ArticleMolecular carcinogenesis2009
Neurofibromin physically interacts with the N-terminal domain of focal adhesion kinase.
Article in Molecular carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
40 citing papers in PubMed, 55 citations in OpenAlex.
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- [Gene therapy strategies and prospects for neurofibromatosis type 1].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2024Article
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- The Contribution of Oxidative Stress toAntioxidants (Basel, Switzerland) · 2023Review
- RAS Signaling Gone Awry in the Skin: The Complex Role of RAS in Cutaneous Neurofibroma Pathogenesis, Emerging Biological Insights.The Journal of investigative dermatology · 2023Review
- The therapeutic potential of neurofibromin signaling pathways and binding partners.Communications biology · 2023Review
- The PYK2 inhibitor PF-562271 enhances the effect of temozolomide on tumor growth in a C57Bl/6-Gl261 mouse glioma model.Journal of neuro-oncology · 2023Article
- Role of nerves in neurofibromatosis type 1-related nervous system tumors.Cellular oncology (Dordrecht, Netherlands) · 2022Review
- Mechanistic insights from animal models of neurofibromatosis type 1 cognitive impairment.Disease models & mechanisms · 2022Review
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- The Crossroads between RAS and RHO Signaling Pathways in Cellular Transformation, Motility and Contraction.Genes · 2021Review
- NF1-RAC1 axis regulates migration of the melanocytic lineage.Translational oncology · 2020Article
- Review
- Nuclear Isoforms of Neurofibromin Are Required for Proper Spindle Organization and Chromosome Segregation.Cells · 2020Article
- Neurofibromin Is an Estrogen Receptor-α Transcriptional Co-repressor in Breast Cancer.Cancer cell · 2020Article
- Pumping the brakes on RAS - negative regulators and death effectors of RAS.Journal of cell science · 2020Review
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- Ras-Specific GTPase-Activating Proteins-Structures, Mechanisms, and Interactions.Cold Spring Harbor perspectives in medicine · 2019Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The NF1 gene that is altered in patients with type 1 neurofibromatosis (NF1) encodes a neurofibromin protein that functions as a tumor suppressor. In this report, we show for the first time physical interaction between neurofibromin and focal adhesion kinase (FAK), the protein that localizes at focal adhesions. We show that neurofibromin associates with the N-terminal domain of FAK, and that the C-terminal domain of neurofibromin directly interacts with FAK. Confocal microscopy demonstrates colocalization of NF1 and FAK in the cytoplasm, perinuclear and nuclear regions inside the cells. Nf1+/+ MEF cells expressed less cell growth during serum deprivation conditions, and adhered less on collagen and fibronectin-treated plates than Nf1(-/-) MEF cells, associated with changes in actin and FAK staining. In addition, Nf1+/+ MEF cells detached more significantly than Nf1(-/-) MEF cells by disruption of FAK signaling with the dominant-negative inhibitor of FAK, C-terminal domain of FAK (FAK-CD). Thus, the results demonstrate the novel interaction of neurofibromin and FAK and suggest their involvement in cell adhesion, cell growth, and other cellular events and pathways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.