Bcl-x(L) prevents cell death following growth factor withdrawal by facilitating mitochondrial ATP/ADP exchange

Matthew G. Vander Heiden, Navdeep S. Chandel, Paul T. Schumacker, Craig B. Thompson*

*Corresponding author for this work

Research output: Contribution to journalArticle

426 Scopus citations

Abstract

Growth factor withdrawal is associated with a metabolic arrest that can result in apoptosis. Cell death is preceded by loss of outer mitochondrial membrane integrity and cytochrome c release. These mitochondrial events appear to follow a relative increase in mitochondrial membrane potential. This change in membrane potential results from the failure of the adenine nucleotide translocator (ANT)/voltage-dependent anion channel (VDAC) complex to maintain ATP/ADP exchange. Bcl-x(L) expression allows growth factor- deprived cells to maintain sufficient mitochondrial ATP/ADP exchange to sustain coupled respiration. These data demonstrate that mitochondrial adenylate transport is under active regulation. Efficient exchange of ADP for ATP is promoted by Bcl-x(L) expression permitting oxidative phosphorylation to be regulated by cellular ATP/ADP levels and allowing mitochondria to adapt to changes in metabolic demand.

Original languageEnglish (US)
Pages (from-to)159-167
Number of pages9
JournalMolecular cell
Volume3
Issue number2
DOIs
StatePublished - Feb 1999

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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