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Mouse (Murine) Monoclonal APC Primary Antibody for IF, ELISA - ABIN1585993
Gaebler, Gruell, Velinzon, Scheid, Nussenzweig, Klein: Isolation of HIV-1-reactive antibodies using cell surface-expressed gp160Δc(BaL.). in Journal of immunological methods 2014
Human Monoclonal APC Primary Antibody for IHC (fro), IP - ABIN152091
Abutaily, Collins, Roche: Cadherins, catenins and APC in pleural malignant mesothelioma. in The Journal of pathology 2003
Show all 2 Pubmed References
Human Polyclonal APC Primary Antibody for ICC, IF - ABIN4280975
Liu, Tackmann, Yang, Zhang: Disruption of the RP-MDM2-p53 pathway accelerates APC loss-induced colorectal tumorigenesis. in Oncogene 2016
we provide mechanistic insight into the role of APC mutations and Wnt (show WNT2 Antibodies) signaling in hematopoietic stem cells (HSC (show FUT1 Antibodies)) biology. As Wnt (show WNT2 Antibodies) 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 Antibodies) activity in cortical progenitors sets the appropriate Wnt (show WNT2 Antibodies) tone necessary for normal cerebral cortical development.
Dll4 (show DLL4 Antibodies) seems to promote Apc (Min/+) tumorigenesis.
In cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 (show RAD52 Antibodies) 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 Antibodies) 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 Antibodies) in the presence of mutated Apc, promoting colorectal cancer cell proliferation.
By sequencing Apc and Ctnnb1 (show CTNNB1 Antibodies) genes, we found that most PhIP (show PHIP Antibodies)-induced small intestinal tumors in obese mice carried only a single heterozygous mutation in Apc . Our findings demonstrate that PhIP (show PHIP Antibodies)-induced small intestinal carcinogenesis in hCYP1A-db/db (show LEPR Antibodies) mice is promoted by obesity and involves Apc mutation and inactivation by DNA hypermethylation
Elevated coexpression of KITENIN (show Vangl1 Antibodies) and ErbB4 (show ERBB4 Antibodies)-CYT (show CYGB Antibodies)-2 promotes the transition of colon adenoma to adenocarcinoma within an APC loss-associated tumor microenvironment
The activation of canonical Wnt (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling by deletion of Apc in cardiomyocytes led to ventricular hyperplasia.
A novel APC promoter 1B deletion is associated with familial adenomatous polyposis in generations of a large Italian family.
Study is the first to demonstrate that EphB6 (show EPHB6 Antibodies) overexpression together with Apc gene mutations may enhance proliferation, invasion and metastasis by colorectal epithelial cells.
Utilizing zebrafish to examine the genetic relationship between MPC1 (show BRP44L Antibodies) and Adenomatous polyposis coli (APC), a key tumor suppressor in colorectal cancer, the authors found that apc controls the levels of mpc1 (show BRP44L Antibodies) and that knock down of mpc1 (show BRP44L Antibodies) recapitulates phenotypes of impaired apc function including failed intestinal differentiation.
Multiple pilomatrixomas in a survivor of WNT (show WNT2 Antibodies)-activated medulloblastoma leading to the discovery of a germline APC mutation and the diagnosis of familial adenomatous polyposis
FZR1 (show FZR1 Antibodies) inhibits BRAF (show BRAF Antibodies) oncogenic functions via both APC-dependent proteolysis and APC-independent disruption of BRAF (show BRAF Antibodies) dimers, whereas hyperactivated ERK (show EPHB2 Antibodies) and CDK4 (show CDK4 Antibodies) reciprocally suppress APC(FZR1 (show FZR1 Antibodies)) 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 Antibodies) 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
the Amer2 (show AMER2 Antibodies)-EB1 (show MAPRE1 Antibodies)-APC complex regulates cell migration by altering microtubule stability.
Data show that importin-beta (show KPNB1 Antibodies) 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 Antibodies) are involved in the Wnt (show WNT2 Antibodies) pathway
depletion of APC from cystostatic factor (CSF (show CSF2 Antibodies)) Xenopus extracts leads to a decrease in microtubule density and changes in tubulin (show TUBB Antibodies) distribution in spindles and asters formed in such extracts
An interaction of tumor-associated N-terminal APC fragments (N-APC) with Mad2 (show MAD2L1 Antibodies), an essential mitotic checkpoint (show BUB3 Antibodies) 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