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Human Polyclonal NF2 Primary Antibody pour 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. dans Developmental cell 2010
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Human NF2 Primary Antibody pour IHC - ABIN966567
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. dans Molecular and cellular biology 2005
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Human Polyclonal NF2 Primary Antibody pour IHC - ABIN966568
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. dans The Journal of biological chemistry 2001
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Human Polyclonal NF2 Primary Antibody pour IP, IHC - ABIN104130
Wang, Lu, Tang, Wang, Wu: The phosphorylation status of merlin in sporadic vestibular Schwannomas. dans Molecular and cellular biochemistry 2009
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Cow (Bovine) Polyclonal NF2 Primary Antibody pour WB - ABIN2789402
Vasilyeva, Murzina, Kireev, Pivovarov: Influence of Membrane Receptor Lateral Diffusion on the Short-Term Depression of Acetylcholine-Induced Current in Helix Neurons. dans Cellular and molecular neurobiology 2017
Human Polyclonal NF2 Primary Antibody pour IHC, ELISA - ABIN1532019
Yu, Zeidel, Hill: Cellular expression profile for interstitial cells of cajal in bladder - a cell often misidentified as myocyte or myofibroblast. dans PLoS ONE 2012
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Zebrafish (Danio rerio) Polyclonal NF2 Primary Antibody pour 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. dans Development (Cambridge, England) 2005
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.
The acquired sensitivity to erlotinib supports the known crosstalk between MET and the HER family of receptors. For the first time, we show inactivation of NF2 during acquisition of resistance to MET-TKI that may explain the refractoriness to erlotinib in these cells.
Genetic data coupled with transcriptomic data allowed the identification of a new malignant pleural mesothelioma (MPM)molecular subgroup, C2(LN), characterized by a co-occurring mutation in the LATS2 and NF2 genes in the same MPM. MPM patients of this subgroup presented a poor prognosis. Coinactivation of LATS2 and NF2 leads to loss of cell contact inhibition between MPM cells
The occurrance and evolvement of sporadic intraspinal Schwannomas have a close relationship with mutations of the NF2 gene.
In this study, the authors perform an exome, methylation and RNA-seq analysis of 31 cases of radiation-induced meningioma and show NF2 rearrangement, an observation previously unreported in the sporadic tumors.
An independent set of Sarcomatoid Renal Cell Carcinoma demonstrated mutations in NF2. NF2 mutations were mutually exclusive with TP53 but not with VHL mutations.
sustained activation of Wnt/beta-catenin signaling due to abrogation of Merlin-mediated inhibition of LRP6 phosphorylation may be a cause of Neurofibromatosis type II disease.
Study demonstrated a high frequency of structural variants, including novel truncating fusions of NF2, and an HRR-independent evolution of AC3 signature in low-dose radiation-induced meningiomas.
Four of the five had a mutation in the NF2 gene. Three had a family history of NF2; one of these patients also had a family history of intracranial aneurysm with NF2
Moesin and merlin regulate urokinase receptor-dependent endothelial cell migration, adhesion and angiogenesis
Molecular analyses for NF2 mutations in blood of the irradiated individuals failed to detect disease-causing mutations
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