Use your antibodies-online credentials, if available.
No Products on your Comparison List.
Your basket is empty.
Find out more
Show all synonyms
Select your origin of interest
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 (show NFATC1 Proteins) localization.
In summary, we show that Pten loss per se in Lgr5 (show LGR5 Proteins)+ 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 (show SPP1 Proteins) 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 (show SPP1 Proteins)(+/-) and Min/OPN (show SPP1 Proteins)(-/-) mice was lower than that of Min/OPN (show SPP1 Proteins)(+/+) mice. Colorectal tumor incidences and multiplicities in Min/OPN (show SPP1 Proteins)(+/-) and Min/OPN (show SPP1 Proteins)(-/-) mice were significantly lower than those in Min/OPN (show SPP1 Proteins)(+/+) 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 (show WNT2 Proteins) signaling in hematopoietic stem cells (HSC (show FUT1 Proteins)) biology. As Wnt (show WNT2 Proteins) 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 (show CTNNB1 Proteins) activity in cortical progenitors sets the appropriate Wnt (show WNT2 Proteins) tone necessary for normal cerebral cortical development.
Dll4 (show DLL4 Proteins) seems to promote Apc (Min/+) tumorigenesis.
In cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 (show RAD52 Proteins) gene suppressed tumor growth and prolonged lifespan.
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.
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 (show WNT2 Proteins) signaling pathway in cervical cancer cells infected by high risk HPV16.
miR (show MLXIP Proteins)-3607 contributes to lung cancer cell proliferation by inhibiting APC.
USP7 (show USP7 Proteins) depletion in APC-mutated colorectal cancer inhibits Wnt (show WNT2 Proteins) activation by restoring beta-catenin (show CTNNB1 Proteins) 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 (show MLH1 Proteins)) 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 (show CTNNB1 Proteins) destruction complexes.
Data show that tumor suppressor adenomatous polyposis coli (APC) loss results in up-regulation of IL-6 (show IL6 Proteins) signal transducer (IL-6ST/gp130 (show IL6ST Proteins)), thereby activating YAP (show YAP1 Proteins) (YY1 (show YY1 Proteins)-associated) protein (YAP (show YAP1 Proteins)) which are simultaneously up-regulated in the majority of colorectal cancer (CRC (show CALR Proteins)).
the Amer2 (show AMER2 Proteins)-EB1 (show MAPRE1 Proteins)-APC complex regulates cell migration by altering microtubule stability.
Data show that importin-beta (show KPNB1 Proteins) 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 Proteins) are involved in the Wnt (show WNT2 Proteins) pathway
depletion of APC from cystostatic factor (CSF (show CSF2 Proteins)) Xenopus extracts leads to a decrease in microtubule density and changes in tubulin (show TUBB Proteins) distribution in spindles and asters formed in such extracts
An interaction of tumor-associated N-terminal APC fragments (N-APC) with Mad2 (show MAD2L1 Proteins), an essential mitotic checkpoint (show BUB3 Proteins) 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