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10.1038/srep15213 http://scihub22266oqcxt.onion/10.1038/srep15213 C4609990!4609990 !26477494     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26477494 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26477494 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Sci+Rep 2015 ; 5 (ä): 15213 Nephropedia Template TP {{tp|p=26477494 |t=2015. Cytoplasmic sphingosine-1-phosphate pathway modulates neuronal autophagy |pdf=|usr=}}{{26477494 }} gab.com Text Cytoplasmic sphingosine-1-phosphate pathway modulates neuronal autophagy JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26477494 #FOAvip Autophagy is an important homeostatic mechanism that eliminates long-lived proteins, protein aggregates and damaged organelles. Its dysregulation is involved in many neurodegenerative disorders. Autophagy is therefore a promising target for blunting neurodegeneration. We searched for novel autophagic pathways in primary neurons and identified the cytosolic sphingosine-1-phosphate (S1P) pathway as a regulator of neuronal autophagy. S1P, a bioactive lipid generated by sphingosine kinase 1 (SK1) in the cytoplasm, is implicated in cell survival. We found that SK1 enhances flux through autophagy and that S1P-metabolizing enzymes decrease this flux. When autophagy is stimulated, SK1 relocalizes to endosomes/autophagosomes in neurons. Expression of a dominant-negative form of SK1 inhibits autophagosome synthesis. In a neuron model of Huntington's disease, pharmacologically inhibiting S1P-lyase protected neurons from mutant huntingtin-induced neurotoxicity. These results identify the S1P pathway as a novel regulator of neuronal autophagy and provide a new target for developing therapies for neurodegenerative disorders. Twit Text FOAVip Cytoplasmic sphingosine-1-phosphate pathway modulates neuronal autophagy ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=26477494 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26477494 #FOAvip English Wikipedia <ref>{{Cite pmid|26477494 }}</ref> Cytoplasmic sphingosine-1-phosphate pathway modulates neuronal autophagy #MMPMID26477494 Moruno Manchon JF ; Uzor NE ; Dabaghian Y ; Furr-Stimming EE ; Finkbeiner S ; Tsvetkov AS Sci Rep 2015[Oct]; 5 (ä): 15213 PMID26477494 show ga Autophagy is an important homeostatic mechanism that eliminates long-lived proteins, protein aggregates and damaged organelles. Its dysregulation is involved in many neurodegenerative disorders. Autophagy is therefore a promising target for blunting neurodegeneration. We searched for novel autophagic pathways in primary neurons and identified the cytosolic sphingosine-1-phosphate (S1P) pathway as a regulator of neuronal autophagy. S1P, a bioactive lipid generated by sphingosine kinase 1 (SK1) in the cytoplasm, is implicated in cell survival. We found that SK1 enhances flux through autophagy and that S1P-metabolizing enzymes decrease this flux. When autophagy is stimulated, SK1 relocalizes to endosomes/autophagosomes in neurons. Expression of a dominant-negative form of SK1 inhibits autophagosome synthesis. In a neuron model of Huntington's disease, pharmacologically inhibiting S1P-lyase protected neurons from mutant huntingtin-induced neurotoxicity. These results identify the S1P pathway as a novel regulator of neuronal autophagy and provide a new target for developing therapies for neurodegenerative disorders. |*Autophagy/drug effects/genetics [MESH] |*Signal Transduction [MESH] |Aldehyde-Lyases/antagonists & inhibitors/metabolism [MESH] |Animals [MESH] |Biomarkers [MESH] |Cell Survival/drug effects [MESH] |Cytoplasm [MESH] |Endoplasmic Reticulum/metabolism [MESH] |Endosomes/metabolism [MESH] |Enzyme Inhibitors/pharmacology [MESH] |Gene Expression [MESH] |Lysophospholipids/*metabolism [MESH] |Neurons/*metabolism [MESH] |Phagosomes/metabolism [MESH] |Phosphotransferases (Alcohol Group Acceptor)/genetics/metabolism [MESH] |Protein Binding [MESH] |Protein Transport [MESH] |Rats [MESH]Cytoplasmic sphingosine-1-phosphate pathway modulates neuronal autopha(epmc).pdf DeepDyve Pubget Overpricing