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Association between wild type and mutant APC gene products
L K Su1, K A Johnson, K J Smith
1Department of Oncology, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21231.
Cancer Research
|June 15, 1993
Summary
Mutations in the Adenomatous Polyposis Coli (APC) gene cause inherited polyposis and sporadic colorectal tumors. Truncated APC proteins can bind to normal APC, potentially inactivating it.
Area of Science:
- Oncology
- Genetics
- Molecular Biology
Background:
- Germline mutations in the Adenomatous Polyposis Coli (APC) gene predispose individuals to colorectal tumors (familial adenomatous polyposis).
- APC gene mutations are also crucial in the development of sporadic colorectal cancers.
- Most identified APC mutations lead to truncated APC proteins.
Purpose of the Study:
- To investigate the in vivo interaction between truncated and wild-type APC proteins.
- To identify the specific regions of the APC protein involved in oligomerization.
Main Methods:
- In vitro protein expression.
- Immunoprecipitation assays.
- Analysis of APC protein truncations and interactions.
Main Results:
- Truncated APC proteins can associate with wild-type APC in vivo.
- The first 171 residues of APC are sufficient for oligomerization.
- The first 45 amino acids of APC are necessary for this interaction.
Conclusions:
- Most mutant APC proteins are capable of binding to wild-type APC.
- This interaction may lead to dominant-negative inactivation of wild-type APC function.
- Understanding this mechanism is crucial for colorectal cancer research.