ArticleMolecular biology of the cell2006
The Ras-GRF1 exchange factor coordinates activation of H-Ras and Rac1 to control neuronal morphology.
Article in Molecular biology of the cell, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 34 citations in OpenAlex.
- RasGRF1 mediates brain-derived neurotrophic factor-induced axonal growth in primary cultured cortical neurons.Biochemistry and biophysics reports · 2019Article
- Ras and Rap1: A tale of two GTPases.Seminars in cancer biology · 2019Review
- Chronic Kappa opioid receptor activation modulates NR2B: Implication in treatment resistant depression.Scientific reports · 2016Article
- Human iPS Cell-Derived Neurons Uncover the Impact of Increased Ras Signaling in Costello Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- How to Target Activated Ras Proteins: Direct Inhibition vs. Induced Mislocalization.Mini reviews in medicinal chemistry · 2016Review
- ATDC (Ataxia Telangiectasia Group D Complementing) Promotes Radioresistance through an Interaction with the RNF8 Ubiquitin Ligase.The Journal of biological chemistry · 2015Article
- Ras guanine nucleotide releasing factor 1 (RasGrf1) enhancement of Trk receptor-mediated neurite outgrowth requires activation of both H-Ras and Rac.Journal of molecular neuroscience : MN · 2013Article
- Activated Ras as a Therapeutic Target: Constraints on Directly Targeting Ras Isoforms and Wild-Type versus Mutated Proteins.ISRN oncology · 2013Review
- Imprinted Rasgrf1 expression in neonatal mice affects olfactory learning and memory.Genes, brain, and behavior · 2011Article
- Prefrontal cortical inputs to the basal amygdala undergo pruning during late adolescence in the rat.The Journal of comparative neurology · 2010Article
- A novel geranylgeranyl transferase inhibitor in combination with lovastatin inhibits proliferation and induces autophagy in STS-26T MPNST cells.The Journal of pharmacology and experimental therapeutics · 2010Article
- Restoration of E-cadherin cell-cell junctions requires both expression of E-cadherin and suppression of ERK MAP kinase activation in Ras-transformed breast epithelial cells.Neoplasia (New York, N.Y.) · 2008Article
- p21-Activated kinase 1 coordinates aberrant cell survival and pericellular proteolysis in a three-dimensional culture model for premalignant progression of human breast cancer.Neoplasia (New York, N.Y.) · 2008Article
- Very-KIND, a KIND domain containing RasGEF, controls dendrite growth by linking Ras small GTPases and MAP2.The Journal of cell biology · 2007Article
- Imprint switch mutations at Rasgrf1 support conflict hypothesis of imprinting and define a growth control mechanism upstream of IGF1.Mammalian genome : official journal of the International Mammalian Genome SocietyArticle
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Ras-GRF1 exchange factor has regulated guanine nucleotide exchange factor (GEF) activity for H-Ras and Rac1 through separate domains. Both H-Ras and Rac1 activation have been linked to synaptic plasticity and thus could contribute to the function of Ras-GRF1 in neuronal signal transduction pathways that underlie learning and memory. We defined the effects of Ras-GRF1 and truncation mutants that include only one of its GEF activities on the morphology of PC12 phaeochromocytoma cells. Ras-GRF1 required coexpression of H-Ras to induce morphological effects. Ras-GRF1 plus H-Ras induced a novel, expanded morphology in PC12 cells, which was characterized by a 10-fold increase in soma size and by neurite extension. A truncation mutant of Ras-GRF1 that included the Ras GEF domain, GRFdeltaN, plus H-Ras produced neurite extensions, but did not expand the soma. This neurite extension was blocked by inhibition of MAP kinase activation, but was independent of dominant-negative Rac1 or RhoA. A truncation mutant of Ras-GRF1 that included the Rac GEF domains, GRFdeltaC, produced the expanded phenotype in cotransfections with H-Ras. Cell expansion was inhibited by wortmannin or dominant-negative forms of Rac1 or Akt. GRFdeltaC binds H-Ras.GTP in both pulldown assays from bacterial lysates and by coimmunoprecipitation from HEK293 cells. These results suggest that coordinated activation of H-Ras and Rac1 by Ras-GRF1 may be a significant controller of neuronal cell size.
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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.