Cell Signaling Technology

Product Pathways - Wnt / Hedgehog / Notch

APC Antibody #2504

Applications Reactivity MW (kDa) Source
W IP H (M) (R) (Mk) 160 truncated APC in SW480 cells. 310 full-length APC. Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.

Specificity / Sensitivity

APC Antibody detects endogenous levels of total APC protein.

Source / Purification

Polyclonal antibodies are produced by immunizing rabbits with a synthetic peptide (KLH-coupled) corresponding to the sequence of human APC. Antibodies are purified by protein A and peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis (lane 1) and Immunoprecipitation (lanes 2-3) of extracts from SW480 cells. APC was immunoprecipitated with APC Antibody (lane 2) or with rabbit IgG (lane 3) to confirm specificity. Western blot was detection was performed using APC Antibody.

Background

The Adenomatous Polyposis Coli (APC) tumor suppressor gene is mutated in most familial and sporadic colorectal cancers, and encodes a large cytoplasmic protein, which is implicated in cell migration, cell adhesion, and proliferation (1). APC binds directly to microtubules, and lack of APC leads to defective mitotic spindles and aneuploidy due to mis-segregation of chromosomes (2). APC is well characterized as a scaffolding protein, binds to beta-catenin and is involved in the regulation of its intracellular concentration: in the absence of a Wnt signal, GSK3beta phosphorylates all three members of the APC-beta-catenin-axin complex and this phosphorylation of beta-catenin creates a recognition site for ubiquitin, the signal for proteosome mediated degradation. In the presence of a Wnt signal, dishevelled inactivates GSK3beta and beta-catenin can now coordinate gene transcription of proteins important for the control of cell cycle progression and proliferations such as cyclin D1 and c-myc (3).

  1. Shih, I. M. et al. (2000) Cancer Res. 60, 1671-1676.
  2. Kaplan, K. B. et al. (2001) Nat Cell Biol. 3, 429-432.
  3. Fodde, R. (2002) Eur J Cancer. 38, 86-871.

Application References

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