Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2005 Jun;37(3):121-8.
doi: 10.1007/s10863-005-6565-9.

Genetic dissection of the permeability transition pore

Affiliations
Review

Genetic dissection of the permeability transition pore

Michael Forte et al. J Bioenerg Biomembr. 2005 Jun.

Abstract

The permeability transition pore (PTP) regulates the structural re-organization of mitochondria in response to changes in cellular Ca(2+) and is thought to be an important participant in mitochondrial responses to cell death signals. Although the proteins forming the PTP have yet to be rigorously identified, recent examination of the response of mitochondria, cells and tissues lacking putative components of the PTP have been reported. Studies on mitochondria lacking cyclophilin D (CyP-D) have proved that this protein is the target for PTP inhibition by CsA; yet they have also unequivocally demonstrated that the PTP can form and open in the absence of CyP-D. Likewise, studies in mice lacking the two adenine nucleotide translocators expressed in this species have shown that a functional PTP can form in the absence of these proteins. Thus, the inner mitochondrial membrane components of the PTP remain to be identified, and the absence of CyP-D may not preclude PTP opening in vivo--a finding that questions the conclusion that the PTP participates in cell death pathways only in response to a restricted set of challenges.

PubMed Disclaimer

Similar articles

Cited by

References

    1. J Biol Chem. 2001 Jan 26;276(4):2571-5 - PubMed
    1. Neuroscience. 1999;90(4):1325-38 - PubMed
    1. Sci STKE. 2004 Jan 13;2004(215):re1 - PubMed
    1. J Biol Chem. 1996 Mar 1;271(9):4846-9 - PubMed
    1. J Biol Chem. 1993 Jan 15;268(2):1005-10 - PubMed

LinkOut - more resources