calpain has been researched along with Neurilemmoma* in 2 studies
1 review(s) available for calpain and Neurilemmoma
| Article | Year |
|---|---|
Calpain-dependent proteolysis of NF2 protein: involvement in schwannomas and meningiomas.
The neurofibromatosis type 2 (NF2) protein, known as merlin or schwannomin, is a tumor suppressor, and the NF2 gene has been found to be mutated in the majority of schwannomas and meningiomas, including both sporadically occurring and familial NF2 cases. Although the development of these tumors depends on the loss of merlin, the presence of tumors lacking detectable NF2 mutations suggests different mechanisms for inactivating merlin. Recent studies have demonstrated cleavage of merlin by calpain, a calcium-dependent neutral cysteine protease, and marked activation of the calpain system resulting in the degradation of merlin in these tumors. Increased turnover of merlin by calpain in some schwannomas and meningiomas exemplifies tumorigenesis linked to the calpain-mediated proteolytic pathway. Topics: Calpain; Genes, Neurofibromatosis 2; Humans; Membrane Proteins; Meningioma; Mutation; Neurilemmoma; Neurofibromatosis 2; Neurofibromin 2; Peptide Hydrolases | 2000 |
1 other study(ies) available for calpain and Neurilemmoma
| Article | Year |
|---|---|
The involvement of calpain-dependent proteolysis of the tumor suppressor NF2 (merlin) in schwannomas and meningiomas.
Neurofibromatosis type 2 (NF2) protein, also known as merlin or schwannomin, is a tumor suppressor, and NF2 is mutated in most schwannomas and meningiomas. Although these tumors are dependent on NF2, some lack detectable NF2 mutations, which indicates that alternative mechanisms exist for inactivating merlin. Here, we demonstrate cleavage of merlin by the ubiquitous protease calpain and considerable activation of the calpain system resulting in the loss of merlin expression in these tumors. Increased proteolysis of merlin by calpain in some schwannomas and meningiomas exemplifies tumorigenesis linked to the calpain-mediated proteolytic pathway. Topics: Base Sequence; Brain Neoplasms; Calpain; Cell Line; DNA Primers; Enzyme Activation; Genes, Neurofibromatosis 2; Glioma; Glutathione Transferase; Humans; Membrane Proteins; Meningioma; Molecular Sequence Data; Mutagenesis, Site-Directed; Neurilemmoma; Neurofibromin 2; Polymerase Chain Reaction; Recombinant Fusion Proteins; RNA, Messenger; Templates, Genetic; Transcription, Genetic; Transfection; Tumor Cells, Cultured | 1998 |