Browse our anti-Neurofibromin 2 (NF2) Antibodies

Human Neurofibromin 2 (NF2) interaction partners

1. Merlin loss increased oxidative stress causing aberrant activation of Hedgehog (show SHH Antibodies) signaling in in vitro.

2. 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.

3. 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]

4. Study identified missense NF2 mutations in 1.9% hepatocellular carcinoma (HCC (show FAM126A Antibodies)) and 5.3% intrahepatic cholangiocarcinoma (ICC). Allele frequency of NF2 IVS4-39 A/A was significantly higher in HCCs (show HCCS Antibodies). Also, NF2/Merlin showed a dual role as a tumorigenic gene and tumor-suppressor gene; Merlin was expressed at higher levels in HCC (show FAM126A Antibodies) tumors ; while the rate of Merlin upregulation was lower in poorly differentiated ICCs.

5. This study demonstrates that simultaneous inhibition of c-Met and Src (show SRC Antibodies) signaling in MD-MSCs triggers apoptosis and reveals vulnerable pathways that could be exploited to develop NF2 therapies.

6. These results indicate that Merlin/YAP (show YAP1 Antibodies)/cMyc (show MYC Antibodies)/mTOR (show FRAP1 Antibodies) signaling axis promotes human cholangiocarcinoma (CCA (show FBN2 Antibodies)) cell proliferation by overriding contact inhibition. We propose that overriding cMycmediated contact inhibition is implicated in the development of CCA (show FBN2 Antibodies).

7. 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.

8. Methylation of NF2 and DNMT1 (show DNMT1 Antibodies) was markedly increased, and miR (show MLXIP Antibodies)-152-3p was downregulated in GBM tissues and glioma cells. Both knockdown of DNMT1 (show DNMT1 Antibodies) and overexpression miR (show MLXIP Antibodies)-152-3p showed that demethylation activated the expression of NF2.

9. 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.

10. 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

Mouse (Murine) Neurofibromin 2 (NF2) interaction partners

1. Results demonstrate that loss of merlin function in Schwann Cells (SCs (show TWIST1 Antibodies)) leads to increased endoneurial space and ultrastructural myelin alterations in the sciatic nerve before and after injury. Loss of merlin function in SCs (show TWIST1 Antibodies) delays neural recovery following injury. Nevertheless, there were no significant functional or electrophysiological differences in neural regeneration attributable to Nf2 mutation in SCs (show TWIST1 Antibodies).

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 (show SMARCB1 Antibodies) loss causes rhabdoid tumors whereas loss at later stages combined with Nf2 gene inactivation causes shwannomas.

6. Rho attenuates the interaction between Amot (show AMOT Antibodies) and Nf2 by binding to the coiled-coil domain of Amot (show AMOT Antibodies).

7. co-deletion of Rac1 (show RAC1 Antibodies) 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 Antibodies).

8. Merlin controls the repair capacity of Schwann cells after injury by regulating Hippo/YAP (show YAP1 Antibodies) 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 (show NGFR Antibodies)) expression.

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 (show WNT2 Antibodies)/beta-catenin (show CTNNB1 Antibodies) signaling activity during the pattern formation in early embryos.