ArticleProceedings of the National Academy of Sciences of the United States of America1993
Residues crucial for Ras interaction with GDP-GTP exchangers.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 45 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
- 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
- An NF-κB pathway-mediated positive feedback loop amplifies Ras activity to pathological levels in mice.The Journal of clinical investigation · 2012Article
- Sensitivity of wild type and mutant ras alleles to Ras specific exchange factors: Identification of factor specific requirements.Oncogene · 2001Article
- Decreased GTPase activity of K-ras mutants deriving from human functional adrenocortical tumours.British journal of cancer · 2000Article
- Distinct subclasses of small GTPases interact with guanine nucleotide exchange factors in a similar manner.Molecular and cellular biology · 1998Article
- Targeting signal transduction for disease therapy.Medical oncology (Northwood, London, England) · 1997Review
- Differential activation of yeast adenylyl cyclase by Ras1 and Ras2 depends on the conserved N terminus.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Identification of residues critical for Ras(17N) growth-inhibitory phenotype and for Ras interaction with guanine nucleotide exchange factors.Molecular and cellular biology · 1994Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cdc25 is essential for Ras-mediated activation of adenylyl cyclase in the yeast Saccharomyces cerevisiae. This protein acts by catalyzing GDP-GTP exchange on yeast Ras. Harvey (Ha) ras expressed in S. cerevisiae is also recognized by both Cdc25 and Sdc25, a yeast homolog of Cdc25. Thus it is feasible to examine molecular aspects of mammalian Ras modulation by Cdc25 using the RAS/cAMP pathway in yeast as a model system. Here, we describe mutational analysis of Ha-ras for the identification of residues critical for the ability of Ras to interact with Cdc25 and related guanine nucleotide-release proteins. Mutations within codons 97-108 impaired Ras-mediated activation of adenylyl cyclase in the presence but not in the absence of mammalian GTPase-activating protein. Such mutations, therefore, affected the ability of Ras to undergo GDP-GTP exchange catalyzed by the guanine nucleotide exchanger without preventing Ras activation of the effector. Similar mutations were previously shown to impair the ability of c-ras to transform mammalian cells while having a less drastic effect on v-ras.
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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.