Browse our anti-Neurofibromin 2 (NF2) Antibodies

Human Neurofibromin 2 (NF2) interaction partners

1. Expression of c-Myc, neurofibromatosis Type 2, somatostatin receptor 2 and erb-B2 in human meningiomas: relation to grades or histotypes.

2. showed that 77% of NF2 identified variants were detected by coding exons sequencing

3. This is the first report of Merlin functioning as a molecular restraint on cellular metabolism in breast cancer.

4. 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.

5. a correlation between the NF2 status and the growth patterns of sporadic vestibular schwannomas, is reported.

6. Results suggest that fibroblast growth factor receptor 2 (FGFR2) expression might be negatively regulated by neurofibromin 2 (NF2) signaling in the mesothelial cells.

7. lipid binding results in the open conformation of neurofibromin 2 and lipid binding is necessary for inhibiting cell proliferation

8. 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

9. Merlin loss increased oxidative stress causing aberrant activation of Hedgehog signaling in in vitro.

10. 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.

11. 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]

12. 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.

13. 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.

14. 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.

15. 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.

16. 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.

17. 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.

18. 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

19. The occurrance and evolvement of sporadic intraspinal Schwannomas have a close relationship with mutations of the NF2 gene.

20. 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.

Mouse (Murine) Neurofibromin 2 (NF2) interaction partners

1. 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.

2. Data indicate an essential role for NF2 and the Hippo pathway in regulation of branching morphogenesis in the mammalian kidney.

3. Loss of Nf2 causes hyperplasia and ocular abnormalities.

4. 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.

5. Data show that early Smarcb1 loss causes rhabdoid tumors whereas loss at later stages combined with Nf2 gene inactivation causes shwannomas.

6. Rho attenuates the interaction between Amot and Nf2 by binding to the coiled-coil domain of Amot.

7. 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.

8. Merlin controls the repair capacity of Schwann cells after injury by regulating Hippo/YAP signaling activity.

9. NF2 is activated by oxidative stress in cardiomyocytes and myocardium and facilitates apoptosis.

10. loss of axonal contact following nerve injury results in merlin phosphorylation leading to increased p75(NTR) expression.

11. Loss of Nf2 and Cdkn2a/b have synergistic effects with PDGF-B overexpression promoting meningioma malignant transformation.

12. Merlin 1 and 2 act as tumor suppressors and are required for optimal sperm maturation

13. Together our results uncover miRNAs as yet another negative mechanism controlling Merlin tumor suppressor functions.

14. 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.

15. 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.

16. Nf2/Merlin controls spinal cord neural progenitor function in a Rac1/ErbB2-dependent manner.

17. Nf2-Yap signaling plays important roles in controlling the expansion of dorsal root ganglia progenitors and glia during DRG development

18. 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.

19. Findings indicate that merlin is sumoylated and that this post-translational modification is essential for tumor suppression.

20. Cdc42 regulates SC radial sorting in vivo through Neurofibromin 2/merlin dependent signaling pathways

Zebrafish Neurofibromin 2 (NF2) interaction partners

1. Mutation of nf2 gene develops extrahepatic choledochal cysts in the common bile duct

Xenopus laevis Neurofibromin 2 (NF2) interaction partners

1. NF2/Merlin negatively regulates the Wnt/beta-catenin signaling activity during the pattern formation in early embryos.