DIRAS3 (ARHI) Blocks RAS/MAPK Signaling by Binding Directly to RAS and Disrupting RAS Clusters

Margie N. Sutton, Zhen Lu, Yao Cheng Li, Yong Zhou, Tao Huang, Albert S. Reger, Amy M. Hurwitz, Timothy Palzkill, Craig Logsdon, Xiaowen Liang, Joe W. Gray, Xiaolin Nan, John Hancock, Geoffrey M. Wahl, Robert C. Bast

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

Sutton et. al. show that re-expression of DIRAS3 can inhibit the growth of multiple cancer types driven by K-RAS mutations by a direct interaction and disruption of K-RAS higher ordered clusters. This phenotype is driven by an N-terminal extension, which distinguishes DIRAS3 from other RAS-related small GTPases.

Original languageEnglish (US)
Pages (from-to)3448-3459.e6
JournalCell Reports
Volume29
Issue number11
DOIs
StatePublished - Dec 10 2019

Keywords

  • ARHI
  • DIRAS3
  • RAS inhibitor
  • cluster
  • dimer
  • heteromer
  • ovarian cancer
  • pancreatic cancer
  • transformation

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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    Sutton, M. N., Lu, Z., Li, Y. C., Zhou, Y., Huang, T., Reger, A. S., Hurwitz, A. M., Palzkill, T., Logsdon, C., Liang, X., Gray, J. W., Nan, X., Hancock, J., Wahl, G. M., & Bast, R. C. (2019). DIRAS3 (ARHI) Blocks RAS/MAPK Signaling by Binding Directly to RAS and Disrupting RAS Clusters. Cell Reports, 29(11), 3448-3459.e6. https://doi.org/10.1016/j.celrep.2019.11.045