Journal
ELIFE
Volume 4, Issue -, Pages -Publisher
ELIFE SCIENCES PUBLICATIONS LTD
DOI: 10.7554/eLife.08905
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Funding
- Suomen Akatemia (Academy of Finland) [272437, 269862, 279163, 252381, 256440, 281497, 141516, 138584, 270010]
- Sigrid Juseliuksen Saatio
- Syopajarjestot
- Turku Doctoral Programme of Biomedical Sciences
- Texas Medical Center Digestive Disease Center [P30 DK56338]
- Cancer Prevention and Research Institute of Texas (CPRIT) [RP130059]
- Integrative Life Science Doctoral Program (ILS)
- National Doctoral Programme in Informational and Structural Biology
- Cancer Foundation Finland sr [110051, 130067] Funding Source: researchfish
- Academy of Finland (AKA) [270010, 281497, 272437, 138584, 269862, 252381, 281497, 279163, 256440, 138584, 141516, 252381, 272437, 270010, 256440, 279163, 141516, 269862] Funding Source: Academy of Finland (AKA)
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Hotspot mutations of Ras drive cell transformation and tumorigenesis. Less frequent mutations in Ras are poorly characterized for their oncogenic potential. Yet insight into their mechanism of action may point to novel opportunities to target Ras. Here, we show that several cancer-associated mutations in the switch III region moderately increase Ras activity in all isoforms. Mutants are biochemically inconspicuous, while their clustering into nanoscale signaling complexes on the plasma membrane, termed nanocluster, is augmented. Nanoclustering dictates downstream effector recruitment, MAPK-activity, and tumorigenic cell proliferation. Our results describe an unprecedented mechanism of signaling protein activation in cancer.
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