Product Pathways - Cell Cycle / Checkpoint
PBK/TOPK Antibody #4942
PhosphoSitePlus® protein, site, and accession data: PBK
| Applications | Reactivity | Sensitivity | MW (kDa) | Source |
|---|---|---|---|---|
| W IHC-P | H M R | Endogenous | 40 | Rabbit |
Applications Key:
W=Western Blotting
IHC-P=Immunohistochemistry (Paraffin)
Reactivity Key:
H=Human
M=Mouse
R=Rat
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.
Protocols
- 4942:
- IHC / Paraffin, Western Blotting
Specificity / Sensitivity
PBK/TOPK Antibody detects endogenous levels of total PBK/TOPK protein.
Source / Purification
Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to amino acids at the carboxy-terminus of human PBK/TOPK. Antibodies are purified by protein A and peptide affinity chromatography.
Western Blotting
Western blot analysis of extracts from NIH/3T3 and PC12 cells, using PBK/TOPK Antibody.
IHC-P (paraffin)
Immunohistochemical analysis of paraffin-embedded human colon carcinoma, showing membrane and cytoplasmic localization, using PBK/TOPK Antibody.
IHC-P (paraffin)
Immunohistochemical analysis of paraffin-embedded human lung carcinoma, using PBK/TOPK Antibody.
IHC-P (paraffin)
Immunohistochemical analysis of paraffin-embedded ME-180 cells, using PBK/TOPK Antibody (left), or no primary antibody (right).
IHC-P (paraffin)
Immunohistochemical analysis of paraffin-embedded human breast carcinoma, using PBK/TOPK Antibody preincubated with an irrelevant control peptide (left) or antigen specific peptide (right).
IHC-P (paraffin)
Immunohistochemical analysis of paraffin-embedded human prostate carcinoma, using PBK/TOPK Antibody.
Background
PBK/TOPK is a serine/threonine kinase that is phosphorylated and active during mitosis (1). PBK/TOPK is composed of kinase subdomains and a carboxy-terminal PDZ-Binding domain, which is thought to interact with the tumor suppressor protein hDlg (1). Increased PBK/TOPK expression has been observed in highly proliferative malignant cell lines, and PBK/TOPK expression is strongly downregulated during terminal differentiation of HL-60 leukemic cells (2,3). PMA-induced kinase activity toward PBK/TOPK has been observed (4), and cdc2/cyclinB has been shown to phosphorylate PBK/TOPK in vitro, presumably at Thr9 (1). Potential substrates of PBK/TOPK include p38 MAPK and c-Myc (3,4).
- Gaudet, S. et al. (2000) Proc. Natl. Acad. Sci. U S A 97, 5167-5172.
- Simons-Evelyn, M. et al. (2001) Blood Cells Mol. Dis. 27, 825-829.
- Nandi, A. et al. (2004) Blood Cells Mol. Dis. 32, 240-245.
- Abe, Y. et al. (2000) J. Biol. Chem. 276, 21525-21531.
- Matsumoto, S. et al. (2004) Biochem Biophys Res Commun. 325, 997-1004.
Application References
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For Research Use Only. Not For Use In Diagnostic Procedures.