Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1016/j.celrep.2020.108411 http://scihub22266oqcxt.onion/10.1016/j.celrep.2020.108411 33238121!7793167!33238121     free     free     free Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 235.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Rep 2020 ; 33 (8): 108411 Nephropedia Template TP {{tp|p=33238121|t=2020. Mitochondrial Ca(2+) Signaling Is an Electrometabolic Switch to Fuel Phagosome Killing |pdf=|usr=}}{{33238121}} gab.com Text Mitochondrial Ca(2+) Signaling Is an Electrometabolic Switch to Fuel Phagosome Killing JO: Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=33238121 #FOAvip Phagocytes reallocate metabolic resources to kill engulfed pathogens, but the intracellular signals that rapidly switch the immunometabolic program necessary to fuel microbial killing are not understood. We report that macrophages use a fast two-step Ca(2+) relay to meet the bioenergetic demands of phagosomal killing. Upon detection of a fungal pathogen, macrophages rapidly elevate cytosolic Ca(2+) (phase 1), and by concurrently activating the mitochondrial Ca(2+) (mCa(2+)) uniporter (MCU), they trigger a rapid influx of Ca(2+) into the mitochondria (phase 2). mCa(2+) signaling reprograms mitochondrial metabolism, at least in part, through the activation of pyruvate dehydrogenase (PDH). Deprived of mCa(2+) signaling, Mcu(-/-) macrophages are deficient in phagosomal reactive oxygen species (ROS) production and defective at killing fungi. Mice lacking MCU in their myeloid cells are highly susceptible to disseminated candidiasis. In essence, this study reveals an elegant design principle that MCU-dependent Ca(2+) signaling is an electrometabolic switch to fuel phagosome killing. Twit Text FOAVip Mitochondrial Ca(2+) Signaling Is an Electrometabolic Switch to Fuel Phagosome Killing ????Cell Rep http://www.kidney.de/pget.php?&tw=1&pmid=33238121 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33238121 #FOAvip English Wikipedia <ref>{{Cite pmid|33238121}}</ref> Mitochondrial Ca(2+) Signaling Is an Electrometabolic Switch to Fuel Phagosome Killing #MMPMID33238121 Seegren PV; Downs TK; Stremska ME; Harper LR; Cao R; Olson RJ; Upchurch CM; Doyle CA; Kennedy J; Stipes EL; Leitinger N; Periasamy A; Desai BN Cell Rep 2020[Nov]; 33 (8): 108411 PMID33238121show ga Phagocytes reallocate metabolic resources to kill engulfed pathogens, but the intracellular signals that rapidly switch the immunometabolic program necessary to fuel microbial killing are not understood. We report that macrophages use a fast two-step Ca(2+) relay to meet the bioenergetic demands of phagosomal killing. Upon detection of a fungal pathogen, macrophages rapidly elevate cytosolic Ca(2+) (phase 1), and by concurrently activating the mitochondrial Ca(2+) (mCa(2+)) uniporter (MCU), they trigger a rapid influx of Ca(2+) into the mitochondria (phase 2). mCa(2+) signaling reprograms mitochondrial metabolism, at least in part, through the activation of pyruvate dehydrogenase (PDH). Deprived of mCa(2+) signaling, Mcu(-/-) macrophages are deficient in phagosomal reactive oxygen species (ROS) production and defective at killing fungi. Mice lacking MCU in their myeloid cells are highly susceptible to disseminated candidiasis. In essence, this study reveals an elegant design principle that MCU-dependent Ca(2+) signaling is an electrometabolic switch to fuel phagosome killing. |Animals[MESH] |Calcium/*metabolism[MESH] |Candida albicans/*pathogenicity[MESH] |Mice[MESH] |Mitochondria/*metabolism[MESH] |Phagosomes/*metabolism[MESH]Mitochondrial Ca(2+) Signaling Is an Electrometabolic Switch to Fuel P(epmc).pdf DeepDyve Pubget Overpricing