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10.1016/j.immuni.2018.02.012 http://scihub22266oqcxt.onion/10.1016/j.immuni.2018.02.012 C6049611!6049611 !29523440     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29523440 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunometabolic Hubs that Orchestrate the Rapid Recall Response of Memory CD8(+) T Cells |pdf=|usr=}}{{29523440 }} gab.com Text Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunometabolic Hubs that Orchestrate the Rapid Recall Response of Memory CD8(+) T Cells JO: Immunity http://www.kidney.de/pget.php?&tw=1&pmid=29523440 #FOAvip Glycolysis is linked to the rapid response of memory CD8(+) T cells, but the molecular and subcellular structural elements enabling enhanced glucose metabolism in nascent activated memory CD8(+) T cells are unknown. We found that rapid activation of protein kinase B (PKB or AKT) by mammalian target of rapamycin complex 2 (mTORC2) led to inhibition of glycogen synthase kinase 3? (GSK3?) at mitochondria-endoplasmic reticulum (ER) junctions. This enabled recruitment of hexokinase I (HK-I) to the voltage-dependent anion channel (VDAC) on mitochondria. Binding of HK-I to VDAC promoted respiration by facilitating metabolite flux into mitochondria. Glucose tracing pinpointed pyruvate oxidation in mitochondria, which was the metabolic requirement for rapid generation of interferon-? (IFN-?) in memory T cells. Subcellular organization of mTORC2-AKT-GSK3? at mitochondria-ER contact sites, promoting HK-I recruitment to VDAC, thus underpins the metabolic reprogramming needed for memory CD8(+) T cells to rapidly acquire effector function. Twit Text FOAVip Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunometabolic Hubs that Orchestrate the Rapid Recall Response of Memory CD8(+) T Cells ????Immunity http://www.kidney.de/pget.php?&tw=1&pmid=29523440 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29523440 #FOAvip English Wikipedia <ref>{{Cite pmid|29523440 }}</ref> Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunometabolic Hubs that Orchestrate the Rapid Recall Response of Memory CD8(+) T Cells #MMPMID29523440 Bantug GR ; Fischer M ; Grählert J ; Balmer ML ; Unterstab G ; Develioglu L ; Steiner R ; Zhang L ; Costa ASH ; Gubser PM ; Burgener AV ; Sauder U ; Löliger J ; Belle R ; Dimeloe S ; Lötscher J ; Jauch A ; Recher M ; Hönger G ; Hall MN ; Romero P ; Frezza C ; Hess C Immunity 2018[Mar]; 48 (3 ): 542-555.e6 PMID29523440 show ga Glycolysis is linked to the rapid response of memory CD8(+) T cells, but the molecular and subcellular structural elements enabling enhanced glucose metabolism in nascent activated memory CD8(+) T cells are unknown. We found that rapid activation of protein kinase B (PKB or AKT) by mammalian target of rapamycin complex 2 (mTORC2) led to inhibition of glycogen synthase kinase 3? (GSK3?) at mitochondria-endoplasmic reticulum (ER) junctions. This enabled recruitment of hexokinase I (HK-I) to the voltage-dependent anion channel (VDAC) on mitochondria. Binding of HK-I to VDAC promoted respiration by facilitating metabolite flux into mitochondria. Glucose tracing pinpointed pyruvate oxidation in mitochondria, which was the metabolic requirement for rapid generation of interferon-? (IFN-?) in memory T cells. Subcellular organization of mTORC2-AKT-GSK3? at mitochondria-ER contact sites, promoting HK-I recruitment to VDAC, thus underpins the metabolic reprogramming needed for memory CD8(+) T cells to rapidly acquire effector function. |*Energy Metabolism [MESH] |*Immunologic Memory [MESH] |*Signal Transduction [MESH] |CD8-Positive T-Lymphocytes/*immunology/*metabolism [MESH] |Cell Respiration [MESH] |Endoplasmic Reticulum/*metabolism/ultrastructure [MESH] |Glycogen Synthase Kinase 3 beta/metabolism [MESH] |Glycolysis [MESH] |Intracellular Membranes/metabolism [MESH] |Lymphocyte Activation [MESH] |Mechanistic Target of Rapamycin Complex 2/metabolism [MESH] |Mitochondria/*metabolism/ultrastructure [MESH] |Models, Biological [MESH] |Proto-Oncogene Proteins c-akt/metabolism [MESH]Mitochondria-Endoplasmic Reticulum Contact Sites Function as Immunomet(epmc).pdf DeepDyve Pubget Overpricing