ER-stress and apoptosis: molecular mechanisms and potential relevance in infection |
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| Institution: | 1. Associate professor, Division of Orthodontics, College of Dentistry, Ohio State University, Columbus, Ohio;2. Research fellow, Department of Orthodontics and Dentofacial Orthopedics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan;3. Professor and chair, Department of Orthodontics and Dentofacial Orthopedics, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University, Okayama, Japan;4. Professor and chair, Division of Orthodontics, College of Dentistry, Ohio State University, Columbus, Ohio;5. Professor and chair, Division of Orthodontics and Dentofacial Orthopedics, Graduate School of Dentistry, Tohoku University, Sendai, Japan;6. Professor and chair, Division of Oral and Craniofacial Anatomy, Graduate School of Dentistry, Tohoku University, Sendai, Japan;7. Professor and Chair, Department of Orthodontics, Graduate School of Dentistry, Osaka University, Osaka, Japan;1. Department of Biochemistry, Molecular and Structural Biology, Jožef Stefan Institute, Ljubljana SI-1000, Slovenia;2. Jožef Stefan International Postgraduate School, Jamova 39, SI-1000 Ljubljana, Slovenia;3. Centre of Excellence for Integrated Approaches in Chemistry and Biology of Proteins (CIPKeBiP), Jamova 39, SI-1000 Ljubljana, Slovenia;4. Department of Chemistry and Biochemistry, Faculty of Chemistry and Chemical Technology, University of Ljubljana, Cesta v Mestni log 88A, SI-1000 Ljubljana, Slovenia;1. 4th Department of Internal Medicine, Athens University Medical School, ATTIKON University General Hospital, Athens, Greece;2. Cardiac and Thoracic Surgery Unit, Athens University Medical School, ATTIKON University General Hospital, Athens, Greece;3. Integrated Research and Treatment Centre, Centre for Sepsis Control and Care (CSCC), Jena University Hospital, Jena, Germany |
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| Abstract: | During ER-stress, one of the responses a cell can choose is apoptosis. Apoptosis generally is a cell's preferred response when other control mechanisms are overwhelmed. We now have a reasonably clear molecular picture what is happening once the apoptotic apparatus has been started. Unclear however are the majority of the upstream pathways that connect other signalling to apoptosis. During ER-stress, confirmed apoptosis-regulating targets are pro- and anti-apoptotic proteins of the Bcl-2-family, whose concerted action induces apoptosis. I will here discuss how mitochondrial apoptosis is triggered, how this is linked to the ER-stress response and in what way this may be relevant during microbial infections. |
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| Keywords: | ER-stress Apoptosis Bcl-2 Infection |
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