Results 51 to 60 of about 24,916 (232)

RNA polymerase I inhibition induces terminal differentiation, growth arrest, and vulnerability to senolytics in colorectal cancer cells

open access: yesMolecular Oncology, 2022
Ribosomal biogenesis and protein synthesis are deregulated in most cancers, suggesting that interfering with translation machinery may hold significant therapeutic potential. Here, we show that loss of the tumor suppressor adenomatous polyposis coli (APC)
Christoph Otto   +15 more
doaj   +1 more source

Identification of cis-HOX-HOXC10 axis as a therapeutic target for colorectal tumor-initiating cells without APC mutations

open access: yesCell Reports, 2021
Summary: Colorectal cancer (CRC) is one of the most common cancers worldwide, in which adenomatous polyposis coli (APC) mutations are frequently and uniquely observed.
Zhenzhen Chen   +8 more
doaj   +1 more source

Adenomatous Polyposis Coli as a Scaffold for Microtubule End-Binding Proteins

open access: yesJournal of Molecular Biology, 2019
End-binding proteins (EBs), referred to as the core components of the microtubule plus-end tracking protein network, interact with the C-terminus of the adenomatous polyposis coli (APC) tumor suppressor. This interaction is disrupted in colon cancers expressing truncated APC.
Serre, Laurence   +2 more
openaire   +5 more sources

Interaction between Ku80 protein and a widely used antibody to adenomatous polyposis coli [PDF]

open access: yesBritish Journal of Cancer, 2003
The adenomatous polyposis coli (APC) gene and its expressed product are highly studied because of its role as a tumour-suppressor protein. Inherited mutations in APC lead to the condition known as familial adenomatous polyposis (FAP), which predisposes the affected individuals to colorectal cancer.
Roberts, G T, Davies, M L, Wakeman, J A
openaire   +2 more sources

APCI1307K Mutations and Forkhead Box Gene (FOXO1A): Another Piece of an Interesting Correlation

open access: yesThe International Journal of Biological Markers, 2012
Purpose Germline nonsense and frameshift mutations in the adenomatous polyposis coli (APC) gene are found in approximately 90% of individuals affected by familial adenomatous polyposis (FAP) and a genotype-phenotype relationship has been observed ...
Marco Agostini   +16 more
doaj   +1 more source

APC-driven actin nucleation powers collective cell dynamics in colorectal cancer cells

open access: yesiScience, 2023
Summary: Cell remodeling relies on dynamic rearrangements of cell contacts powered by the actin cytoskeleton. The tumor suppressor adenomatous polyposis coli (APC) nucleate actin filaments (F-actin) and localizes at cell junctions.
Lautaro Baro   +4 more
doaj   +1 more source

Fruits, vegetables, and hMLH1 protein-deficient and -proficient colon cancer: The Netherlands cohort study. [PDF]

open access: yes, 2005
BACKGROUND: Clinical and pathologic differences exist between colon carcinomas deficient and proficient in the mismatch repair protein hMLH1. Animal and in vitro studies suggest that fruits, vegetables, folate, and antioxidants are associated with ...
Brandt, P.A. van den   +31 more
core   +1 more source

Germline Missense Changes in the APC Gene and Their Relationship to Disease

open access: yesHereditary Cancer in Clinical Practice, 2004
Familial adenomatous polyposis (FAP) is characterized by the presence of hundreds to thousands of adenomas that carpet the entire colon and rectum. Nonsense and frameshift mutations in the adenomatous polyposis coli (APC) gene account for the majority of
Scott Rodney J   +7 more
doaj   +1 more source

Rare mutations predisposing to familial adenomatous polyposis in Greek FAP patients

open access: yesBMC Cancer, 2005
Background Familial Adenomatous Polyposis (FAP) is caused by germline mutations in the APC (Adenomatous Polyposis Coli) gene. The vast majority of APC mutations are point mutations or small insertions / deletions which lead to truncated protein products.
Danielidis Ioannis   +11 more
doaj   +1 more source

The Ubiquitin-Proteasome Pathway and Serine Kinase Activity Modulate Adenomatous Polyposis Coli Protein-mediated Regulation of β-Catenin-Lymphocyte Enhancer-binding Factor Signaling*

open access: yesJournal of Biological Chemistry, 1999
The tumor suppressor function of the adenomatous polyposis coli protein (APC) depends, in part, on its ability to bind and regulate the multifunctional protein, β-catenin.
V. Easwaran   +3 more
semanticscholar   +1 more source

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