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10.1038/s41586-019-1498-3 http://scihub22266oqcxt.onion/10.1038/s41586-019-1498-3 31435016!6726485!31435016     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nature 2019 ; 572 (7771): 609-613 Nephropedia Template TP {{tp|p=31435016|t=2019. Identification of an ATP-sensitive potassium channel in mitochondria |pdf=|usr=}}{{31435016}} gab.com Text Identification of an ATP-sensitive potassium channel in mitochondria JO: Nature http://www.kidney.de/pget.php?&tw=1&pmid=31435016 #FOAvip Mitochondria provide chemical energy for endoergonic reactions in the form of ATP, and their activity must meet cellular energy requirements, but the mechanisms that link organelle performance to ATP levels are poorly understood. Here we confirm the existence of a protein complex localized in mitochondria that mediates ATP-dependent potassium currents (that is, mitoK(ATP)). We show that-similar to their plasma membrane counterparts-mitoK(ATP) channels are composed of pore-forming and ATP-binding subunits, which we term MITOK and MITOSUR, respectively. In vitro reconstitution of MITOK together with MITOSUR recapitulates the main properties of mitoK(ATP). Overexpression of MITOK triggers marked organelle swelling, whereas the genetic ablation of this subunit causes instability in the mitochondrial membrane potential, widening of the intracristal space and decreased oxidative phosphorylation. In a mouse model, the loss of MITOK suppresses the cardioprotection that is elicited by pharmacological preconditioning induced by diazoxide. Our results indicate that mitoK(ATP) channels respond to the cellular energetic status by regulating organelle volume and function, and thereby have a key role in mitochondrial physiology and potential effects on several pathological processes. Twit Text FOAVip Identification of an ATP-sensitive potassium channel in mitochondria ????Nature http://www.kidney.de/pget.php?&tw=1&pmid=31435016 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=31435016 #FOAvip English Wikipedia <ref>{{Cite pmid|31435016}}</ref> Identification of an ATP-sensitive potassium channel in mitochondria #MMPMID31435016 Paggio A; Checchetto V; Campo A; Menabo R; Di Marco G; Di Lisa F; Szabo I; Rizzuto R; De Stefani D Nature 2019[Aug]; 572 (7771): 609-613 PMID31435016show ga Mitochondria provide chemical energy for endoergonic reactions in the form of ATP, and their activity must meet cellular energy requirements, but the mechanisms that link organelle performance to ATP levels are poorly understood. Here we confirm the existence of a protein complex localized in mitochondria that mediates ATP-dependent potassium currents (that is, mitoK(ATP)). We show that-similar to their plasma membrane counterparts-mitoK(ATP) channels are composed of pore-forming and ATP-binding subunits, which we term MITOK and MITOSUR, respectively. In vitro reconstitution of MITOK together with MITOSUR recapitulates the main properties of mitoK(ATP). Overexpression of MITOK triggers marked organelle swelling, whereas the genetic ablation of this subunit causes instability in the mitochondrial membrane potential, widening of the intracristal space and decreased oxidative phosphorylation. In a mouse model, the loss of MITOK suppresses the cardioprotection that is elicited by pharmacological preconditioning induced by diazoxide. Our results indicate that mitoK(ATP) channels respond to the cellular energetic status by regulating organelle volume and function, and thereby have a key role in mitochondrial physiology and potential effects on several pathological processes. |Adenosine Triphosphate/*metabolism[MESH] |Animals[MESH] |Cardiotonic Agents/pharmacology[MESH] |Diazoxide/pharmacology[MESH] |Electrophysiological Phenomena[MESH] |Heart/drug effects/physiology[MESH] |Ischemic Preconditioning, Myocardial[MESH] |Male[MESH] |Membrane Potential, Mitochondrial[MESH] |Mice[MESH] |Mitochondria, Heart/drug effects/*metabolism/pathology/physiology[MESH] |Organ Size/drug effects[MESH] |Oxidative Phosphorylation[MESH] |Potassium Channels/chemistry/*metabolism[MESH] |Potassium/metabolism[MESH]Identification of an ATP-sensitive potassium channel in mitochondria (epmc).pdf DeepDyve Pubget Overpricing