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Adenomatous polyposis coli protein

Liu, J., et al., Siah-1 mediates a novel beta-catenin degradation pathway linking p53 to the adenomatous polyposis coli protein. Mol Cell, 2001, 7f5 , 927-36. [Pg.90]

Orbit/MAST proteins, also known as CLIP-associated proteins (CLASPs), are involved in the regulation of microtubule dynamics and bind to microtubule plus ends via CLIP115 or CLIP170. Active CLASP suppresses microtubule assembly and axon outgrowth (Lee et al., 2004), whereas activated adenomatous polyposis coli protein (APC see below) promotes microtubule assembly and axon outgrowth. [Pg.286]

APC, antigen-presenting cells are bone-marrow-derived cells, macrophages and dendritic cells which process foreign antigens and present them to T cells, OR, adenomatous polyposis coli protein, enoded by the human ape gene. [Pg.304]

S. Miinemitsu, I. Albert, B. Souza, B. Rubinfeld, and P. Polakis. Regulation of intracellular beta-catenin levels by the adenomatous polyposis coli (APC) tumor-suppressor protein. Proc Natl Acad Set, USA, 92 (7), 3046-3050, 1995. [Pg.293]

Hassan A, Yerian LM, Kuan SF, et al. Immunohistochemical evaluation of adenomatous polyposis coli, beta-catenin, c-Myc, cyclin Dl, p53, and retinoblastoma protein expression in syndromic and sporadic fundic gland polyps. Hum Pathol. 2004 35 328-334. [Pg.533]

Adenomatous Polyposis Coli Rodent Model Adenomatous polyposis coli (APC) is a dual-function tumor suppressor gene and encodes a protein that has been implicated in a variety of cellular functions including cellular proliferation, differentiation, cytoskeleton regulation, migration, and apoptosis (Neufeld, 2009 Minde et al., 2011 Perez-Sayans et al., 2012). Mechanistically, APC regulates levels of p-catenin, an important mediator of... [Pg.277]

There are two major forms of hereditary susceptibility to colon cancer.00 Familial adenomatous polyposis is caused by defects in the APC gene (see Chapter 32). The more common hereditary nonpolyposis colorectal cancer (HNPCC), which includes many endometrial, stomach, and urinary tract tumors, results from defects in DNA mismatch repair. -)) The proteins hMSH2 and hMSLl are homologs of the E.coli MutS and MutL (main text). [Pg.1585]


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