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  Mcl-1 Is a Key Regulator of Apoptosis Resistance in Chlamydia trachomatis-Infected Cells

Rajalingam, K., Sharma, M., Lohmann, C., Oswald, M., Thieck, O., Froelich, C. J., et al. (2008). Mcl-1 Is a Key Regulator of Apoptosis Resistance in Chlamydia trachomatis-Infected Cells. PLoS ONE, 3(9): e3102. doi:10.1371/journal.pone.0003102.

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PLoS_One_2008_3_e3102.pdf (Publisher version), 548KB
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Copyright: © 2008 Rajalingam et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Rajalingam, Krishnaraj1, Author              
Sharma, Manu1, Author              
Lohmann, Christine1, Author              
Oswald, Monique1, Author              
Thieck, Oliver1, Author              
Froelich, Christopher J., Author
Rudel, Thomas1, Author              
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1Department of Molecular Biology, Max Planck Institute for Infection Biology, Max Planck Society, ou_1664147              

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 Abstract: Chlamydia are obligate intracellular bacteria that cause variety of human diseases. Host cells infected with Chlamydia are protected against many different apoptotic stimuli. The induction of apoptosis resistance is thought to be an important immune escape mechanism allowing Chlamydia to replicate inside the host cell. Infection with C. trachomatis activates the Raf/MEK/ERK pathway and the PI3K/AKT pathway. Here we show that inhibition of these two pathways by chemical inhibitors sensitized C. trachomatis infected cells to granzyme B-mediated cell death. Infection leads to the Raf/MEK/ERK-mediated up-regulation and PI3K-dependent stabilization of the anti-apoptotic Bcl-2 family member Mcl-1. Consistently, interfering with Mcl-1 up-regulation sensitized infected cells for apoptosis induced via the TNF receptor, DNA damage, granzyme B and stress. Our data suggest that Mcl-1 up-regulation is primarily required to maintain apoptosis resistance in C. trachomatis-infected cells.

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Language(s): eng - English
 Dates: 2008-09
 Publication Status: Published in print
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 Rev. Type: Peer
 Identifiers: eDoc: 411656
DOI: 10.1371/journal.pone.0003102
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Title: PLoS ONE
Source Genre: Journal
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Pages: - Volume / Issue: 3 (9) Sequence Number: e3102 Start / End Page: - Identifier: ISSN: 1932-6203