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Human Polyclonal NF2 Primary Antibody für IP, IHC - ABIN104130
Wang, Lu, Tang, Wang, Wu: The phosphorylation status of merlin in sporadic vestibular Schwannomas. in Molecular and cellular biochemistry 2009
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Human Polyclonal NF2 Primary Antibody für IHC - ABIN966568
Xiao, Gallagher, Shetler, Skele, Altomare, Pestell, Jhanwar, Testa: The NF2 tumor suppressor gene product, merlin, inhibits cell proliferation and cell cycle progression by repressing cyclin D1 expression. in Molecular and cellular biology 2005
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Human NF2 Primary Antibody für IHC - ABIN966567
Ratner, Bryan, Weber, Nguyen, Barnes, Pitt, Gelber, Cheung, Prince: Cystic fibrosis pathogens activate Ca2+-dependent mitogen-activated protein kinase signaling pathways in airway epithelial cells. in The Journal of biological chemistry 2001
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Human Polyclonal NF2 Primary Antibody für ICC, IF - ABIN4339287
Zhang, Bai, David, Dong, Zheng, Cai, Giovannini, Liu, Anders, Pan: The Merlin/NF2 tumor suppressor functions through the YAP oncoprotein to regulate tissue homeostasis in mammals. in Developmental cell 2010
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Zebrafish (Danio rerio) Polyclonal NF2 Primary Antibody für IHC (p), ELISA - ABIN547975
Sadler, Amsterdam, Soroka, Boyer, Hopkins: A genetic screen in zebrafish identifies the mutants vps18, nf2 and foie gras as models of liver disease. in Development (Cambridge, England) 2005
Cow (Bovine) Polyclonal NF2 Primary Antibody für WB - ABIN2789402
Vasilyeva, Murzina, Kireev, Pivovarov: Influence of Membrane Receptor Lateral Diffusion on the Short-Term Depression of Acetylcholine-Induced Current in Helix Neurons. in Cellular and molecular neurobiology 2017
Human Polyclonal NF2 Primary Antibody für IHC, ELISA - ABIN1532019
Yu, Zeidel, Hill: Cellular expression profile for interstitial cells of cajal in bladder - a cell often misidentified as myocyte or myofibroblast. in PLoS ONE 2012
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reduction or deletion of TbetaR2 or NF2 induces the TbetaR1-mediated oncogenic pathway, and therefore inhibition of the unbalanced TGFbeta signaling is a putative strategy for NF2-related cancers
Merlin regulates contact inhibition and is an integral part of cell-cell junctions, while ERM proteins, ezrin, radixin and moesin, assist in the formation and maintenance of specialized plasma membrane structures and membrane vesicle structures. [review]
Study in human colorectal carcinoma and lung adenocarcinoma cells revealed downregulation of NF2 by miR92a3p via its wildtype 3'UTR, but not NF23'UTR with mutated miR92a3p MRE. miR92a3p overexpression in cancer cells promoted migration, proliferation and resistance to apoptosis, as well as altered Factin organization compared with controls.
we identify nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB)-inducing kinase (NIK) as a potential drug target driving NF-kappaB signaling and Merlin-deficient schwannoma genesis
Expression of c-Myc, neurofibromatosis Type 2, somatostatin receptor 2 and erb-B2 in human meningiomas: relation to grades or histotypes.
showed that 77% of NF2 identified variants were detected by coding exons sequencing
This is the first report of Merlin functioning as a molecular restraint on cellular metabolism in breast cancer.
Data indicate that mutations affecting SMARCB1 play a role in the development or progression of a small subset of spinal schwannomas and that biallelic inactivation of SMARCB1 may cooperate with deficiency of NF2 function in schwannoma tumorigenesis.
a correlation between the NF2 status and the growth patterns of sporadic vestibular schwannomas, is reported.
Results suggest that fibroblast growth factor receptor 2 (FGFR2) expression might be negatively regulated by neurofibromin 2 (NF2) signaling in the mesothelial cells.
lipid binding results in the open conformation of neurofibromin 2 and lipid binding is necessary for inhibiting cell proliferation
Cell viability results showed that three agents (GSK2126458, Panobinostat, CUDC-907) had the greatest activity across schwannoma and meningioma cell systems, but merlin status did not significantly influence response
Merlin loss increased oxidative stress causing aberrant activation of Hedgehog signaling in in vitro.
NF2 promoter gene mutations occurred in medulloblastoma (MB) patients. The NF2 mRNA expression was higher in the controls than in patients; however NF2 protein expression was significantly higher in patients than in the controls. NF2 protein was mainly expressed in the nucleus in MB patients, while the NF2 protein was mainly expressed in the cytoplasm in the controls.
Study summarizes the current knowledge of molecular events triggered by NF2/merlin inactivation, which lead to the development of mesothelioma and other cancers. Genetic alterations in NF2 that abrogate merlin's functional activity are found in about 40% of malignant mesothelioma (MM), indicating the importance of NF2 inactivation in MM development and progression. [review]
Study identified missense NF2 mutations in 1.9% hepatocellular carcinoma (HCC) and 5.3% intrahepatic cholangiocarcinoma (ICC). Allele frequency of NF2 IVS4-39 A/A was significantly higher in HCCs. Also, NF2/Merlin showed a dual role as a tumorigenic gene and tumor-suppressor gene; Merlin was expressed at higher levels in HCC tumors ; while the rate of Merlin upregulation was lower in poorly differentiated ICCs.
This study demonstrates that simultaneous inhibition of c-Met and Src signaling in MD-MSCs triggers apoptosis and reveals vulnerable pathways that could be exploited to develop NF2 therapies.
These results indicate that Merlin/YAP/cMyc/mTOR signaling axis promotes human cholangiocarcinoma (CCA) cell proliferation by overriding contact inhibition. We propose that overriding cMycmediated contact inhibition is implicated in the development of CCA.
The genetic alterations observed in the NF2 gene indicated that spinal schwannomas are associated with genetic alterations also found in other schwannomas and type 2 Neurofibromatosis, which reinforces the etiological role of this gene.
Methylation of NF2 and DNMT1 was markedly increased, and miR-152-3p was downregulated in GBM tissues and glioma cells. Both knockdown of DNMT1 and overexpression miR-152-3p showed that demethylation activated the expression of NF2.
Results demonstrate that loss of merlin function in Schwann Cells (SCs) leads to increased endoneurial space and ultrastructural myelin alterations in the sciatic nerve before and after injury. Loss of merlin function in SCs delays neural recovery following injury. Nevertheless, there were no significant functional or electrophysiological differences in neural regeneration attributable to Nf2 mutation in SCs.
Data indicate an essential role for NF2 and the Hippo pathway in regulation of branching morphogenesis in the mammalian kidney.
Loss of Nf2 causes hyperplasia and ocular abnormalities.
studies suggest that NF2 normally limits biliary morphogenesis by coordinating lumen expansion and cell architecture. This work provides fundamental insight into how biliary fate and tubulogenesis are coordinated during development and will guide analyses of disease-associated and experimentally induced biliary pathologies.
Data show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined with Nf2 gene inactivation causes shwannomas.
Rho attenuates the interaction between Amot and Nf2 by binding to the coiled-coil domain of Amot.
co-deletion of Rac1 with Nf2 blocks tumor initiation but paradoxically exacerbates hepatomegaly induced by Nf2 loss, which can be suppressed either by treatment with pro-oxidants or by co-deletion of Yap.
Merlin controls the repair capacity of Schwann cells after injury by regulating Hippo/YAP signaling activity.
NF2 is activated by oxidative stress in cardiomyocytes and myocardium and facilitates apoptosis.
loss of axonal contact following nerve injury results in merlin phosphorylation leading to increased p75(NTR) expression.
Loss of Nf2 and Cdkn2a/b have synergistic effects with PDGF-B overexpression promoting meningioma malignant transformation.
Merlin 1 and 2 act as tumor suppressors and are required for optimal sperm maturation
Together our results uncover miRNAs as yet another negative mechanism controlling Merlin tumor suppressor functions.
Merlin and Ezrin are components of a mechanism where mechanical forces associated with cell junctions are transduced across the cell cortex via cortical actomyosin cytoskeleton to control lateral mobility and activity of epidermal growth factor receptor.
The study describe a novel NF2 mouse model recapitulating schwannoma phenotypes found in human patients where tumors develop in the cranial nerve VIII and/or the spinal roots.
Nf2/Merlin controls spinal cord neural progenitor function in a Rac1/ErbB2-dependent manner.
Nf2-Yap signaling plays important roles in controlling the expansion of dorsal root ganglia progenitors and glia during DRG development
CD44 cytoplasmic tail cleaved by RIP could release DCAF1 from merlin by competing for binding to the merlin FERM domain, which results in the inhibition of merlin-mediated suppression of tumorigenesis.
Findings indicate that merlin is sumoylated and that this post-translational modification is essential for tumor suppression.
Cdc42 regulates SC radial sorting in vivo through Neurofibromin 2/merlin dependent signaling pathways
Mutation of nf2 gene develops extrahepatic choledochal cysts in the common bile duct
NF2/Merlin negatively regulates the Wnt/beta-catenin signaling activity during the pattern formation in early embryos.
This gene encodes a protein that is similar to some members of the ERM (ezrin, radixin, moesin) family of proteins that are thought to link cytoskeletal components with proteins in the cell membrane. This gene product has been shown to interact with cell-surface proteins, proteins involved in cytoskeletal dynamics and proteins involved in regulating ion transport. This gene is expressed at high levels during embryonic development\; in adults, significant expression is found in Schwann cells, meningeal cells, lens and nerve. Mutations in this gene are associated with neurofibromatosis type II which is characterized by nervous system and skin tumors and ocular abnormalities. Two predominant isoforms and a number of minor isoforms are produced by alternatively spliced transcripts.
, moesin-ezrin-radixin like
, moesin-ezrin-radixin-like protein
, moesin-ezrin-radizin-like protein
, neurofibromin 2 (bilateral acoustic neuroma)
, neurofibromin 2
, neurofibromatosis 2
, LOW QUALITY PROTEIN: merlin
, neurofibromin 2 (merlin) S homeolog