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10.1016/j.mcn.2015.02.008 http://scihub22266oqcxt.onion/10.1016/j.mcn.2015.02.008 C4492119!4492119!25697646     free     free     free 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       Mol+Cell+Neurosci 2015 ; 66 (0 0): 62-71 Nephropedia Template TP {{tp|p=25697646|t=2015. Pathologic and Therapeutic Implications for the Cell Biology of Parkin |pdf=|usr=}}{{25697646}} gab.com Text Pathologic and Therapeutic Implications for the Cell Biology of Parkin JO: Mol Cell Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25697646 #FOAvip Mutations in the E3 ligase parkin are the most common cause of autosomal recessive Parkinson's disease (PD), but it is believed that parkin dysfunction may also contribute to idiopathic PD. Since its discovery, parkin has been implicated in supporting multiple neuroprotective pathways, many revolving around the maintenance of mitochondrial health quality control and governance of cell survival. Recent advances across the structure, biochemistry, and cell biology of parkin have provided great insights into the etiology of parkin-linked and idiopathic PD and may ultimately generate novel therapeutic strategies to slow or halt disease progression. This review describes the various pathways in which parkin acts and the mechanisms by which parkin may be targeted for therapeutic intervention. Twit Text FOAVip Pathologic and Therapeutic Implications for the Cell Biology of Parkin ????Mol Cell Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25697646 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25697646 #FOAvip English Wikipedia <ref>{{Cite pmid|25697646}}</ref> Pathologic and Therapeutic Implications for the Cell Biology of Parkin #MMPMID25697646 Charan RA; LaVoie MJ Mol Cell Neurosci 2015[May]; 66 (0 0): 62-71 PMID25697646show ga Mutations in the E3 ligase parkin are the most common cause of autosomal recessive Parkinson's disease (PD), but it is believed that parkin dysfunction may also contribute to idiopathic PD. Since its discovery, parkin has been implicated in supporting multiple neuroprotective pathways, many revolving around the maintenance of mitochondrial health quality control and governance of cell survival. Recent advances across the structure, biochemistry, and cell biology of parkin have provided great insights into the etiology of parkin-linked and idiopathic PD and may ultimately generate novel therapeutic strategies to slow or halt disease progression. This review describes the various pathways in which parkin acts and the mechanisms by which parkin may be targeted for therapeutic intervention. äPathologic and Therapeutic Implications for the Cell Biology of Parkin(epmc).pdf DeepDyve Pubget Overpricing