Journal
INFECTION AND IMMUNITY
Volume 73, Issue 3, Pages 1861-1864Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/IAI.73.3.1861-1864.2005
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Funding
- NHLBI NIH HHS [R01HL64883, R01 HL064883] Funding Source: Medline
- NIAID NIH HHS [R21 AI057450, R01 AI047997, R21AI57450] Funding Source: Medline
- NIAMS NIH HHS [R01AR47997] Funding Source: Medline
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We have previously correlated Chlamydia trachomatis antiapoptotic activity with the blockade of mitochondrial cytochrome c release and the inhibition of Bax and Bak activation. We now report that C. trachomatis infection leads to degradation of Bik, Puma, and Bim, three upstream proapoptotic BH3-only proteins of the Bcl-2 family that can transmit death signals to mitochondria by inhibiting the Bcl-2 antiapoptotic proteins and/or activating the Bcl-2 proapoptotic members, such as Bax and Bak. This observation has provided new information on the chlamydial antiapoptosis mechanisms.
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