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demonstrated that despite having both Kras and Pik3ca (show PIK3CA ELISA Kits) mutations at the time of tumor initiation from loss of APC
Suggest that the early activation of Hsf1 (show HSF1 ELISA Kits) dependent cell stress pathway by mono-allelic mutations in APC can affect cell programming in a way that contributes to cancer onset.
Adenomatous polyposis coli mutation leads to myopia development in mice.
findings indicate Ctnnb1 (show CTNNB1 ELISA Kits) gene dose exerts tissue-specific differences in Apc mutation-instigated tumorigenesis
Microsatellite instability in the Apc gene does not significantly affect chlorinated water-induced colonic tumorigenesis.
Lung mesenchyme-specific Apc conditional knockout resulted in abnormal lung morphogenesis and fetal lethality at mid-gestation.
our results suggest that both T cell development in a functional thymus and IL-17A (show IL17A ELISA Kits) control the ability of Treg to inhibit intestinal tumorigenesis in Apc (/Min+) mice.
the effect of Apc loss in MMTV-PyMT mouse breast cancer cells on gene expression changes of ATP-binding cassette transporters and immunofluorescence to determine proliferative and apoptotic response of cells to cisplatin, doxorubicin and paclitaxel
The results demonstrate that in muscle stem cells, APC dampens canonical Wnt (show WNT2 ELISA Kits) signaling to allow cell cycle progression. And that APC is absolutely necessary for regenerative myogenesis.
APC loss leads to a DNA damage signature and genomic instability in the liver and additional loss of p53 (show TP53 ELISA Kits) leads to an increase in the DNA damage signal but not to an immediate increase in the genomic instability phenotype.
analysis of the causative APC gene defects associated with familial adenomatous coli in a Chinese pedigree
A male-specific association of the APC rs383830 polymorphism with coronary heart disease in the Chinese population has been found.
APC promoter methylation is associated with the risk of hepatocellular carcinoma.
A founder mutation within the APC promoter is associated with familial adenomatous polyposis in the United States.
GSK3 acts through APC motifs R2 and B to regulate APC:Axin interactions, promoting high-throughput of betacatenin to destruction.
Expression of APC is decreased in mutation negative cases and this appears to be a promising indicator of FAP predisposition, while for MUTYH (show MUTYH ELISA Kits) gene, mutation is associated to reduced mRNA expression.
two novel mutations in APC gene identified in Chinese families with familial adenomatous polyposis.
shows that RAR-beta (show RARB ELISA Kits) methylation detected in lung tissue may be used as a predictive marker for non-small cell lung cancer diagnosis and that APC methylation in tumor sample may be a useful marker
the findings that were derived from this large study cohort suggest that the I1307K variant in the APC gene is a global risk factor for cancer, with an OR of over 2.5, and mostly in males.
the Amer2 (show AMER2 ELISA Kits)-EB1 (show MAPRE1 ELISA Kits)-APC complex regulates cell migration by altering microtubule stability.
Data show that importin-beta (show KPNB1 ELISA Kits) binds to Apc and negatively regulates the MT-assembly and spindle-promoting activity of Apc in a Ran-regulatable manner.
APC and Axin (show AXIN1 ELISA Kits) are involved in the Wnt (show WNT2 ELISA Kits) pathway
depletion of APC from cystostatic factor (CSF (show CSF2 ELISA Kits)) Xenopus extracts leads to a decrease in microtubule density and changes in tubulin (show TUBB ELISA Kits) distribution in spindles and asters formed in such extracts
An interaction of tumor-associated N-terminal APC fragments (N-APC) with Mad2 (show MAD2L1 ELISA Kits), an essential mitotic checkpoint (show BUB3 ELISA Kits) protein, providing a direct molecular support for linking APC mutations to the generation of chromosome instability, is reported.
This gene encodes a tumor suppressor protein that acts as an antagonist of the Wnt signaling pathway. It is also involved in other processes including cell migration and adhesion, transcriptional activation, and apoptosis. Defects in this gene cause familial adenomatous polyposis (FAP), an autosomal dominant pre-malignant disease that usually progresses to malignancy. Disease-associated mutations tend to be clustered in a small region designated the mutation cluster region (MCR) and result in a truncated protein product.
adenomatosis polyposis coli
, adenomatous polyposis coli protein
, multiple intestinal neoplasia
, adenomatosis polyposis coli tumor suppressor
, deleted in polyposis 2.5
, protein phosphatase 1, regulatory subunit 46
, adenomatous polyposis coli homolog