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Mouse (Murine) Monoclonal APC Primary Antibody für 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 für 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 für ICC, IF - ABIN4280975
Liu, Tackmann, Yang, Zhang: Disruption of the RP-MDM2-p53 pathway accelerates APC loss-induced colorectal tumorigenesis. in Oncogene 2016
In summary, we show that Pten loss per se in Lgr5 (zeige LGR5 Antikörper)+ 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 (zeige SPP1 Antikörper) 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 (zeige SPP1 Antikörper)(+/-) and Min/OPN (zeige SPP1 Antikörper)(-/-) mice was lower than that of Min/OPN (zeige SPP1 Antikörper)(+/+) mice. Colorectal tumor incidences and multiplicities in Min/OPN (zeige SPP1 Antikörper)(+/-) and Min/OPN (zeige SPP1 Antikörper)(-/-) mice were significantly lower than those in Min/OPN (zeige SPP1 Antikörper)(+/+) 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 (zeige WNT2 Antikörper) signaling in hematopoietic stem cells (HSC (zeige FUT1 Antikörper)) biology. As Wnt (zeige WNT2 Antikörper) 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 Antikörper) activity in cortical progenitors sets the appropriate Wnt (zeige WNT2 Antikörper) tone necessary for normal cerebral cortical development.
Dll4 (zeige DLL4 Antikörper) seems to promote Apc (Min/+) tumorigenesis.
In cancer-prone, heterozygous APC mutant mice, homozygous deletion of the Rad52 (zeige RAD52 Antikörper) 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 Antikörper) deletion resulted in the development of a distinct type of pancreatic premalignant precursors, mucinous cystic neoplasms (MCNs)
We conclude that among multiple genomic alterations in CRC (zeige CALR Antikörper), strongest associations with clinical outcome were observed for common mutations in APC.
Studies reveal that the proportion of APC promoter 1A methylation in non-small cell lung cancer (NSCLC) tissues was higher than in autologous controls, indicating that promoter 1A methylation of the APC gene may play an important role in NSCLC carcinogenesis. [meta-analysis]
E-cadherin (zeige CDH1 Antikörper) inhibits beta-catenin (zeige CTNNB1 Antikörper) in the context of disruption of the APC-destruction complex, and that this function is also EC1 domain dependent. Both binding functions of E-cadherin (zeige CDH1 Antikörper) may be required for its tumour suppressor activity.
analysis of the largest deletion of the APC gene in the Chinese population associated with familial adenomatous polyposis in a five generation family
APC promoter methylation was associated with breast cancer risk, and it could be a valuable biomarker for diagnosis, treatment and prognosis of breast cancer (Meta-Analysis)
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 (zeige EPHB6 Antikörper) 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 (zeige BRP44L Antikörper) and Adenomatous polyposis coli (APC), a key tumor suppressor in colorectal cancer, the authors found that apc controls the levels of mpc1 (zeige BRP44L Antikörper) and that knock down of mpc1 (zeige BRP44L Antikörper) recapitulates phenotypes of impaired apc function including failed intestinal differentiation.
Multiple pilomatrixomas in a survivor of WNT (zeige WNT2 Antikörper)-activated medulloblastoma leading to the discovery of a germline APC mutation and the diagnosis of familial adenomatous polyposis
FZR1 (zeige FZR1 Antikörper) inhibits BRAF (zeige BRAF Antikörper) oncogenic functions via both APC-dependent proteolysis and APC-independent disruption of BRAF (zeige BRAF Antikörper) dimers, whereas hyperactivated ERK (zeige EPHB2 Antikörper) and CDK4 (zeige CDK4 Antikörper) reciprocally suppress APC(FZR1 (zeige FZR1 Antikörper)) E3 ligase activity
the Amer2 (zeige AMER2 Antikörper)-EB1 (zeige MAPRE1 Antikörper)-APC complex regulates cell migration by altering microtubule stability.
Data show that importin-beta (zeige KPNB1 Antikörper) 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 Antikörper) are involved in the Wnt (zeige WNT2 Antikörper) pathway
depletion of APC from cystostatic factor (CSF (zeige CSF2 Antikörper)) Xenopus extracts leads to a decrease in microtubule density and changes in tubulin (zeige TUBB Antikörper) distribution in spindles and asters formed in such extracts
An interaction of tumor-associated N-terminal APC fragments (N-APC) with Mad2 (zeige MAD2L1 Antikörper), an essential mitotic checkpoint (zeige BUB3 Antikörper) 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