F-ATP synthase and the permeability transition pore: fewer doubts, more certainties

被引：42

作者：

Carraro, Michela ^{[1
]}

Checchetto, Vanessa ^{[2
]}

Szabo, Ildiko ^{[2
]}

Bernardi, Paolo ^{[1
]}

机构：

[1] Univ Padua, Dept Biomed Sci, Via Ugo Bassi 58-B, I-35131 Padua, Italy

[2] Univ Padua, Dept Biol, Padua, Italy

来源：

FEBS LETTERS | 2019年 / 593卷 / 13期

关键词：

ATP synthase; calcium; channel; cyclophilin; mitochondria; permeability transition; INNER MITOCHONDRIAL-MEMBRANE; COMPRISE VDAC MOLECULES; DEPENDENT ANION CHANNEL; CYCLOSPORINE-A; CYCLOPHILIN-D; SUBUNIT-C; BENZODIAZEPINE-RECEPTOR; PHOSPHATE CARRIER; OXIDATIVE-PHOSPHORYLATION; CA-2+-DEPENDENT PORE;

D O I：

10.1002/1873-3468.13485

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Whether the mitochondrial permeability transition pore (PTP), also called mitochondrial megachannel (MMC), originates from the F-ATP synthase is a matter of controversy. This hypothesis is supported both by site-directed mutagenesis of specific residues of F-ATP synthase affecting regulation of the PTP/MMC and by deletion of specific subunits causing dramatic changes in channel conductance. In contrast, human cells lacking an assembled F-ATP synthase apparently display persistence of the PTP. We discuss recent data that shed new light on this controversy, supporting the conclusion that the PTP/MMC originates from a Ca2+-dependent conformational change in F-ATP synthase allowing its reversible transformation into a high-conductance channel.

引用

页码：1542 / 1553

页数：12

共 127 条

[71] Genetic deletion of the mitochondrial phosphate carrier desensitizes the mitochondrial permeability transition pore and causes cardiomyopathy [J].

Kwong, J. Q. ;

Davis, J. ;

Baines, C. P. ;

Sargent, M. A. ;

Karch, J. ;

Wang, X. ;

Huang, T. ;

Molkentin, J. D. .

CELL DEATH AND DIFFERENTIATION, 2014, 21 (08) :1209-1217

[72]

LEHNINGER AL, 1959, J BIOL CHEM, V234, P2465

[73]

LEHNINGER AL, 1959, J BIOL CHEM, V234, P2459

[74] Recent progress in elucidating the molecular mechanism of the mitochondrial permeability transition pore [J].

Leung, Anna W. C. ;

Halestrap, Andrew P. .

BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 2008, 1777 (7-8) :946-952

[75] Ligand-selective modulation of the permeability transition pore by arginine modification.: Opposing effects of p-hydroxyphenylglyoxal and phenylglyoxal. [J].

Linder, MD ;

Morkunaite-Haimi, S ;

Kinnumen, PKJ ;

Bernardi, P ;

Eriksson, O .

JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (02) :937-942

[76] The permeability transition pore complex:: A target for apoptosis regulation by caspases and Bcl-2-related proteins [J].

Marzo, I ;

Brenner, C ;

Zamzami, N ;

Susin, SA ;

Beutner, G ;

Brdiczka, D ;

Rémy, R ;

Xie, ZH ;

Reed, JC ;

Kroemer, G .

JOURNAL OF EXPERIMENTAL MEDICINE, 1998, 187 (08) :1261-1271

[77] Induction of the permeability transition pore in cells depleted of mitochondrial DNA [J].

Masgras, Ionica ;

Rasola, Andrea ;

Bernardi, Paolo .

BIOCHIMICA ET BIOPHYSICA ACTA-BIOENERGETICS, 2012, 1817 (10) :1860-1866

[78] EQUIVALENT PORE RADIUS OF INTACT AND DAMAGED MITOCHONDRIA AND MECHANISM OF ACTIVE SHRINKAGE [J].

MASSARI, S ;

AZZONE, GF .

BIOCHIMICA ET BIOPHYSICA ACTA, 1972, 238 (01) :23-+

[79] ISOLATION OF THE MITOCHONDRIAL BENZODIAZEPINE RECEPTOR - ASSOCIATION WITH THE VOLTAGE-DEPENDENT ANION CHANNEL AND THE ADENINE-NUCLEOTIDE CARRIER [J].

MCENERY, MW ;

SNOWMAN, AM ;

TRIFILETTI, RR ;

SNYDER, SH .

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1992, 89 (08) :3170-3174

[80]

McGeoch J E, 2001, Eur J Paediatr Neurol, V5 Suppl A, P147, DOI 10.1053/ejpn.2000.0452

← 3 4 5 6 7 8 9 10 11 12 →