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Titolo:
Targeting of the pro-apoptotic VDAC-like porin (PorB) of Neisseria gonorrhoeae to mitochondria of infected cells
Autore:
Muller, A; Gunther, D; Brinkmann, V; Hurwitz, R; Meyer, TF; Rudel, T;
Indirizzi:
Max Planck Inst Infect Biol, Dept Mol Biol, D-10117 Berlin, Germany Max Planck Inst Infect Biol Berlin Germany D-10117 10117 Berlin, Germany Max Planck Inst Infect Biol, Cent Support Unit, D-10117 Berlin, Germany Max Planck Inst Infect Biol Berlin Germany D-10117 10117 Berlin, Germany
Titolo Testata:
EMBO JOURNAL
fascicolo: 20, volume: 19, anno: 2000,
pagine: 5332 - 5343
SICI:
0261-4189(20001016)19:20<5332:TOTPVP>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
PERMEABILITY TRANSITION PORE; CYTOCHROME-C; POLY(ADP-RIBOSE) POLYMERASE; RHODOBACTER-CAPSULATUS; NUCLEAR APOPTOSIS; EPITHELIAL-CELLS; CHANNEL PROTEIN; ALPHA-FODRIN; PILC PROTEIN; DEATH;
Keywords:
apoptosis; mitochondria; Neisseria; permeability transition; voltage-dependent anion channel (VDAC)-like porin;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
73
Recensione:
Indirizzi per estratti:
Indirizzo: Meyer, TF Max Planck Inst Infect Biol, Dept Mol Biol, Schumannstr 21-22, D-10117 Berlin, Germany Max Planck Inst Infect Biol Schumannstr 21-22 Berlin Germany D-10117
Citazione:
A. Muller et al., "Targeting of the pro-apoptotic VDAC-like porin (PorB) of Neisseria gonorrhoeae to mitochondria of infected cells", EMBO J, 19(20), 2000, pp. 5332-5343

Abstract

Infection of cell cultures with Neisseria gonorrhoeae results in apoptosisthat is mediated by the PorB porin. During the infection process porin translocates from the outer bacterial membrane into host cell membranes where its channel activity is regulated by nucleotide binding and voltage-dependent gating, features that are shared by the mitochondrial voltage-dependent anion channel (VDAC). Here we show that porin is selectively and efficiently transported to mitochondria of infected cells. Prevention of porin translocation also blocked the induction of apoptosis. Mitochondria of cells treated with porin both in vitro and in vivo were depleted of cytochrome c and underwent permeability transition. Overexpression of Bcl-2 blocked porin-induced apoptosis. The release of cytochrome c occurred independently of active caspases but was completely prevented by Bcl-2. Our data suggest that the Neisseria porin can, like its eukaryotic homologue, function at the mitochondrial checkpoint to mediate apoptosis.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 13:11:47