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we provide mechanistic insight into the role of APC mutations and Wnt (zeige WNT2 ELISA Kits) signaling in hematopoietic stem cells (HSC (zeige FUT1 ELISA Kits)) biology. As Wnt (zeige 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 (zeige CTNNB1 ELISA Kits) activity in cortical progenitors sets the appropriate Wnt (zeige WNT2 ELISA Kits) tone necessary for normal cerebral cortical development.
Dll4 (zeige DLL4 ELISA Kits) seems to promote Apc (Min/+) tumorigenesis.
In cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 (zeige 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 (zeige 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 (zeige TGFBR2 ELISA Kits) in the presence of mutated Apc, promoting colorectal cancer cell proliferation.
By sequencing Apc and Ctnnb1 (zeige CTNNB1 ELISA Kits) genes, we found that most PhIP (zeige PHIP ELISA Kits)-induced small intestinal tumors in obese mice carried only a single heterozygous mutation in Apc . Our findings demonstrate that PhIP (zeige PHIP ELISA Kits)-induced small intestinal carcinogenesis in hCYP1A-db/db (zeige LEPR ELISA Kits) mice is promoted by obesity and involves Apc mutation and inactivation by DNA hypermethylation
Elevated coexpression of KITENIN (zeige Vangl1 ELISA Kits) and ErbB4 (zeige ERBB4 ELISA Kits)-CYT (zeige CYGB ELISA Kits)-2 promotes the transition of colon adenoma to adenocarcinoma within an APC loss-associated tumor microenvironment
The activation of canonical Wnt (zeige WNT2 ELISA Kits)/beta-catenin (zeige CTNNB1 ELISA Kits) signaling by deletion of Apc in cardiomyocytes led to ventricular hyperplasia.
Utilizing zebrafish to examine the genetic relationship between MPC1 (zeige BRP44L ELISA Kits) and Adenomatous polyposis coli (APC), a key tumor suppressor in colorectal cancer, the authors found that apc controls the levels of mpc1 (zeige BRP44L ELISA Kits) and that knock down of mpc1 (zeige BRP44L ELISA Kits) recapitulates phenotypes of impaired apc function including failed intestinal differentiation.
Multiple pilomatrixomas in a survivor of WNT (zeige WNT2 ELISA Kits)-activated medulloblastoma leading to the discovery of a germline APC mutation and the diagnosis of familial adenomatous polyposis
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 (zeige 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.
the Amer2 (zeige AMER2 ELISA Kits)-EB1 (zeige MAPRE1 ELISA Kits)-APC complex regulates cell migration by altering microtubule stability.
Data show that importin-beta (zeige 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 (zeige AXIN1 ELISA Kits) are involved in the Wnt (zeige WNT2 ELISA Kits) pathway
depletion of APC from cystostatic factor (CSF (zeige CSF2 ELISA Kits)) Xenopus extracts leads to a decrease in microtubule density and changes in tubulin (zeige 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 (zeige MAD2L1 ELISA Kits), an essential mitotic checkpoint (zeige 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