Ras Family of Genes and Proteins: Structure, Function and Regulation
A special issue of Cells (ISSN 2073-4409).
Deadline for manuscript submissions: 30 September 2025 | Viewed by 1163
Special Issue Editors
Interests: RAS oncogenes; RAS signaling pathways; RAS activation by guanine nucleotide exchange factors (GEFs); mammalian GEFs of the SOS and GRF families; inhibitors of RAS-driven tumors; RAS and GEF inhibitors; cancer molecular biology; signal transduction
Special Issues, Collections and Topics in MDPI journals
Interests: RAS GTPases; signaling; guanine nucleotide exchange factors; RASopathies; lung development; inhibitor screening; interactome
Special Issues, Collections and Topics in MDPI journals
Interests: cancer biology and immunotherapy research; RAS proteins and GEF activation mechanisms; inhibitors of RAS-driven tumors; signal transduction mechanisms in RAS-associated pathways; preclinical assays for evaluating RAS-related therapeutics; integration of immunology and RAS signaling in tumor microenvironment
Special Issues, Collections and Topics in MDPI journals
Special Issue Information
Dear Colleagues,
RAS oncogenes, discovered in the 1980s, are directly responsible for about 30% of all human cancers, including some of the most lethal ones.
RAS research is now entering its fifth decade behind multiple prior discoveries including the pioneering isolation and characterization of the canonical HRAS, NRAS, and KRAS oncogenes and their cellular counterparts, the demonstration of their malignant activation by point mutations, the preferential association of specific RAS oncogenes with certain tumor types, and the characterization of the essential roles played by different RAS proteins in cellular signaling processes controlling proliferation, differentiation, or survival.
Indeed, a major part of our current understanding of the role of RAS genes and proteins in physiological and pathological cellular processes stems from the detailed characterization of RTK-RAS-ERK signaling pathways involving, in particular functional interactions between the different RAS isoforms and the specific positive and negative regulators of the GAP and GEF families. Although early therapeutic approaches using farnesyl transferase inhibitors were deeply disappointing, suggesting the notion that RAS was undruggable, we are currently witnessing a paradigm shift in the clinical management of RAS-dependent cancers due to the recent development of a plethora of new, specific inhibitors capable of directly targeting different forms of the RAS oncoproteins, as well as some of their upstream and downstream regulators.
The aim of this Special Issue, in this era of renovated optimism in the RAS field, is to assemble original data and reviews fostering a deeper knowledge about the structure, function, and regulation of all members of the RAS superfamily of genes and proteins, as well as the cellular modulators of the GAP and GEF families. It is likely that any new progress concerning basic knowledge on these issues will also be quickly translated into improvements in diagnostics, prognostics, or treatments of RAS-driven tumors.
Dr. Eugenio Santos
Dr. Alberto Fernández-Medarde
Dr. Rosula Garcia-Navas
Guest Editors
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Keywords
- HRAS
- NRAS
- KRAS
- RAS-driven tumors
- rasopathies
- RAS signaling
- RAS inhibitors
- GAP
- GEF
- SOS
- GRF
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