Cell Signaling Technology

Product Pathways - Cell Cycle / Checkpoint

PBK/TOPK Antibody #4942

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

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 Blotting

Western blot analysis of extracts from NIH/3T3 and PC12 cells, using PBK/TOPK Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human colon carcinoma, showing membrane and cytoplasmic localization, using PBK/TOPK Antibody.

IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded human lung carcinoma, using PBK/TOPK Antibody.


IHC-P (paraffin)

IHC-P (paraffin)

Immunohistochemical analysis of paraffin-embedded ME-180 cells, using PBK/TOPK Antibody (left), or no primary antibody (right).

IHC-P (paraffin)

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)

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).

  1. Gaudet, S. et al. (2000) Proc. Natl. Acad. Sci. U S A 97, 5167-5172.
  2. Simons-Evelyn, M. et al. (2001) Blood Cells Mol. Dis. 27, 825-829.
  3. Nandi, A. et al. (2004) Blood Cells Mol. Dis. 32, 240-245.
  4. Abe, Y. et al. (2000) J. Biol. Chem. 276, 21525-21531.
  5. Matsumoto, S. et al. (2004) Biochem Biophys Res Commun. 325, 997-1004.

Application References

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Companion Products


For Research Use Only. Not For Use In Diagnostic Procedures.

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