ArticleMolecular and cellular biology1994
Neurofibromin can inhibit Ras-dependent growth by a mechanism independent of its GTPase-accelerating function.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 102 citations in OpenAlex.
- Phase II study of sorafenib in patients with metastatic or recurrent sarcomas.Journal of clinical oncology : official journal of the American Society of Clinical Oncology · 2009Trial
- Altered body as a source of interactional problems in the family of individuals with neurofibromatosis type 1 - A polish study.PloS one · 2024Article
- Gliosarcoma: The Distinct Genomic Alterations Identified by Comprehensive Analysis of Copy Number Variations.Analytical cellular pathology (Amsterdam) · 2022Article
- Alterations in brain morphology by MRI in adults with neurofibromatosis 1.Orphanet journal of rare diseases · 2021Article
- Gliosarcoma Is Driven by Alterations in PI3K/Akt, RAS/MAPK Pathways and Characterized by Collagen Gene Expression Signature.Cancers · 2019Article
- Treatment-related adverse effects with pazopanib, sorafenib and sunitinib in patients with advanced soft tissue sarcoma: a pooled analysis.Cancer management and research · 2018Article
- Quantitative Proteomics Reveals Fundamental Regulatory Differences in Oncogenic HRAS and Isocitrate Dehydrogenase (IDH1) Driven Astrocytoma.Molecular & cellular proteomics : MCP · 2017Article
- Dermatofibrosarcoma protuberans (DFSP) successfully treated with sorafenib: case report.Clinical sarcoma research · 2013Article
- Article
- The GAP-related domain of neurofibromin attenuates proliferation and downregulates N- and K-Ras activation in Nf1-negative AML cells.Leukemia research · 2007Article
- Aberrant growth and differentiation of oligodendrocyte progenitors in neurofibromatosis type 1 mutants.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain.Genes & development · 2001Article
- Article
- Single cell Ras-GTP analysis reveals altered Ras activity in a subpopulation of neurofibroma Schwann cells but not fibroblasts.The Journal of biological chemistry · 2000Article
- The neurofibromatosis type 1 (Nf1) tumor suppressor is a modifier of carcinogen-induced pigmentation and papilloma formation in C57BL/6 mice.The Journal of investigative dermatology · 2000Article
- Urinary bladder transitional cell carcinogenesis is associated with down-regulation of NF1 tumor suppressor gene in vivo and in vitro.The American journal of pathology · 1999Article
- p21 ras and phosphatidylinositol-3 kinase are required for survival of wild-type and NF1 mutant sensory neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Structural analysis of the GAP-related domain from neurofibromin and its implications.The EMBO journal · 1998Article
- Signal-transducing protein phosphorylation cascades mediated by Ras/Rho proteins in the mammalian cell: the potential for multiplex signalling.The Biochemical journal · 1996Review
- Suppression of tumorigenicity by the wild-type tuberous sclerosis 2 (Tsc2) gene and its C-terminal region.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The NF1 gene, which is altered in patients with type 1 neurofibromatosis, has been postulated to function as a tumor suppressor gene. The NF1 protein product neurofibromin stimulates the intrinsic GTPase activity of active GTP-bound Ras, thereby inactivating it. Consistent with a tumor suppressor function, we have found that the introduction of NF1 in melanoma cell lines that are deficient in neurofibromin inhibited their growth and induced their differentiation. In addition, overexpression of neurofibromin in NIH 3T3 cells was growth inhibitory but did not alter the level of GTP.Ras in the cells. Transformation by v-ras, whose protein product is resistant to GTPase stimulation by neurofibromin, was inhibited in a cell line overexpressing neurofibromin, while transformation by v-raf was not altered. The results demonstrate that NF1 is a tumor suppressor gene that can inhibit Ras-dependent growth by a regulatory mechanism that is independent of neurofibromin's ability to stimulate Ras GTPase.
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