ER-stress and apoptosis: molecular mechanisms and potential relevance in infection

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 howe...

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Published inMicrobes and infection Vol. 16; no. 10; pp. 805 - 810
Main Author Häcker, Georg
Format Journal Article
LanguageEnglish
Published France Elsevier Masson SAS 01.10.2014
Subjects
Apoptosis
Apoptosis - physiology
Bcl-2
Communicable Diseases - metabolism
Endoplasmic Reticulum - metabolism
Endoplasmic Reticulum Stress - physiology
ER-stress
Humans
Infection
Mitochondria - genetics
Mitochondria - metabolism
Proto-Oncogene Proteins c-bcl-2 - metabolism
Bcl-2
Infection
ER-stress
Apoptosis
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Summary: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.
Bibliography:ObjectType-Article-1
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ISSN:1286-4579
1769-714X
DOI:10.1016/j.micinf.2014.08.009