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10.3390/cells9112349 http://scihub22266oqcxt.onion/10.3390/cells9112349 33114389!7693032!33114389     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=33114389&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       Cells 2020 ; 9 (11): ? Nephropedia Template TP {{tp|p=33114389|t=2020. Selective Autophagy by Close Encounters of the Ubiquitin Kind |pdf=|usr=}}{{33114389}} gab.com Text Selective Autophagy by Close Encounters of the Ubiquitin Kind JO: Cells http://www.kidney.de/pget.php?&tw=1&pmid=33114389 #FOAvip Autophagy, a bulk degradation process within eukaryotic cells, is responsible for cellular turnover and nutrient liberation during starvation. Increasing evidence indicate that this process can be extremely discerning. Selective autophagy segregates and eliminates protein aggregates, damaged organelles, and invading organisms. The specificity of this process is largely mediated by post-translational modifications (PTMs), which are recognized by autophagy receptors. These receptors grant autophagy surgical precision in cargo selection, where only tagged substrates are engulfed within autophagosomes and delivered to the lysosome for proteolytic breakdown. A growing number of selective autophagy receptors have emerged including p62, NBR1, OPTN, NDP52, TAX1BP1, TOLLIP, and more continue to be uncovered. The most well-documented PTM is ubiquitination and selective autophagy receptors are equipped with a ubiquitin binding domain and an LC3 interacting region which allows them to physically bridge cargo to autophagosomes. Here, we review the role of ubiquitin and ubiquitin-like post-translational modifications in various types of selective autophagy. Twit Text FOAVip Selective Autophagy by Close Encounters of the Ubiquitin Kind ????Cells http://www.kidney.de/pget.php?&tw=1&pmid=33114389 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=33114389 #FOAvip English Wikipedia <ref>{{Cite pmid|33114389}}</ref> Selective Autophagy by Close Encounters of the Ubiquitin Kind #MMPMID33114389 Vainshtein A; Grumati P Cells 2020[Oct]; 9 (11): ? PMID33114389show ga Autophagy, a bulk degradation process within eukaryotic cells, is responsible for cellular turnover and nutrient liberation during starvation. Increasing evidence indicate that this process can be extremely discerning. Selective autophagy segregates and eliminates protein aggregates, damaged organelles, and invading organisms. The specificity of this process is largely mediated by post-translational modifications (PTMs), which are recognized by autophagy receptors. These receptors grant autophagy surgical precision in cargo selection, where only tagged substrates are engulfed within autophagosomes and delivered to the lysosome for proteolytic breakdown. A growing number of selective autophagy receptors have emerged including p62, NBR1, OPTN, NDP52, TAX1BP1, TOLLIP, and more continue to be uncovered. The most well-documented PTM is ubiquitination and selective autophagy receptors are equipped with a ubiquitin binding domain and an LC3 interacting region which allows them to physically bridge cargo to autophagosomes. Here, we review the role of ubiquitin and ubiquitin-like post-translational modifications in various types of selective autophagy. |*Autophagy[MESH] |Animals[MESH] |Apoptosis Regulatory Proteins/metabolism[MESH] |Autophagosomes/metabolism[MESH] |Endoplasmic Reticulum/metabolism[MESH] |Humans[MESH] |Mitochondria/genetics/metabolism[MESH] |Mitophagy[MESH] |Protein Binding[MESH] |Protein Processing, Post-Translational[MESH] |Ubiquitin/*metabolism[MESH]Selective Autophagy by Close Encounters of the Ubiquitin Kind (epmc).pdf DeepDyve Pubget Overpricing