title: APC as a mobile scaffold: regulation and function at the nucleus, centrosomes, and mitochondria.
abstract: Genetic mutations of adenomatous polyposis coli (APC) predispose to high risk of human colon cancer. APC is a large tumor suppressor protein and truncating mutations disrupt its normal roles in regulating cell migration, DNA replication/repair, mitosis, apoptosis, and turnover of oncogenic β-catenin. APC is targeted to multiple subcellular sites, and here we discuss recent evidence implicating novel protein interactions and functions of APC in the nucleus and at centrosomes and mitochondria. The ability of APC to shuttle between these and other cell locations is hypothesized to be integral to its cellular function.
authors.affiliation: Westmead Institute for Cancer Research, University of Sydney, Westmead Millennium Institute at Westmead Hospital, New South Wales, Australia.
authors.forename: Christina
authors.initials: C
authors.lastname: Lui
authors.forename: Kate
authors.initials: K
authors.lastname: Mills
authors.forename: Mariana G
authors.initials: MG
authors.lastname: Brocardo
authors.forename: Manisha
authors.initials: M
authors.lastname: Sharma
authors.forename: Beric R
authors.initials: BR
authors.lastname: Henderson
mesh_terms: D025601:Adenomatous Polyposis Coli Protein / Q000378:metabolism*; D000818:Animals; D002465:Cell Movement / Q000502:physiology*; D002467:Cell Nucleus / Q000378:metabolism*; D018385:Centrosome / Q000378:metabolism*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*
chemical_list: D025601:Adenomatous Polyposis Coli Protein