![[Feedback]](/icons/banner/feedbackACT.gif){kind=icon}
![[For Subscribers]](/icons/banner/subscriberACT.gif){kind=icon}
![[Archive]](/icons/banner/archiveACT.gif){kind=icon}
![[Search]](/icons/banner/searchACT.gif){kind=icon}
|
|
|
|
|
||
A more recent version of this article appeared on July 1, 2004
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Submitted on December 1, 2003
Revised on April 8, 2004
Accepted on April 9, 2004
1 Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261, Dept. of Biochemistry, Chosun University School of Medicine, Gwangju, 501-759, Korea
2 Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261
3 Dept. of Biochemistry, Chosun University School of Medicine, Gwangju, 501-759, Korea
4 Korea Basic Science Institute Gwangju branch, Chonnam National University 300 Yongbong-Dong, Book-Gu, Gwangju, 500-757, Korea
5 Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261
* Corresponding author. E-mail address: xmyin{at}pitt.edu.
Release of cytochrome c from the mitochondrial intermembrane space is critical to apoptosis induced by a variety of death stimuli. Bid is a BH3-only prodeath Bcl-2 family protein that can potently activate this efflux. In the current study, we investigated the mitochondrial localization of Bid and its interactions with mitochondrial phospholipids, focusing on their relationships with Bid-induced cytochrome c release. We found that Bid binding to the mitochondria required only three of its eight helical structures (
4-6), but not the BH3 domain, and the binding could not be inhibited by the antideath molecule Bcl-xL. Membrane fractionations indicated that tBid bound to mitochondrial outer membranes at both contact and noncontact sites. Bid could interact with specific cardiolipin species on intact mitochondria as identified by mass spectrometry. Like the binding to the mitochondria, this interaction could not be blocked by the mutation in the BH3 domain or by Bcl-xL. However, a cardiolipin-specific dye, 10-N-nonyl acridine orange, could preferentially suppress Bid binding to the mitochondrial contact site and inhibit Bid-induced mitochondrial cristae reorganization and cytochrome c release. These findings thus suggest that interactions of Bid with mitochondrial cardiolipin at the contact site can contribute significantly to its functions.
This article has been cited by other articles:
|
|
 |
|
  F. Gonzalvez, Z. T. Schug, R. H. Houtkooper, E. D. MacKenzie, D. G. Brooks, R. J.A. Wanders, P. X. Petit, F. M. Vaz, and E. Gottlieb Cardiolipin provides an essential activating platform for caspase-8 on mitochondria J. Cell Biol., November 17, 2008; 183(4): 681 - 696. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. Scorrano Caspase-8 goes cardiolipin: a new platform to provide mitochondria with microdomains of apoptotic signals? J. Cell Biol., November 17, 2008; 183(4): 579 - 581. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Terrones, A. Etxebarria, A. Landajuela, O. Landeta, B. Antonsson, and G. Basanez BIM and tBID Are Not Mechanistically Equivalent When Assisting BAX to Permeabilize Bilayer Membranes J. Biol. Chem., March 21, 2008; 283(12): 7790 - 7803. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Gillick and M. Crompton Evaluating cytochrome c diffusion in the intermembrane spaces of mitochondria during cytochrome c release J. Cell Sci., March 1, 2008; 121(5): 618 - 626. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. D. Freel, D. A. Richardson, M. J. Thomenius, E. C. Gan, S. R. Horn, M. R. Olson, and S. Kornbluth Mitochondrial Localization of Reaper to Promote Inhibitors of Apoptosis Protein Degradation Conferred by GH3 Domain-Lipid Interactions J. Biol. Chem., January 4, 2008; 283(1): 367 - 379. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Cao, J. Xing, X. Xiao, A. K. F. Liou, Y. Gao, X.-M. Yin, R. S. B. Clark, S. H. Graham, and J. Chen Critical Role of Calpain I in Mitochondrial Release of Apoptosis-Inducing Factor in Ischemic Neuronal Injury J. Neurosci., August 29, 2007; 27(35): 9278 - 9293. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P. A. Watson, J. E. B. Reusch, S. A. McCune, L. A. Leinwand, S. W. Luckey, J. P. Konhilas, D. A. Brown, A. J. Chicco, G. C. Sparagna, C. S. Long, et al. Restoration of CREB function is linked to completion and stabilization of adaptive cardiac hypertrophy in response to exercise Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H246 - H259. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. K. Rostovtseva, N. Kazemi, M. Weinrich, and S. M. Bezrukov Voltage Gating of VDAC Is Regulated by Nonlamellar Lipids of Mitochondrial Membranes J. Biol. Chem., December 8, 2006; 281(49): 37496 - 37506. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. J. Oh, S. Barbuto, K. Pitter, J. Morash, L. D. Walensky, and S. J. Korsmeyer A Membrane-targeted BID BCL-2 Homology 3 Peptide Is Sufficient for High Potency Activation of BAX in Vitro J. Biol. Chem., December 1, 2006; 281(48): 36999 - 37008. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Petrosillo, N. Di Venosa, M. Pistolese, G. Casanova, E. Tiravanti, G. Colantuono, A. Federici, G. Paradies, and F. M. Ruggiero Protective effect of melatonin against mitochondrial dysfunction associated with cardiac ischemia- reperfusion: role of cardiolipin FASEB J, February 1, 2006; 20(2): 269 - 276. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Garcia-Saez, M. Coraiola, M. Dalla Serra, I. Mingarro, G. Menestrina, and J. Salgado Peptides Derived from Apoptotic Bax and Bid Reproduce the Poration Activity of the Parent Full-Length Proteins Biophys. J., June 1, 2005; 88(6): 3976 - 3990. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Mashima, T. Oh-hara, S. Sato, M. Mochizuki, Y. Sugimoto, K. Yamazaki, J.-i. Hamada, M. Tada, T. Moriuchi, Y. Ishikawa, et al. p53-Defective Tumors With a Functional Apoptosome-Mediated Pathway: A New Therapeutic Target J Natl Cancer Inst, May 18, 2005; 97(10): 765 - 777. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Lucken-Ardjomande and J.-C. Martinou Newcomers in the process of mitochondrial permeabilization J. Cell Sci., February 1, 2005; 118(3): 473 - 483. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. J. Oh, S. Barbuto, N. Meyer, R.-S. Kim, R. J. Collier, and S. J. Korsmeyer Conformational Changes in BID, a Pro-apoptotic BCL-2 Family Member, upon Membrane Binding: A SITE-DIRECTED SPIN LABELING STUDY J. Biol. Chem., January 7, 2005; 280(1): 753 - 767. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Petrosillo, F. M. Ruggiero, M. Pistolese, and G. Paradies Ca2+-induced Reactive Oxygen Species Production Promotes Cytochrome c Release from Rat Liver Mitochondria via Mitochondrial Permeability Transition (MPT)-dependent and MPT-independent Mechanisms: ROLE OF CARDIOLIPIN J. Biol. Chem., December 17, 2004; 279(51): 53103 - 53108. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Enoksson, J. D. Robertson, V. Gogvadze, P. Bu, A. Kropotov, B. Zhivotovsky, and S. Orrenius Caspase-2 Permeabilizes the Outer Mitochondrial Membrane and Disrupts the Binding of Cytochrome c to Anionic Phospholipids J. Biol. Chem., November 26, 2004; 279(48): 49575 - 49578. [Abstract] [Full Text] [PDF]
|
|
