Results 31 to 40 of about 24,916 (232)

An APC Mutation in a Large Chinese Kindred With Familial Adenomatous Polyposis Was Identified Using Both Next Generation Sequencing and Simple STR Marker Haplotypes

open access: yesFrontiers in Genetics, 2020
BackgroundFamilial adenomatous polyposis (FAP) is an autosomal dominant disorder characterized primarily by the development of numerous adenomatous polyps in the colon and a high risk for colorectal cancer.
Qitao Zhan   +10 more
doaj   +1 more source

T cell migration and effector function differences in familial adenomatous polyposis patients with APC gene mutations

open access: yesFrontiers in Immunology, 2023
Familial adenomatous polyposis (FAP) is an inherited disease characterized by the development of large number of colorectal adenomas with high risk of evolving into colorectal tumors. Mutations of the Adenomatous polyposis coli (APC) gene is often at the
Céline Cuche   +27 more
doaj   +1 more source

Adenomatous Polyposis Coli (APC) in cell migration

open access: yesEuropean Journal of Cell Biology, 2022
Adenomatous Polyposis Coli (APC) protein is mostly known as a tumor suppressor that regulates Wnt signaling, but is also an important cytoskeletal protein.
Xingyuan Fang, Tatyana M. Svitkina
doaj   +1 more source

Trabid patient mutations impede the axonal trafficking of adenomatous polyposis coli to disrupt neurite growth

open access: yeseLife, 2023
ZRANB1 (human Trabid) missense mutations have been identified in children diagnosed with a range of congenital disorders including reduced brain size, but how Trabid regulates neurodevelopment is not understood.
Daniel Frank   +15 more
doaj   +1 more source

Interactions and functions of the adenomatous polyposis coli (APC) protein at a glance [PDF]

open access: yesJournal of Cell Science, 2013
Since its discovery as the major tumour suppressor in colorectal cancer, the adenomatous polyposis coli (APC) protein has emerged as a multi-functional protein that directly or indirectly regulates the cellular processes that govern epithelial tissues ([McCartney and Nathke, 2008][1]).
Nelson, Scott, Näthke, Inke S.
openaire   +3 more sources

Mitochondrial Targeting of Adenomatous Polyposis Coli Protein Is Stimulated by Truncating Cancer Mutations [PDF]

open access: yesJournal of Biological Chemistry, 2008
The adenomatous polyposis coli (APC) protein tumor suppressor is mutated in the majority of colon cancers. Most APC gene mutations cause deletion of the C terminus and disrupt APC regulation of β-catenin turnover, microtubule dynamics, and chromosome ...
Mariana Brocardo   +5 more
openaire   +2 more sources

Gene expression analyses on skin lesions from patients with familial adenomatous polyposis [PDF]

open access: yes, 2014
Familial adenomatous polyposis coli (FAP) is an autosomal dominant colorectal cancer predisposition syndrome caused by germline mutations in the APC gene.
Stegmann, Danielle Alexandra
core   +1 more source

Loss of APC induces polyploidy as a result of a combination of defects in mitosis and apoptosis [PDF]

open access: yes, 2007
Mutations in the adenomatous polyposis coli (APC) tumor suppressor gene initiate a majority of colorectal cancers. Acquisition of chromosomal instability is an early event in these tumors.
Newton, Ian P.   +32 more
core   +1 more source

A pan-cancer analysis on the carcinogenic effect of human adenomatous polyposis coli.

open access: yesPLoS ONE, 2022
Adenomatous polyposis coli (APC) is the most commonly mutated gene in colon cancer and can cause familial adenomatous polyposis (FAP). Hypermethylation of the APC promoter can also promote the development of breast cancer, indicating that APC is not ...
Yinci Zhang   +3 more
doaj   +2 more sources

Advances and Insights of APC-Asef Inhibitors for Metastatic Colorectal Cancer Therapy

open access: yesFrontiers in Molecular Biosciences, 2021
In Colorectal cancer (CRC), adenomatous polyposis coli (APC) directly interacts with the Rho guanine nucleotide exchange factor 4 (Asef) and releases its GEF activity.
Xiuyan Yang   +7 more
doaj   +1 more source

Home - About - Disclaimer - Privacy