy-terminal segment (1). Frequent gene locus rearrangement, deletion, and null mutation of BAP1 have been found in lung and breast cancers (1,2). In vivo mutation analysis of cancer cell line survival and animal tumorigenesis indicates that both the deubiquitinase activity and the nuclear localization signal are required for BAP1 function as a tumor suppressor (3). BAP1 does not have direct deubiquitination activity towards the autoubiquitinated BRCA1/BARD1 E3 complex (4), but its interaction with BARD1 inhibits BRCA1/BARD1 E3 activity by interfering with the complex dimerization process (5). In addition to its interaction with BRCA1/BARD1, BAP1 has also been shown to interact with and deubiquitinate HCF-1, thereby controlling its stability (6).
- Jensen, D.E. et al. (1998) Oncogene 16, 1097-112.
- Buchhagen, D.L. et al. (1994) Int J Cancer 57, 473-9.
- Ventii, K.H. et al. (2008) Cancer Res 68, 6953-62.
- Mallery, D.L. et al. (2002) EMBO J 21, 6755-62.
- Nishikawa, H. et al. (2009) Cancer Res 69, 111-9.
- Misaghi, S. et al. (2009) Mol Cell Biol 29, 2181-92.
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