4.7 Article

RB goes mitochondrial

Journal

GENES & DEVELOPMENT
Volume 27, Issue 9, Pages 975-979

Publisher

COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1101/gad.219451.113

Keywords

MOMP; apoptosis; cancer; pRB; retinoblastoma protein

Funding

  1. National Institutes of Health (NIH)/National Cancer Institute [R01 CA114102]
  2. California Institute for Regenerative Medicine [RB1-01385]
  3. NIH [R01 CA140875, R21 CA169673]
  4. Department of Defense
  5. Leukemia and Lymphoma Society

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The retinoblastoma tumor suppressor RB is well known for its capacity to restrict cell cycle progression at the G1/S transition of the cell cycle by controlling the transcription of cell cycle genes. In this issue of Genes & Development, Hilgendorf and colleagues (pp. 1003-1015) have identified a novel tumor suppressor function for RB independent of its role as a transcriptional regulator, in which RB directly activates the apoptosis regulator Bax at the mitochondria to promote cell death.

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