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10.1016/j.tins.2014.03.004 http://scihub22266oqcxt.onion/10.1016/j.tins.2014.03.004 C4075431!4075431 !24735649     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24735649 &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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\24735649 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Trends+Neurosci 2014 ; 37 (6 ): 315-24 Nephropedia Template TP {{tp|p=24735649 |t=2014. Parkin and PINK1: much more than mitophagy |pdf=|usr=}}{{24735649 }} gab.com Text Parkin and PINK1: much more than mitophagy JO: Trends Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=24735649 #FOAvip Parkinson's disease (PD) is a progressive neurodegenerative disease that causes a debilitating movement disorder. Although most cases of PD appear to be sporadic, rare Mendelian forms have provided tremendous insight into disease pathogenesis. Accumulating evidence suggests that impaired mitochondria underpin PD pathology. In support of this theory, data from multiple PD models have linked Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin, two recessive PD genes, in a common pathway impacting mitochondrial health, prompting a flurry of research to identify their mitochondrial targets. Recent work has focused on the role of PINK1 and parkin in mediating mitochondrial autophagy (mitophagy); however, emerging evidence casts parkin and PINK1 as key players in multiple domains of mitochondrial health and quality control. Twit Text FOAVip Parkin and PINK1: much more than mitophagy ????Trends Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=24735649 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24735649 #FOAvip English Wikipedia <ref>{{Cite pmid|24735649 }}</ref> Parkin and PINK1: much more than mitophagy #MMPMID24735649 Scarffe LA ; Stevens DA ; Dawson VL ; Dawson TM Trends Neurosci 2014[Jun]; 37 (6 ): 315-24 PMID24735649 show ga Parkinson's disease (PD) is a progressive neurodegenerative disease that causes a debilitating movement disorder. Although most cases of PD appear to be sporadic, rare Mendelian forms have provided tremendous insight into disease pathogenesis. Accumulating evidence suggests that impaired mitochondria underpin PD pathology. In support of this theory, data from multiple PD models have linked Phosphatase and tensin homolog (PTEN)-induced putative kinase 1 (PINK1) and parkin, two recessive PD genes, in a common pathway impacting mitochondrial health, prompting a flurry of research to identify their mitochondrial targets. Recent work has focused on the role of PINK1 and parkin in mediating mitochondrial autophagy (mitophagy); however, emerging evidence casts parkin and PINK1 as key players in multiple domains of mitochondrial health and quality control. |Animals [MESH] |Humans [MESH] |Mitochondria/*physiology [MESH] |Mitochondrial Diseases/physiopathology [MESH] |Parkinson Disease/*physiopathology [MESH] |Protein Kinases/*metabolism [MESH]Parkin and PINK1: much more than mitophagy (epmc).pdf DeepDyve Pubget Overpricing