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10.1016/j.redox.2017.04.033 http://scihub22266oqcxt.onion/10.1016/j.redox.2017.04.033 C5426049!5426049!28476010     free     free     free       Redox+Biol 2017 ; 12 (ä): 908-15 Nephropedia Template TP {{tp|p=28476010|t=2017. Redox signaling in acute oxygen sensing |pdf=|usr=}}{{28476010}} gab.com Text Redox signaling in acute oxygen sensing JO: Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=28476010 #FOAvip Acute oxygen (O2) sensing is essential for individuals to survive under hypoxic conditions. The carotid body (CB) is the main peripheral chemoreceptor, which contains excitable and O2-sensitive glomus cells with O2-regulated ion channels. Upon exposure to acute hypoxia, inhibition of K+ channels is the signal that triggers cell depolarization, transmitter release and activation of sensory fibers that stimulate the brainstem respiratory center to produce hyperventilation. The molecular mechanisms underlying O2 sensing by glomus cells have, however, remained elusive. Here we discuss recent data demonstrating that ablation of mitochondrial Ndufs2 gene selectively abolishes sensitivity of glomus cells to hypoxia, maintaining responsiveness to hypercapnia or hypoglycemia. These data suggest that reactive oxygen species and NADH generated in mitochondrial complex I during hypoxia are signaling molecules that modulate membrane K+ channels. We propose that the structural substrates for acute O2 sensing in CB glomus cells are ?O2-sensing microdomains? formed by mitochondria and neighboring K+ channels in the plasma membrane. Twit Text FOAVip Redox signaling in acute oxygen sensing ????Redox Biol http://www.kidney.de/pget.php?&tw=1&pmid=28476010 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28476010 #FOAvip English Wikipedia <ref>{{Cite pmid|28476010}}</ref> Redox signaling in acute oxygen sensing #MMPMID28476010 Gao L; González-Rodríguez P; Ortega-Sáenz P; López-Barneo J Redox Biol 2017[Aug]; 12 (ä): 908-15 PMID28476010show ga Acute oxygen (O2) sensing is essential for individuals to survive under hypoxic conditions. The carotid body (CB) is the main peripheral chemoreceptor, which contains excitable and O2-sensitive glomus cells with O2-regulated ion channels. Upon exposure to acute hypoxia, inhibition of K+ channels is the signal that triggers cell depolarization, transmitter release and activation of sensory fibers that stimulate the brainstem respiratory center to produce hyperventilation. The molecular mechanisms underlying O2 sensing by glomus cells have, however, remained elusive. Here we discuss recent data demonstrating that ablation of mitochondrial Ndufs2 gene selectively abolishes sensitivity of glomus cells to hypoxia, maintaining responsiveness to hypercapnia or hypoglycemia. These data suggest that reactive oxygen species and NADH generated in mitochondrial complex I during hypoxia are signaling molecules that modulate membrane K+ channels. We propose that the structural substrates for acute O2 sensing in CB glomus cells are ?O2-sensing microdomains? formed by mitochondria and neighboring K+ channels in the plasma membrane. äRedox signaling in acute oxygen sensing (epmc).pdf DeepDyve Pubget Overpricing