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10.1074/jbc.M114.555284 http://scihub22266oqcxt.onion/10.1074/jbc.M114.555284 C4110295!4110295 !24936055     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24936055 &cmd=llinks): Failed to open stream: HTTP request failed! 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Activation of AMP-activated protein kinase regulates hippocampal neuronal pH by recruiting Na(+)/H(+) exchanger NHE5 to the cell surface |pdf=|usr=}}{{24936055 }} gab.com Text Activation of AMP-activated protein kinase regulates hippocampal neuronal pH by recruiting Na(+)/H(+) exchanger NHE5 to the cell surface JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=24936055 #FOAvip Strict regulation of intra- and extracellular pH is an important determinant of nervous system function as many voltage-, ligand-, and H(+)-gated cationic channels are exquisitely sensitive to transient fluctuations in pH elicited by neural activity and pathophysiologic events such as hypoxia-ischemia and seizures. Multiple Na(+)/H(+) exchangers (NHEs) are implicated in maintenance of neural pH homeostasis. However, aside from the ubiquitous NHE1 isoform, their relative contributions are poorly understood. NHE5 is of particular interest as it is preferentially expressed in brain relative to other tissues. In hippocampal neurons, NHE5 regulates steady-state cytoplasmic pH, but intriguingly the bulk of the transporter is stored in intracellular vesicles. Here, we show that NHE5 is a direct target for phosphorylation by the AMP-activated protein kinase (AMPK), a key sensor and regulator of cellular energy homeostasis in response to metabolic stresses. In NHE5-transfected non-neuronal cells, activation of AMPK by the AMP mimetic AICAR or by antimycin A, which blocks aerobic respiration and causes acidification, increased cell surface accumulation and activity of NHE5, and elevated intracellular pH. These effects were effectively blocked by the AMPK antagonist compound C, the NHE inhibitor HOE694, and mutation of a predicted AMPK recognition motif in the NHE5 C terminus. This regulatory pathway was also functional in primary hippocampal neurons, where AMPK activation of NHE5 protected the cells from sustained antimycin A-induced acidification. These data reveal a unique role for AMPK and NHE5 in regulating the pH homeostasis of hippocampal neurons during metabolic stress. Twit Text FOAVip Activation of AMP-activated protein kinase regulates hippocampal neuronal pH by recruiting Na(+)/H(+) exchanger NHE5 to the cell surface ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=24936055 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24936055 #FOAvip English Wikipedia <ref>{{Cite pmid|24936055 }}</ref> Activation of AMP-activated protein kinase regulates hippocampal neuronal pH by recruiting Na(+)/H(+) exchanger NHE5 to the cell surface #MMPMID24936055 Jinadasa T ; Szabó EZ ; Numat M ; Orlowski J J Biol Chem 2014[Jul]; 289 (30 ): 20879-97 PMID24936055 show ga Strict regulation of intra- and extracellular pH is an important determinant of nervous system function as many voltage-, ligand-, and H(+)-gated cationic channels are exquisitely sensitive to transient fluctuations in pH elicited by neural activity and pathophysiologic events such as hypoxia-ischemia and seizures. Multiple Na(+)/H(+) exchangers (NHEs) are implicated in maintenance of neural pH homeostasis. However, aside from the ubiquitous NHE1 isoform, their relative contributions are poorly understood. NHE5 is of particular interest as it is preferentially expressed in brain relative to other tissues. In hippocampal neurons, NHE5 regulates steady-state cytoplasmic pH, but intriguingly the bulk of the transporter is stored in intracellular vesicles. Here, we show that NHE5 is a direct target for phosphorylation by the AMP-activated protein kinase (AMPK), a key sensor and regulator of cellular energy homeostasis in response to metabolic stresses. In NHE5-transfected non-neuronal cells, activation of AMPK by the AMP mimetic AICAR or by antimycin A, which blocks aerobic respiration and causes acidification, increased cell surface accumulation and activity of NHE5, and elevated intracellular pH. These effects were effectively blocked by the AMPK antagonist compound C, the NHE inhibitor HOE694, and mutation of a predicted AMPK recognition motif in the NHE5 C terminus. This regulatory pathway was also functional in primary hippocampal neurons, where AMPK activation of NHE5 protected the cells from sustained antimycin A-induced acidification. These data reveal a unique role for AMPK and NHE5 in regulating the pH homeostasis of hippocampal neurons during metabolic stress. |AMP-Activated Protein Kinases/antagonists & inhibitors/genetics/*metabolism [MESH] |Amino Acid Motifs [MESH] |Aminoimidazole Carboxamide/analogs & derivatives/metabolism [MESH] |Animals [MESH] |Antifungal Agents/pharmacology [MESH] |Antimycin A/pharmacology [MESH] |Cell Line [MESH] |Guanidines/pharmacology [MESH] |Hippocampus/cytology/*metabolism [MESH] |Humans [MESH] |Hydrogen-Ion Concentration [MESH] |Mice [MESH] |Neurons/cytology/*metabolism [MESH] |Phosphorylation/drug effects/genetics [MESH] |Protein Structure, Tertiary [MESH] |Ribonucleotides/genetics/metabolism [MESH] |Sodium-Hydrogen Exchangers/genetics/*metabolism [MESH] |Stress, Physiological/drug effects/genetics [MESH]Activation of AMP-activated protein kinase regulates hippocampal neuro(epmc).pdf DeepDyve Pubget Overpricing