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A new phase in KRAS signaling
Krista A Budinich1, Liling Wan2
1Department of Cancer Biology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Abramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA; Epigenetics Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA 19104, USA.
Trends in Cancer
|August 10, 2026
Summary
Kirsten rat sarcoma virus oncogene homolog (KRAS) farnesylation drives cytoplasmic condensates, promoting KRAS processing, trafficking, and signaling. This discovery reveals condensate formation as a novel mechanism for regulating RAS activity.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Kirsten rat sarcoma virus oncogene homolog (KRAS) is a key regulator of cell signaling.
- Understanding KRAS biology involves its lipidation, membrane association, and signaling pathways.
Purpose of the Study:
- To investigate the role of phase separation in KRAS biology.
- To unify distinct aspects of KRAS processing, trafficking, and signaling.
Main Methods:
- Investigated KRAS lipidation and its impact on phase separation.
- Analyzed the formation of cytoplasmic KRAS condensates.
- Examined the effects of condensates on KRAS processing, trafficking, and signaling.
Main Results:
- Farnesylation of KRAS drives the formation of cytoplasmic condensates.
- These KRAS condensates are crucial for KRAS processing and membrane trafficking.
- Condensate formation enhances KRAS signaling output.
Conclusions:
- Phase separation is a critical mechanism controlling KRAS activity.
- Cytoplasmic KRAS condensates represent a novel regulatory hub for RAS signaling.