Overexpression of Bcl-2 suppresses the calcium activation of a mitochondrial megachannel

Robert C. Murphy, Erasmus Schneider, Kathleen W. Kinnally

Research output: Contribution to journalArticlepeer-review

Abstract

The molecular mechanism(s) by which Bcl-2 regulates apoptosis is poorly understood. Bcl-2 suppresses apoptosis by inhibiting calcium activation of the permeability transition of mitochondria. In this patch-clamp study, overexpression of Bcl-2 in mitochondria of cultured cells suppressed calcium activation of a high conductance channel that may underlie the permeability transition. All other single channel parameters were identical when multiple conductance channel activities of mitochondria from control and Bcl-2 overexpressing cells were compared. Bcl-2 forms channels in artificial membranes; however, no novel channel activities could be linked to Bcl-2 overexpression, suggesting Bcl-2 does not form channels in native inner membranes of mitochondria.

Original languageEnglish (US)
Pages (from-to)73-76
Number of pages4
JournalFEBS Letters
Volume497
Issue number2-3
DOIs
StatePublished - May 25 2001

Keywords

  • Apoptosis
  • Bcl-2
  • Channel
  • Mitochondrion
  • Patch clamp

ASJC Scopus subject areas

  • Biophysics
  • Structural Biology
  • Biochemistry
  • Molecular Biology
  • Genetics
  • Cell Biology

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