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Elevated coexpression of KITENIN (show Vangl1 ELISA Kits) and ErbB4 (show ERBB4 ELISA Kits)-CYT (show CYGB ELISA Kits)-2 promotes the transition of colon adenoma to adenocarcinoma within an APC loss-associated tumor microenvironment
The activation of canonical Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling by deletion of Apc in cardiomyocytes led to ventricular hyperplasia.
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
Both TIMP3 (show TIMP3 ELISA Kits) and APC methylation were associated with lymph node metastasis and higher clinical stage of tumors. Patients with methylation at TIMP3 (show TIMP3 ELISA Kits) or APC had worse prognoses as compared to those without these alterations.
AXIN1 (show AXIN1 ELISA Kits) is expressed in meningioma along with APC and E-cadherin (show CDH1 ELISA Kits)
we identified three novel mutations as well as two recurrent mutations in the APC in five Chinese familial adenomatous polyposis families
In oral squamous cell carcinoma there is no statistically significant differences in the expression level of MGMT (show MGMT ELISA Kits), p16, and APC genes in tumor samples compared to margin samples.
Notably, other mutations including MET, APC, CDH1 (show CDH1 ELISA Kits), and FBXW7 (show FBXW7 ELISA Kits) were also identified in Taiwanese oral squamous cell carcinoma patients.
Results of APC and DCC LOH, KRAS and microsatellite instability indicate our colorectal cancer cases were typical of sporadic cancers following the 'chromosomal instability' pathway.
Full-length APC promotes assembly of the Miro-1 (show RHOT1 ELISA Kits)/Milton-2 complex.
Studied promoter methylation of ITF2 (show TCF4 ELISA Kits) and APC and associated microsatellite instability in two case-case studies nested in colorectal cancer.
While binding to gamma-tubulin (show TUBG1 ELISA Kits) may help target APC to the site of microtubule nucleation complexes, additional C-terminal sequences of APC are required to stimulate and stabilize microtubule growth.
Our data represent the first comprehensive study delineating the mutation spectra of both APC and MUTYH (show MUTYH ELISA Kits) in Hungarian familial adenomatous polyposis families
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