Connecting with an old partner in a new way

Cancer Cell. 2013 May 13;23(5):559-61. doi: 10.1016/j.ccr.2013.04.023.

Abstract

In this issue of Cancer Cell, Hao and colleagues report a non-canonical interaction between the insulin receptor substrate 1 and certain oncogenic variants of the p110α catalytic subunit of phosphoinositide 3-kinase (PI3K). A cell-penetrant peptide that disrupts this interaction downregulates PI3K signaling and inhibits tumor growth in mice.

Publication types

  • Research Support, Non-U.S. Gov't
  • Comment

MeSH terms

  • Class I Phosphatidylinositol 3-Kinases
  • Humans
  • Insulin Receptor Substrate Proteins / metabolism*
  • Phosphatidylinositol 3-Kinases / genetics*

Substances

  • IRS1 protein, human
  • Insulin Receptor Substrate Proteins
  • Phosphatidylinositol 3-Kinases
  • Class I Phosphatidylinositol 3-Kinases
  • PIK3CA protein, human