Journal of Bioenergetics and Biomembranes

, Volume 37, Issue 3, pp 129–142

On the Role of VDAC in Apoptosis: Fact and Fiction

  • Tatiana K. Rostovtseva
  • Wenzhi Tan
  • Marco Colombini

DOI: 10.1007/s10863-005-6566-8

Cite this article as:
Rostovtseva, T.K., Tan, W. & Colombini, M. J Bioenerg Biomembr (2005) 37: 129. doi:10.1007/s10863-005-6566-8


Research on VDAC has accelerated as evidence grows of its importance in mitochondrial function and in apoptosis. New investigators entering the field are often confounded by the VDAC literature and its many apparent conflicts and contradictions. This review is an effort to shed light on the situation and identify reliable information from more questionable claims. Our views on the most important controversial issues are as follows: VDAC is only present in the mitochondrial outer membrane. VDAC functions as a monomer. VDAC functions normally with or without Ca2+. It does not form channels that mediate the flux of proteins through membranes (peptides and unfolded proteins are excluded from this statement). Closure of VDAC, not VDAC opening, leads to mitochondria outer membrane permeabilization and apoptosis.


ApoptosisVDACmitochondriaouter membranecalciumarsenic trioxidepermeability transitionBcl-2

Copyright information

© Springer Science + Business Media, Inc. 2005

Authors and Affiliations

  • Tatiana K. Rostovtseva
    • 1
    • 3
  • Wenzhi Tan
    • 2
  • Marco Colombini
    • 2
  1. 1.Laboratory of Physical and Structural Biology, NICHDNational Institutes of HealthBethesda
  2. 2.Department of BiologyUniversity of MarylandCollege Park
  3. 3.Laboratory of Physical and Structural Biology, NICHD, NIHBethesda