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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 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 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
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
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 (Montrer NFATC1 Anticorps) localization.
In summary, we show that Pten loss per se in Lgr5 (Montrer LGR5 Anticorps)+ 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 (Montrer SPP1 Anticorps) 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 (Montrer SPP1 Anticorps)(+/-) and Min/OPN (Montrer SPP1 Anticorps)(-/-) mice was lower than that of Min/OPN (Montrer SPP1 Anticorps)(+/+) mice. Colorectal tumor incidences and multiplicities in Min/OPN (Montrer SPP1 Anticorps)(+/-) and Min/OPN (Montrer SPP1 Anticorps)(-/-) mice were significantly lower than those in Min/OPN (Montrer SPP1 Anticorps)(+/+) 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 (Montrer WNT2 Anticorps) signaling in hematopoietic stem cells (HSC (Montrer FUT1 Anticorps)) biology. As Wnt (Montrer WNT2 Anticorps) 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 (Montrer CTNNB1 Anticorps) activity in cortical progenitors sets the appropriate Wnt (Montrer WNT2 Anticorps) tone necessary for normal cerebral cortical development.
Dll4 (Montrer DLL4 Anticorps) seems to promote Apc (Min/+) tumorigenesis.
In cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 (Montrer RAD52 Anticorps) gene suppressed tumor growth and prolonged lifespan.
In the two wild type (WT) cases, two novel alterations were detected: a complex deletion of APC and a pathogenic mutation of LAMTOR2 (Montrer LAMTOR2 Anticorps). Focusing on WT DT subtype, deep sequencing of CTNNB1 (Montrer CTNNB1 Anticorps), APC and LAMTOR2 (Montrer LAMTOR2 Anticorps) 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 (Montrer TBC1D9 Anticorps)/CLCX-1 signaling pathway.
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 (Montrer WNT2 Anticorps) signaling pathway in cervical cancer cells infected by high risk HPV16.
miR (Montrer MLXIP Anticorps)-3607 contributes to lung cancer cell proliferation by inhibiting APC.
USP7 (Montrer USP7 Anticorps) depletion in APC-mutated colorectal cancer inhibits Wnt (Montrer WNT2 Anticorps) activation by restoring beta-catenin (Montrer CTNNB1 Anticorps) 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 (Montrer MLH1 Anticorps)) 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 (Montrer CTNNB1 Anticorps) destruction complexes.
the Amer2 (Montrer AMER2 Anticorps)-EB1 (Montrer MAPRE1 Anticorps)-APC complex regulates cell migration by altering microtubule stability.
Data show that importin-beta (Montrer KPNB1 Anticorps) binds to Apc and negatively regulates the MT-assembly and spindle-promoting activity of Apc in a Ran-regulatable manner.
APC and Axin (Montrer AXIN1 Anticorps) are involved in the Wnt (Montrer WNT2 Anticorps) pathway
depletion of APC from cystostatic factor (CSF (Montrer CSF2 Anticorps)) Xenopus extracts leads to a decrease in microtubule density and changes in tubulin (Montrer TUBB Anticorps) distribution in spindles and asters formed in such extracts
An interaction of tumor-associated N-terminal APC fragments (N-APC) with Mad2 (Montrer MAD2L1 Anticorps), an essential mitotic checkpoint (Montrer BUB3 Anticorps) 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