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10.1371/journal.pone.0194423 http://scihub22266oqcxt.onion/10.1371/journal.pone.0194423 C5858923!5858923!29554128     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2018 ; 13 (3): ä Nephropedia Template TP {{tp|p=29554128|t=2018. Quantifying autophagy using novel LC3B and p62 TR-FRET assays |pdf=|usr=}}{{29554128}} gab.com Text Quantifying autophagy using novel LC3B and p62 TR-FRET assays JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29554128 #FOAvip Autophagy is a cellular mechanism that can generate energy for cells or clear misfolded or aggregated proteins, and upregulating this process has been proposed as a therapeutic approach for neurodegenerative diseases. Here we describe a novel set of LC3B-II and p62 time-resolved fluorescence resonance energy transfer (TR-FRET) assays that can detect changes in autophagy in the absence of exogenous labels. Lipidated LC3 is a marker of autophagosomes, while p62 is a substrate of autophagy. These assays can be employed in high-throughput screens to identify novel autophagy upregulators, and can measure autophagy changes in cultured cells or tissues after genetic or pharmacological interventions. We also demonstrate that different cells exhibit varying autophagic responses to pharmacological interventions. Overall, it is clear that a battery of readouts is required to make conclusions about changes in autophagy. Twit Text FOAVip Quantifying autophagy using novel LC3B and p62 TR-FRET assays ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29554128 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29554128 #FOAvip English Wikipedia <ref>{{Cite pmid|29554128}}</ref> Quantifying autophagy using novel LC3B and p62 TR-FRET assays #MMPMID29554128 Bresciani A; Spiezia MC; Boggio R; Cariulo C; Nordheim A; Altobelli R; Kuhlbrodt K; Dominguez C; Munoz-Sanjuan I; Wityak J; Fodale V; Marchionini DM; Weiss A PLoS One 2018[]; 13 (3): ä PMID29554128show ga Autophagy is a cellular mechanism that can generate energy for cells or clear misfolded or aggregated proteins, and upregulating this process has been proposed as a therapeutic approach for neurodegenerative diseases. Here we describe a novel set of LC3B-II and p62 time-resolved fluorescence resonance energy transfer (TR-FRET) assays that can detect changes in autophagy in the absence of exogenous labels. Lipidated LC3 is a marker of autophagosomes, while p62 is a substrate of autophagy. These assays can be employed in high-throughput screens to identify novel autophagy upregulators, and can measure autophagy changes in cultured cells or tissues after genetic or pharmacological interventions. We also demonstrate that different cells exhibit varying autophagic responses to pharmacological interventions. Overall, it is clear that a battery of readouts is required to make conclusions about changes in autophagy. äQuantifying autophagy using novel LC3B and p62 TR-FRET assays (epmc).pdf DeepDyve Pubget Overpricing