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Msi-1 (show MSI1 ELISA Kits) contributes to intestinal tumorigenesis driven by Apc loss, and validate the pursuit of Msi-1 (show MSI1 ELISA Kits) inhibitors as chemo-prevention agents to reduce tumor burden.
we provide mechanistic insight into the role of APC mutations and Wnt (show WNT2 ELISA Kits) signaling in hematopoietic stem cells (HSC (show FUT1 ELISA Kits)) biology. As Wnt (show WNT2 ELISA Kits) 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 ELISA Kits) activity in cortical progenitors sets the appropriate Wnt (show WNT2 ELISA Kits) tone necessary for normal cerebral cortical development.
Dll4 (show DLL4 ELISA Kits) seems to promote Apc (Min/+) tumorigenesis.
In cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 (show RAD52 ELISA Kits) 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 (show TP53 ELISA Kits) 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 (show TGFBR2 ELISA Kits) in the presence of mutated Apc, promoting colorectal cancer cell proliferation.
By sequencing Apc and Ctnnb1 (show CTNNB1 ELISA Kits) genes, we found that most PhIP (show PHIP ELISA Kits)-induced small intestinal tumors in obese mice carried only a single heterozygous mutation in Apc . Our findings demonstrate that PhIP (show PHIP ELISA Kits)-induced small intestinal carcinogenesis in hCYP1A-db/db (show LEPR ELISA Kits) mice is promoted by obesity and involves Apc mutation and inactivation by DNA hypermethylation
Elevated coexpression of KITENIN (show Vangl1 ELISA Kits) and ErbB4 (show ERBB4 ELISA Kits)-CYT (show CYGB ELISA Kits)-2 promotes the transition of colon adenoma to adenocarcinoma within an APC loss-associated tumor microenvironment
FZR1 inhibits BRAF oncogenic functions via both APC-dependent proteolysis and APC-independent disruption of BRAF dimers, whereas hyperactivated ERK and CDK4 reciprocally suppress APC(FZR1) E3 ligase activity
Establish a role for APC in coordinating microtubules and actin cytoskeleton at focal adhesions to direct cell migration.
Germline mutation in the APC gene is associated with familial adenomatous polyposis.
beta-catenin (show CTNNB1 ELISA Kits) reactivity was noted in all familial adenomatous polyposis-associated Gardner fibromas and in 1/4 APC wild-type cases
The rs75612255 C allele and rs113017087 C allele in promoter 1A of APC as well as the rs138386816 T allele and rs115658307 T allele in promoter 1B of APC significantly increased luciferase activity in the human erythromyeloblastoid leukaemia cell line K562.
Functional redundancy between Apc and Apc2 regulates tissue homeostasis and prevents tumorigenesis in murine mammary epithelium
Finally, we observed that expression of miR-19a significantly correlates with beta-catenin levels in colorectal cancer specimens, and it is associated to the aggressive stage of tumor progression. Thus, our study reveals that miR-17-92 cluster is directly regulated by APC/b-catenin pathway and could be a potential therapeutic target in colon cancers with aberrant APC/b-catenin signaling.
Findings show that colorectal Cancer patients-derived cells with short APC mutants were either sensitive or responsive to tankyrase inhibitors corroborating the idea that APC with complete deletion of seven 20-AA repeats could be a predictive biomarker for the sensitivity to tankyrase inhibitors.
Our study showed that mutations in the APC gene alter the protein expression and cell cycle regulation in diffuse type gastric adenocarcinoma.
the Amer2 (show AMER2 ELISA Kits)-EB1 (show MAPRE1 ELISA Kits)-APC complex regulates cell migration by altering microtubule stability.
Data show that importin-beta (show KPNB1 ELISA Kits) 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 ELISA Kits) are involved in the Wnt (show WNT2 ELISA Kits) pathway
depletion of APC from cystostatic factor (CSF (show CSF2 ELISA Kits)) Xenopus extracts leads to a decrease in microtubule density and changes in tubulin (show TUBB ELISA Kits) distribution in spindles and asters formed in such extracts
An interaction of tumor-associated N-terminal APC fragments (N-APC) with Mad2 (show MAD2L1 ELISA Kits), an essential mitotic checkpoint (show BUB3 ELISA Kits) 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