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APC regulator of Wnt signaling pathway

The APC gene provides instructions for making the APC protein, which plays a critical role in several cellular processes. The APC protein acts as a tumour suppressor, which means that it keeps cells from growing and dividing too fast or in an uncontrolled way. This protein blocks a chemical signaling pathway known as Wnt signaling. This pathway promotes cell growth and division (proliferation) and controls the activity (expression) of certain genes. 

Normal function

The APC gene provides instructions for making the APC protein, which plays a critical role in several cellular processes. The APC protein acts as a tumour suppressor, which means that it keeps cells from growing and dividing too fast or in an uncontrolled way. This protein blocks a chemical signaling pathway known as Wnt signaling. This pathway promotes cell growth and division (proliferation) and controls the activity (expression) of certain genes. 

The APC protein attaches (binds) to multiple proteins to form a complex that helps to control levels of another protein called beta-catenin. Beta-catenin is a key part of the Wnt pathway, and it helps control many cell functions, including cell proliferation, gene expression, and the process by which cells mature to carry out specific functions (differentiation). When the APC protein complex binds beta-catenin, it helps break the protein down when it is no longer needed.

The APC protein also plays a role in regulating cell division. The protein interacts with parts of the cell's structural framework (cytoskeleton) to help with proper cell organisation during cell division. This helps ensure that the number of chromosomes in a cell is correct after the cell divides. 

Conditions referring to this gene or chromosome

Other names

adenomatous polyposis coli

APC_HUMAN

WNT signaling pathway regulator

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Lectures complémentaires et références

Historique de l'article

Les informations sur cette page sont rédigées et examinées par des cliniciens qualifiés.
  • 26 août 2025 | Dernière version
  • 1 août 2025 | Publié à l'origine

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