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Bim and Bmf Synergize To Induce Apoptosis in Neisseria Gonorrhoeae Infection

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons81971

Kepp,  Oliver
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons81902

Gottschalk,  Kathleen
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons81840

Churin,  Yuri
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons82110

Rajalingam,  Krishnaraj
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons81827

Brinkmann,  Volker
Core Facilities / Microscopy, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons82028

Machuy,  Nikolaus
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons82130

Rudel,  Thomas
Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society;

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Zitation

Kepp, O., Gottschalk, K., Churin, Y., Rajalingam, K., Brinkmann, V., Machuy, N., et al. (2009). Bim and Bmf Synergize To Induce Apoptosis in Neisseria Gonorrhoeae Infection. PLoS Pathogens, 5(3): e1000348.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-000E-C105-0
Zusammenfassung
Bcl-2 family proteins including the pro-apoptotic BH3-only proteins are central regulators of apoptotic cell death. Here we show by a focused siRNA miniscreen that the synergistic action of the BH3-only proteins Bim and Bmf is required for apoptosis induced by infection with Neisseria gonorrhoeae (Ngo). While Bim and Bmf were associated with the cytoskeleton of healthy cells, they both were released upon Ngo infection. Loss of Bim and Bmf from the cytoskeleton fraction required the activation of Jun-N-terminal kinase-1 (JNK-1), which in turn depended on Rac-1. Depletion and inhibition of Rac-1, JNK-1, Bim, or Bmf prevented the activation of Bak and Bax and the subsequent activation of caspases. Apoptosis could be reconstituted in Bim-depleted and Bmf-depleted cells by additional silencing of antiapoptotic Mcl-1 and Bcl-X-L, respectively. Our data indicate a synergistic role for both cytoskeletal-associated BH3-only proteins, Bim, and Bmf, in an apoptotic pathway leading to the clearance of Ngo-infected cells.