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neurofibromatoses/phosphatase
Linkki tallennetaan leikepöydälle
Sivu 1 alkaen 69 tuloksia
Preliminary observations on genetic alterations in pilocytic astrocytomas associated with neurofibromatosis 1.
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Neurofibromatosis 1 (NF1) is an autosomal dominant disorder that predisposes sufferers to various forms of neoplasia. Among affected individuals, 15%-20% develop astrocytomas, especially pilocytic astrocytomas (PA), which are benign and classified as grade I by the World Health Organization. They
Loss of heterozygosity in tumor cells of a recurrent mandibular giant cell granuloma in neurofibromatosis type 1.
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Neurofibromatosis type 1 (NF1) is an autosomal dominant inherited disease affecting about 1:3000 humans. Neurofibromas are benign soft tissue tumors. Giant cell granuloma (GCG) is a benign tumor-like lesion that is preferentially located in the jaws. GCG can develop in NF1 patients. A 7-year-old
KIBRA protein phosphorylation is regulated by mitotic kinase aurora and protein phosphatase 1.
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Recent genetic studies in Drosophila identified Kibra as a novel regulator of the Hippo pathway, which controls tissue growth and tumorigenesis by inhibiting cell proliferation and promoting apoptosis. The cellular function and regulation of human KIBRA remain largely unclear. Here, we show that
Analysis of cell-mediated mineralization in culture of bone-derived embryonic cells with neurofibromatosis.
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von Recklinghausen neurofibromatosis (NF1) is an autosomal dominant genetic disorder associated with congenital pseudoarthrosis and with short stature. To examine whether the NF1 phenotype includes functional osteogenic defects, embryonic bone-derived cells affected with NF1 were tested in culture
Regulation of the neurofibromatosis type 2 tumor suppressor protein, merlin, by adhesion and growth arrest stimuli.
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The neurofibromatosis type 2 tumor suppressor gene is inactivated in the development of familial and sporadic schwannomas and meningiomas. The encoded protein, Merlin, is closely related to the Ezrin, Radixin, and Moesin family of membrane/cytoskeletal linker proteins. Examination of Merlin in
Efficacy of denosumab therapy for neurofibromatosis type 1 with osteoporosis and history of fractures: a case report.
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UNASSIGNED
The natural history and pathogenesis of the skeletal abnormalities found in neurofibromatosis type 1 (NF1) are poorly understood, and the therapeutic options for these manifestations remain limited. This report first describes the clinical outcomes of denosumab treatment for a patient
Structure-function relationships in the ezrin family and the effect of tumor-associated point mutations in neurofibromatosis 2 protein.
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Ezrin, radixin and moesin (ERM proteins) link cell adhesion molecules to the cytoskeleton, modulate cell morphology and cell growth and are involved in Rho-mediated signal transduction. Merlin, the tumor suppressor in neurofibromatosis 2, is a diverged member of the ezrin family, but its function is
Mammalian target of rapamycin inhibitor abrogates abnormal osteoclastogenesis in neurofibromatosis type 1.
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BACKGROUND
Neurofibromatosis type 1 (NF1) is the most common genetic syndrome predisposing patients to various tumors due to dysregulation of the Ras signaling pathway. Recent research has shown NF1 patients also suffer a spectrum of bone pathologies. The pathogenesis of NF1 bone diseases is largely
The association of neurofibromatosis 1 and spinal deformity with primary hyperparathyroidism and osteomalacia: might melatonin have a role?
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A 35-year-old woman with neurofibromatosis 1 and thoracic kyphoscoliosis had incomplete paraplegia. She had a history of hyperparathyroidism due to a parathyroid adenoma which had been excised 4 years previously. Plain radiographs of the spine revealed kyphoscoliosis from the third to sixth thoracic
[Von Recklinghausen type I neurofibromatosis and neuroendocrine tumor (somatostatinoma) in a 50-year-old woman].
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METHODS
A 50-year-old woman has had diffuse abdominal symptoms for approximately 2 weeks. For 30 years a von Recklinghausen's neurofibromatosis has been known.
METHODS
Clinically and chemically there was a cholestasis (alkaline phosphatase 244 U/l, gamma GT 83 U/l) with uneventful values for
Adult hypophosphataemic osteomalacia with Fanconi syndrome presenting in a patient with neurofibromatosis.
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A patient is described with neurofibromatosis, increasing walking problems and low back pain. Initially, osteoporosis or pressure caused by a neurofibroma was suspected. However, the progressively increasing alkaline phosphatase activity and hypophosphataemia found during laboratory investigations
Molecular cloning of a mouse epithelial protein-tyrosine phosphatase with similarities to submembranous proteins.
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Protein-tyrosine phosphatases (PTPases) form an important class of cell regulatory proteins. We have isolated overlapping cDNA clones that together comprise an 8 kb transcript encoding a novel murine PTPase which is expressed in various organs. Sequence analysis revealed an open reading frame of
Mammalian Ste20-like kinase (Mst2) indirectly supports Raf-1/ERK pathway activity via maintenance of protein phosphatase-2A catalytic subunit levels and consequent suppression of inhibitory Raf-1 phosphorylation.
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Many tumor suppressor proteins act to blunt the effects of mitogenic signaling pathways. Loss of function mutations in the merlin tumor suppressor underlie neurofibromatosis type 2 (NF2), a familial autosomal dominant cancer syndrome. Studies of Drosophila suggest that Hippo (hpo) is required for
Regulation of merlin by protein phosphatase 1-TIMAP and EBP50 in endothelial cells.
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Merlin (moesin-ezrin-radixin like protein), the product of neurofibromatosis type 2 gene, was primarily recognized as a tumor suppressor, but it also functions as a membrane-cytoskeletal linker and regulator of multiple signaling pathways. The activity and localization of merlin is regulated by head
Asfotase-α improves bone growth, mineralization and strength in mouse models of neurofibromatosis type-1.
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Individuals with neurofibromatosis type-1 (NF1) can manifest focal skeletal dysplasias that remain extremely difficult to treat. NF1 is caused by mutations in the NF1 gene, which encodes the RAS GTPase-activating protein neurofibromin. We report here that ablation of Nf1 in bone-forming cells leads
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