Bub1b (D32E8) Rabbit mAb #5421
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 130 |
| Source/Isotype | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Bub1b (D32E8) Rabbit mAb detects endogenous levels of total Bub1b protein.
Species Reactivity:
Human
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to amino acid sequence surrounding Lys370 of human Bub1b.
Background
The Mitotic Checkpoint Complex (MCC), which contains Bub1, Bub1b, Bub3, Mad2, and Cdc20, controls chromosome segregation and monitors kinetochore-microtubule interactions (1). During mitosis, the MCC complex inhibits the ubiquitin ligase activity of the Anaphase Promoting Complex/Cyclosome (APC/C), thereby preventing cells with unaligned chromosomes from prematurely entering anaphase (2). Research studies have shown that Bub1b and Bub1 kinases are mutated in several types of human malignancies including hematopoietic, colorectal, lung, and breast cancers (3). Biallelic mutations in Bub1b have been found in mosaic variegated aneuploidy syndrome and premature chromatid separation syndrome (4). Bub1b mouse germline knockouts are embryonic lethal with heterozygous animals displaying genetic instability, early aging phenotypes, and increased cancer susceptibility (5). Bub3 binds both Bub1 and Bub1b, facilitating their recruitment to kinetochores (6), and is required for functional microtubule-kinetochore interactions (7).
- Fukagawa, T. (2008) Front Biosci 13, 2705-13.
- Chen, R.H. (2007) J Biomed Sci 14, 475-9.
- Dai, W. et al. (2004) Cancer Res 64, 440-5.
- Kops, G.J. et al. (2005) Nat Rev Cancer 5, 773-85.
- Baker, D.J. et al. (2004) Nat Genet 36, 744-9.
- Taylor, S.S. et al. (1998) J Cell Biol 142, 1-11.
- Logarinho, E. et al. (2008) Mol Biol Cell 19, 1798-813.
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