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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
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
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
The activation of canonical Wnt/beta-catenin signaling by deletion of Apc in cardiomyocytes led to ventricular hyperplasia.
demonstrated that despite having both Kras and Pik3ca mutations at the time of tumor initiation from loss of APC
Suggest that the early activation of Hsf1 dependent cell stress pathway by mono-allelic mutations in APC can affect cell programming in a way that contributes to cancer onset.
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 synonymous single nucleotide polymorphism APC486s induced major splicing defects with skipping of exon 12 in APC. The data of the present study suggested that the synonymous polymorphism APC486s was a potential pathogenic alteration that predisposed APC/MUTYH mutationnegative patients to FAP.
A novel heterozygous large deletion segregated with familial adenomatous polyposis in five generations.
Long noncoding RNA lncAPC promotes liver tumor initiating cells self-renewal through EZH2-dependent APC transcriptional inhibition.
elevated expression of miR-494 promotes cell proliferation and tumorigenesis in CRC by suppressing the expression of APC, an inhibitor of beta-catenin signaling. These findings uncover a novel molecular mechanism for the hyperactivation of the Wnt/beta-catenin signaling pathway in CRC.
Study reveal an unexpected role of APC in the directional spread of HIV-1 by promoting the directional assembly of viral components at virological synapses, thereby facilitating cell-to-cell viral transmission.
Because of low sensitivity, APC gene promoter methylation in serum was not suitable for breast cancer (BC) screening. However, as specificity was very high, detection of serum APC gene promoter methylation could be used as tool to confirm BC.
Multivariate analyses revealed that the PIK3CA mutation and clinical T stage were independent favorable prognostic factors (hazard ratio 0.34, 95% confidence interval: 0.12-0.96, p = 0.042). PIK3CA mutations were significantly associated with APC alterations (p = 0.0007) and BRAF mutations (p = 0.0090).
A novel APC frameshift mutation has been identified in a large Chinese family with familial adenomatous polyposis.
In the two wild type (WT) cases, two novel alterations were detected: a complex deletion of APC and a pathogenic mutation of LAMTOR2. Focusing on WT DT subtype, deep sequencing of CTNNB1, APC and LAMTOR2 was conducted on a retrospective series of 11 WT DT using a targeted approach
This study demonstrates a prognostic role for APC.
There is a certain correlation between the APC gene and ovarian tumors, and the APC gene mediates the apoptosis of tumor cells through the MDR-1/CLCX-1 signaling pathway.
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