title: ER-stress and apoptosis: molecular mechanisms and potential relevance in infection.
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.
authors.affiliation: Institute for Medical Microbiology and Hygiene, University Medical Centre Freiburg, Hermann Herder-Str. 11, D-79104 Freiburg, Germany. Electronic address: georg.haecker@uniklinik-freiburg.de.
authors.forename: Georg
authors.initials: G
authors.lastname: Häcker
mesh_terms: D017209:Apoptosis / Q000502:physiology; D003141:Communicable Diseases / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism; D059865:Endoplasmic Reticulum Stress / Q000502:physiology*; D006801:Humans; D008928:Mitochondria / Q000235:genetics / Q000378:metabolism; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism
chemical_list: D019253:Proto-Oncogene Proteins c-bcl-2
keywords: Apoptosis; Bcl-2; ER-stress; Infection