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Mouse (Murine) Monoclonal APC Primary Antibody for IF, ELISA - ABIN533447
Hendriksen, Jansen, Brown, van der Velde, van Ham, Galjart, Offerhaus, Fagotto, Fornerod: Plasma membrane recruitment of dephosphorylated beta-catenin upon activation of the Wnt pathway. in Journal of cell science 2008
Mouse (Murine) Monoclonal APC Primary Antibody for IF, ELISA - ABIN533448
Onuma, Ochiai, Orihashi, Takahashi, Imai, Nakagama, Hippo: Genetic reconstitution of tumorigenesis in primary intestinal cells. in Proceedings of the National Academy of Sciences of the United States of America 2013
Human Polyclonal APC Primary Antibody for ICC, IF - ABIN4280975
Liu, Tackmann, Yang, Zhang: Disruption of the RP-MDM2-p53 pathway accelerates APC loss-induced colorectal tumorigenesis. in Oncogene 2016
Human Polyclonal APC Primary Antibody for IHC - ABIN6711664
Lombardi, Etcheverría, Carrera, Cacabelos, Chacón: Prevention of chronic experimental colitis induced by dextran sulphate sodium (DSS) in mice treated with FR91. in Journal of biomedicine & biotechnology 2012
Human Monoclonal APC Primary Antibody for IHC (fro), IP - ABIN152091
Abutaily, Collins, Roche: Cadherins, catenins and APC in pleural malignant mesothelioma. in The Journal of pathology 2003
Show all 2 Pubmed References
Human Monoclonal APC Primary Antibody for ICC, IHC (fro) - ABIN153070
Nakayama, Abe, Morimoto, Iida, Okabe, Sakimura, Hashimoto: Microglia permit climbing fiber elimination by promoting GABAergic inhibition in the developing cerebellum. in Nature communications 2018
PPARg and APC respectively contributed to microRNA-27a-decreased osteoclast differentiation and bone resorption. Taken together, these results showed that microRNA-27a may play a significant role in the process of estrogen-inhibited osteoclast differentiation and function.
Conditional loss of Apc resulted in the expression of nuclear beta-catenin throughout the developing mouse liver and increased number of cells expressing glutamine synthetase.
mTORC1 inactivation is beneficial in APC loss-dependent colorectal cancer.
Paracrine macrophage Cox-2 activity drives growth and progression of Apc (Min/+) mouse colonic adenomas, linked to increased epithelial cell beta-catenin dysregulation. Stromal cell (macrophage) gene regulation and signalling represent valid targets for chemoprevention of colorectal cancer.
Combined Mutation of Apc, Kras, and Tgfbr2 is associated with Metastasis of Intestinal Cancer.
Plk1 inhibition (RNAi, pharmacological compounds) promotes the development of adenomatous polyps in two independent Apc (Min/+) mouse models.
APC defines Treg differentiation and anti-inflammatory function through microtubule-mediated NFAT localization.
In summary, we show that Pten loss per se in Lgr5+ intestinal stem cells is not required either as a tumor suppressor or for maintaining intestinal homeostasis when Apc is functional, even when combined with obesity.
In this study, the effect of deficiency of OPN on intestinal tumor development in Apc-deficient Min mice was investigated.At 16 weeks of age, the number of small intestinal polyps in Min/OPN(+/-) and Min/OPN(-/-) mice was lower than that of Min/OPN(+/+) mice. Colorectal tumor incidences and multiplicities in Min/OPN(+/-) and Min/OPN(-/-) mice were significantly lower than those in Min/OPN(+/+) mice
The results indicate that C-terminal domain of APC has a role in the regulation of intestinal epithelium homeostasis.
Neonatal APC conditional knock-out (cKO) mice exhibit flexion-extension motor spasms and abnormal high-amplitude electroencephalographic discharges. Frequency of excitatory postsynaptic currents is increased in layer V pyramidal cells. At adult ages, APC cKOs display spontaneous electroclinical seizures. APC cKO is a new genetic model of infantile spasms.
we provide mechanistic insight into the role of APC mutations and Wnt signaling in hematopoietic stem cells (HSC) biology. As Wnt signals are explored in various in vivo and ex vivo expansion protocols for HSCs, our findings also have clinical ramifications.
The results reveal that APC-regulated beta-catenin activity in cortical progenitors sets the appropriate Wnt tone necessary for normal cerebral cortical development.
Dll4 seems to promote Apc (Min/+) tumorigenesis.
In cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 gene suppressed tumor growth and prolonged lifespan.
APC is required by Schwann cells for their timely differentiation to mature, myelinating cells and plays a crucial role in radial axonal sorting and peripheral nervous system myelination.
APC haploinsufficiency coupled with p53 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 in the presence of mutated Apc, promoting colorectal cancer cell proliferation.
By sequencing Apc and Ctnnb1 genes, we found that most PhIP-induced small intestinal tumors in obese mice carried only a single heterozygous mutation in Apc . Our findings demonstrate that PhIP-induced small intestinal carcinogenesis in hCYP1A-db/db mice is promoted by obesity and involves Apc mutation and inactivation by DNA hypermethylation
Elevated coexpression of KITENIN and ErbB4-CYT-2 promotes the transition of colon adenoma to adenocarcinoma within an APC loss-associated tumor microenvironment
This study aimed to evaluate patterns of APC and MUTYH germ-line mutations in Russian patients with colorectal malignancies. APC gene defects were identified in 26/38 (68%) subjects with colon polyposis; 8/26 (31%) APC mutations were associated with 2 known mutational hotspots
APC promoter methylation may be associated with the development and progression of bladder cancer and may serve as a promising noninvasive biomarker using urine samples for the detection of bladder cancer
APC gene mutation is associated with familial adenomatous polyposis.
Recurrent mutations in APC and CTNNB1 in nonintestinal-type intraductal papillary neoplasms of the bile duct (IPNBs) suggest that activation of the Wnt/beta-catenin signaling pathway is relevant to the development and progression of IPNBs.
Tumor location has been proposed as an additional prognostic indicator and -more recently- as a factor with significant influence on the prognostic value of particular molecular markers and/or combination of markers (KRAS, MSI, APC/MSI), allowing the discrimination of specific disease subsets with considerably disparate outcome and the identification of high risk cases
Study of a four generation Chinese family identified a germline novel heterozygous single nucleotide deletion [c.3418delC; p.Pro1140Leufs*25] in exon18 of APC gene, which segregated with the familial adenomatous polyposis phenotypes in the proband and in all the affected family members whereas absent in unaffected family members as well as in normal healthy controls of same ethnic origin.
Apc mutation, leading to uncontrolled Wnt activation and thus to tumorigenesis in the vast majority in colorectal cancer patients, critically induces extracellular vesicle release by activating the Wnt pathway.
The armadillo repeats in full-length APC interact with the APC residues 1362 to 1540 (APC-2,3 repeats), and this interaction competes off and inhibits Asef. Deletion of APC-2,3 repeats permits Asef interactions leading to downstream signaling events, including the induction of Golgi fragmentation through the activation of the Asef-ROCK-MLC2.
Moderate impact APC mutations and non-APC-related causes of increased WNT signaling may have a more important role in serrated neoplasia than the truncating APC mutations common in conventional adenomas.
The authors have identified a subtype of colorectal cancer that is associated with younger age of diagnosis, lack of APC mutation, microsatellite and chromosome stability, lower mutation burden and distinctive methylation changes.
A heterozygous germline APC mutation was found in a three-generation Vietnamese family with familial adenomatous polyposis.
LSINCT5 interacted with EZH2 to suppress the expression of APC, a negative regulator of the Wnt/beta-catenin pathway.
The miR-182 stimulates canonical Wnt signaling pathway by targeting APC gene and enhances the proliferation of cervical cancer cells.
29 patients with hepatoblastoma had received constitutional APC testing. Four (14%) were found to have APC pathogenic truncations of the APC protein and in addition two (7%) had APC missense variants of unknown clinical significance.
Using ICAT as a tool to disengage beta-catenin-mediated APC-Axin interaction, we demonstrate that Wnt quickly inhibits the direct interaction between APC and Axin
the roles of somatic and germline mutations of the APC gene in hereditary as well as sporadic forms of Colorectal cancer (Review)
we identified a novel germline mutation in the APC gene in members of an FAP-affected (Familial adenomatous polyposis) family. This unique heterozygous variant (c.735_736insT; p.Ser246PhefsTer6) was identified in ten out of twenty six family members, ranging in age from 6 to 60 years.
Data revealed that miR-106a was a direct target of LINC01133, which functioned as a ceRNA in regulating gastric cancer (GC) metastasis. Mechanistic analysis demonstrated that miR-106a specifically targeted APC gene, and LINC01133/miR-106a-3p suppressed the EMT and metastasis by inactivating the Wnt/beta-catenin pathway in an APC-dependent manner.
hsa-miR-135b-5p regulates the APC gene in both intestinal and diffuse subtypes of GC. Dysregulation in their expression, and consequently in their respectively signaling pathways, shows how these miRNAs can influence the carcinogenesis of different histological subtypes of gastric cancer.
the Amer2-EB1-APC complex regulates cell migration by altering microtubule stability.
Data show that importin-beta binds to Apc and negatively regulates the MT-assembly and spindle-promoting activity of Apc in a Ran-regulatable manner.
APC and Axin are involved in the Wnt pathway
depletion of APC from cystostatic factor (CSF) Xenopus extracts leads to a decrease in microtubule density and changes in tubulin distribution in spindles and asters formed in such extracts
An interaction of tumor-associated N-terminal APC fragments (N-APC) with Mad2, an essential mitotic checkpoint 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