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Human Polyclonal APC Primary Antibody pour ICC, IF - ABIN4280975
Liu, Tackmann, Yang, Zhang: Disruption of the RP-MDM2-p53 pathway accelerates APC loss-induced colorectal tumorigenesis. dans Oncogene 2016
Mouse (Murine) Monoclonal APC Primary Antibody pour 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. dans Journal of cell science 2008
Mouse (Murine) Monoclonal APC Primary Antibody pour IF, ELISA - ABIN533448
Onuma, Ochiai, Orihashi, Takahashi, Imai, Nakagama, Hippo: Genetic reconstitution of tumorigenesis in primary intestinal cells. dans Proceedings of the National Academy of Sciences of the United States of America 2013
Human Monoclonal APC Primary Antibody pour IF, WB - ABIN393899
Jaulin, Kreitzer: KIF17 stabilizes microtubules and contributes to epithelial morphogenesis by acting at MT plus ends with EB1 and APC. dans The Journal of cell biology 2010
Show all 6 Pubmed References
Human Monoclonal APC Primary Antibody pour IHC (fro), IP - ABIN152091
Abutaily, Collins, Roche: Cadherins, catenins and APC in pleural malignant mesothelioma. dans The Journal of pathology 2003
Show all 2 Pubmed References
Human Monoclonal APC Primary Antibody pour ICC, IHC (fro) - ABIN153070
Nakayama, Abe, Morimoto, Iida, Okabe, Sakimura, Hashimoto: Microglia permit climbing fiber elimination by promoting GABAergic inhibition in the developing cerebellum. dans Nature communications 2018
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.
Adenomatous polyposis coli mutation leads to myopia development in mice.
findings indicate Ctnnb1 gene dose exerts tissue-specific differences in Apc mutation-instigated tumorigenesis
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.
Its mutation is identified in duodenal adenoma and it involves in development of duodenal cancers.
We have investigated if the initial source of intratumoral heterogeneity is consequent to multiple independent lineages derived from different crypts harboring distinct truncal APC and driver KRAS mutations, thus challenging the prevailing monoclonal monocryptal model.
methylation-dependent silencing of the APC gene promoter 1A is a mechanism that contributes to the activation of Wnt signaling pathway in cervical cancer cells infected by high risk HPV16.
miR-3607 contributes to lung cancer cell proliferation by inhibiting APC.
USP7 depletion in APC-mutated colorectal cancer inhibits Wnt activation by restoring beta-catenin ubiquitination, drives differentiation, and suppresses xenograft tumor growth.
Data suggest that the concurrent mutations of the adenomatous polyposis coli protein (APC) and mutL protein homolog 1 (MLH1) genes probably underline the familial adenomatous polyposis (FAP) in the pedigree.
The expression of APC-DeltaC in colon cells reduces the accumulation of mitotic cells upon PLK1 inhibition, accelerates mitotic exit and increases the survival of cells with enhanced chromosomal abnormalities.
our results suggest that the amount of APC expression is the rate-limiting factor for the constitution of beta-catenin destruction complexes.
Data show that tumor suppressor adenomatous polyposis coli (APC) loss results in up-regulation of IL-6 signal transducer (IL-6ST/gp130), thereby activating YAP (YY1-associated) protein (YAP) which are simultaneously up-regulated in the majority of colorectal cancer (CRC).
The results indicate that APC promoter hypermethylation is an early event in carcinogenesis of CRC, could be a valuable diagnostic marker for early-stage CRC. APC methylation is not significantly associated with overall survival in patients with CRC.
the promoters of WIF1, NLK, and APC are highly methylated in the nasopharyngeal cancers (NPC) and gastric carcinoma (GC) cell lines, and the 3 genes are also regulated by miR-BART19-3p expressed by Epstein-Barr virus (EBV); expression of the WIF1, APC, and NLK genes is strongly affected by hypermethylation, and in EBV-associated tumors, the 3 genes are also affected by miR-BART19-3p
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