neurofibromatoses/protease

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Molecular alterations in the neurofibromatosis type 2 gene and its protein rarely occurring in meningothelial meningiomas.

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OBJECTIVE The neurofibromatosis Type 2 (NF2) gene is the only tumor suppressor gene that has been clearly implicated in the development of benign meningiomas. Interestingly, previous data obtained by the authors indicate that reduced NF2 protein expression seldom occurs in meningothelial

A universal expression-purification system based on the coiled-coil interaction of myosin heavy chain.

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We have constructed a series of Escherichia coli expression vectors that produce high yields of fusion proteins containing the C-terminal fragment of light meromyosin (LMM) from rabbit fast skeletal muscle. The fusion proteins retain the ability of LMM to form polymers in low salt and to be soluble

Calpain-dependent proteolysis of NF2 protein: involvement in schwannomas and meningiomas.

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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

The involvement of calpain-dependent proteolysis of the tumor suppressor NF2 (merlin) in schwannomas and meningiomas.

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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

Mast cell interactions with the nervous system: relationship to mechanisms of disease.

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In summary, mast cell interactions in the nervous system are relevant to both physiological processes (i.e. reproduction) and pathologic states (i.e. inflammatory demyelination, painful disorders, toxic and metabolic disease, and tumor angiogenesis). Their physiologic roles may contribute to

Genesis and biology of vestibular schwannomas.

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This review chapter is a synthesis of the recent literature about pathogenesis of schwannomas with emphasis on vestibular schwannomas (VSs). The cornerstone of cellular transformation and proliferation of Schwann cells toward schwannomas has been attributed to the nonexpression of normal

Tight association of loss of merlin expression with loss of heterozygosity at chromosome 22q in sporadic meningiomas.

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Mutations of NF2, the gene for neurofibromatosis 2, are detected in 20-30% of sporadic meningiomas, and almost all mutations lead to loss of merlin expression. However, loss of heterozygosity (LOH) at chromosome 22q is found at a much higher frequency, up to 50-70%, and the possibility of another

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