ArticleMolecular and cellular biology1994
Identification of residues critical for Ras(17N) growth-inhibitory phenotype and for Ras interaction with guanine nucleotide exchange factors.
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 29 papers.
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Who cites it
29 citing papers in PubMed, 90 citations in OpenAlex.
- Targeting KRAS mutations: orchestrating cancer evolution and therapeutic challenges.Signal transduction and targeted therapy · 2025Review
- A Rational Design of α-Helix-Shaped Peptides Employing the Hydrogen-Bond Surrogate Approach: A Modulation Strategy for Ras-RasGRF1 Interaction in Neuropsychiatric Disorders.Pharmaceuticals (Basel, Switzerland) · 2021Article
- 40 Years of RAS-A Historic Overview.Genes · 2021Review
- Mechanistic insights into the effect of phosphorylation on Ras conformational dynamics and its interactions with cell signaling proteins.Computational and structural biotechnology journal · 2021Article
- Direct multiplex imaging and optogenetics of Rho GTPases enabled by near-infrared FRET.Nature chemical biology · 2018Article
- Article
- Epac activation sensitizes rat sensory neurons through activation of Ras.Molecular and cellular neurosciences · 2016Article
- Mutant and wild-type Ras: co-conspirators in cancer.Cancer discovery · 2013Article
- A novel HRAS substitution (c.266C>G; p.S89C) resulting in decreased downstream signaling suggests a new dimension of RAS pathway dysregulation in human development.American journal of medical genetics. Part A · 2012Article
- Signaling pathways that mediate nerve growth factor-induced increase in expression and release of calcitonin gene-related peptide from sensory neurons.Neuroscience · 2010Article
- cPLA2 regulates the expression of type I interferons and intracellular immunity to Chlamydia trachomatis.The Journal of biological chemistry · 2010Article
- Akt mediates Ras downregulation of RhoB, a suppressor of transformation, invasion, and metastasis.Molecular and cellular biology · 2004Article
- EGFR, ErbB2 and Ras but not Src suppress RhoB expression while ectopic expression of RhoB antagonizes oncogene-mediated transformation.Oncogene · 2004Article
- Brain lipid binding protein in axon-Schwann cell interactions and peripheral nerve tumorigenesis.Molecular and cellular biology · 2003Article
- Epstein-Barr virus immediate-early protein BRLF1 induces the lytic form of viral replication through a mechanism involving phosphatidylinositol-3 kinase activation.Journal of virology · 2001Article
- Sensitivity of wild type and mutant ras alleles to Ras specific exchange factors: Identification of factor specific requirements.Oncogene · 2001Article
- A MAP kinase-signaling pathway mediates neurite outgrowth on L1 and requires Src-dependent endocytosis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Regulation of T cell development in the thymus.Immunologic research · 2000Review
- Direct evidence that ERK regulates the production/secretion of interleukin-2 in PHA/PMA-stimulated T lymphocytes.Immunology · 1999Article
- Distinct subclasses of small GTPases interact with guanine nucleotide exchange factors in a similar manner.Molecular and cellular biology · 1998Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The Ras(17N) dominant negative antagonizes endogenous Ras function by forming stable, inactive complexes with Ras guanine nucleotide exchange factors (GEFs; e.g., SOS1). We have used the growth-inhibitory phenotype of Ras(17N) to characterize two aspects of Ras interaction with GEFs. First, we used a nonprenylated version of Ras(17N), designated Ras(17N/186S), which no longer associates with the plasma membrane and lacks the growth-inhibitory phenotype, to address the importance of Ras subcellular location and posttranslational modification for its interaction with GEFs. We observed that addition of an N-terminal myristylation signal to Ras(17N/186S) restored the growth-inhibitory activity of nonprenylated Ras(17N). Thus, membrane association, rather than prenylation, is critical for Ras interaction with Ras GEFs. Second, we used a biological selection approach to identify Ras residues which are critical for Ras(17N) growth inhibition and hence for interaction with Ras GEFs. We identified mutations at residues 75, 76, and 78 that abolished the growth-inhibitory activity of Ras(17N). Since GEF interaction is dispensable for oncogenic but not normal Ras function, our demonstration that single-amino-acid substitutions at these three positions impaired the transforming activity of normal but not oncogenic Ras provides further support for the role of these residues in Ras-GEF interactions. Finally, Ras(WT) proteins with mutations at these residues were no longer activated by mammalian SOS1. Altogether, these results suggest that the Ras intracellular location and Ras residues 75 to 78 are critical for Ras-GEF interaction.
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