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APC haploinsufficiency coupled with p53 (show TP53 ELISA Kits) deletion resulted in the development of a distinct type of pancreatic premalignant precursors, mucinous cystic neoplasms (MCNs)
Gasdermin C is upregulated by inactivation of Tgfbr2 (show TGFBR2 ELISA Kits) in the presence of mutated Apc, promoting colorectal cancer cell proliferation.
By sequencing Apc and Ctnnb1 (show CTNNB1 ELISA Kits) genes, we found that most PhIP (show PHIP ELISA Kits)-induced small intestinal tumors in obese mice carried only a single heterozygous mutation in Apc . Our findings demonstrate that PhIP (show PHIP ELISA Kits)-induced small intestinal carcinogenesis in hCYP1A-db/db (show LEPR ELISA Kits) mice is promoted by obesity and involves Apc mutation and inactivation by DNA hypermethylation
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.
Nine patients with 21- approximately 100 colorectal adenomas (50%) and the two positive controls, showed somatic mosaicism, with identical APC variants in adenomas tested.
These result suggested that miR (show MLXIP ELISA Kits)-590-3p can promote osteogenic differentiation via suppressing APC expression and stabilizing beta-catenin (show CTNNB1 ELISA Kits).
The present findings indicate epigenetic silencing of APC in advanced gallbladder cancer (GBC). The methylation pattern, followed by expression analysis of APC may be suggested for diagnostic, prognostic and therapeutic purposes in GBC in future
miR (show MLXIP ELISA Kits)-106a-5p is involved in the invasive behavior of glioblastoma cells and by targeting APC and activating Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) pathway.
Point Mutations in Exon 1B of APC Reveal Similar mutations in APC promoter 1B occur in rare families with familial adenomatous polyposis
Studies suggest that both loss of tumor suppressive function and gain of function of APC mutants play critical roles in colorectal cancers (CRC (show CALR ELISA Kits)) tumorigenesis.
Loss of heterozygosity of TP53 (show TP53 ELISA Kits), P16, SMAD4 (show SMAD4 ELISA Kits) and APC genes was observed in esophageal adenocarcinoma.
miR (show MLXIP ELISA Kits)-582-5P was upregulated in the colorectal cancer specimens and cell lines and targeted the 3' untranslated region of APC directly.
Loss of APC expression through methylation of its promoter is a widespread phenomenon in Wnt (show WNT2 ELISA Kits)//beta-catenin (show CTNNB1 ELISA Kits) activated tumors.
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