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Mutation of nf2 gene develops extrahepatic choledochal cysts in the common bile duct
Data show that early Smarcb1 (show SMARCB1 ELISA Kits) loss causes rhabdoid tumors whereas loss at later stages combined with Nf2 gene inactivation causes shwannomas.
Rho attenuates the interaction between Amot (show AMOT ELISA Kits) and Nf2 by binding to the coiled-coil domain of Amot (show AMOT ELISA Kits).
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 (show YAP1 ELISA Kits).
Merlin controls the repair capacity of Schwann cells after injury by regulating Hippo/YAP (show YAP1 ELISA Kits) 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 (show NGFR ELISA Kits)) expression.
Loss of Nf2 and Cdkn2a/b have synergistic effects with PDGF-B (show PDGFB ELISA Kits) 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 (show EZR ELISA Kits) 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 (show EGFR ELISA Kits).
An independent set of Sarcomatoid Renal Cell Carcinoma demonstrated mutations in NF2. NF2 mutations were mutually exclusive with TP53 (show TP53 ELISA Kits) but not with VHL (show VHL ELISA Kits) mutations.
sustained activation of Wnt (show WNT2 ELISA Kits)/beta-catenin (show CTNNB1 ELISA Kits) signaling due to abrogation of Merlin-mediated inhibition of LRP6 (show LRP6 ELISA Kits) 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 (show ADCY3 ELISA Kits) 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 (show MSN ELISA Kits) 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
We suggest that PrP(C (show PRNP ELISA Kits)) and its interactor, LR/37/67 kDa, could be potential therapeutic targets for schwannomas and other Merlin-deficient tumours.
These findings uncover the significance of Merlin protein expression and Survivin (show BIRC5 ELISA Kits) labeling index as prognosticators for poor clinical outcome in two independent Malignant pleural mesothelioma cohorts.
NF2 localizes in nucleus when Ser518 is not phosphorylated, while phosphorylated form is present in cytoplasm and plasma membrane. Data suggest that binding of NF2 to TIMAP (show PPP1R16B ELISA Kits) and EBP50 (show SLC9A3R1 ELISA Kits) is critical in nuclear localization of NF2. (NF2 = neurofibromin 2; TIMAP (show PPP1R16B ELISA Kits) = TGF-beta-inhibited membrane-associated protein (show PPP1R16B ELISA Kits); EBP50 (show SLC9A3R1 ELISA Kits) = Ezrin (show EZR ELISA Kits)-Radixin (show RDX ELISA Kits)-Mosein binding phosphoprotein 50)
Low merlin expression is associated with meningioma and schwannoma.
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.
neurofibromin 2 (bilateral acoustic neuroma)
, neurofibromatosis 2
, neurofibromin 2
, moesin-ezrin-radixin-like protein
, moesin-ezrin-radixin like
, moesin-ezrin-radizin-like protein