Mechanistic insights into the role of truncating PREX2 mutations in melanoma

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3 Scopus citations

Abstract

PREX2 is a PTEN binding protein that is significantly mutated in melanoma and pancreatic ductal adenocarcinoma. We recently reported the molecular mechanism of tumorigenesis associated with PREX2 mutations: truncating PREX2 mutations activate its RAC1 guanine nucleotide exchanger activity leading to increased PI3K/AKT signaling and enhanced cell proliferation.

Original languageEnglish (US)
Article numbere1160174
JournalMolecular and Cellular Oncology
Volume3
Issue number3
DOIs
StatePublished - May 3 2016

Keywords

  • Epigenetics
  • Melanoma
  • Mouse models of cancer
  • PI3K
  • PREX2
  • RAC1

ASJC Scopus subject areas

  • Molecular Medicine
  • Cancer Research

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