<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>10(1)</volume><submitter>Khan MM</submitter><pubmed_abstract>Removal of ubiquitinated targets by autophagosomes can be mediated by receptor molecules, like SQSTM1, in a mechanism referred to as selective autophagy. While cytoplasmic protein aggregates, mitochondria, and bacteria are the best-known targets of selective autophagy, their role in the turnover of membrane receptors is scarce. We here showed that fasting-induced wasting of skeletal muscle involves remodeling of the neuromuscular junction (NMJ) by increasing the turnover of muscle-type CHRN (cholinergic receptor, nicotinic/nicotinic acetylcholine receptor) in a TRIM63-dependent manner. Notably, this process implied enhanced production of endo/lysosomal carriers of CHRN, which also contained the membrane remodeler SH3GLB1, the E3 ubiquitin ligase, TRIM63, and the selective autophagy recepto</pubmed_abstract><journal>Autophagy</journal><pagination>123-36</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4389866</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors.</pubmed_title><pmcid>PMC4389866</pmcid><pubmed_authors>Carnio S</pubmed_authors><pubmed_authors>Sandri M</pubmed_authors><pubmed_authors>Khan MM</pubmed_authors><pubmed_authors>Hanashima A</pubmed_authors><pubmed_authors>Reischl M</pubmed_authors><pubmed_authors>Labeit D</pubmed_authors><pubmed_authors>Rudolf R</pubmed_authors><pubmed_authors>Labeit S</pubmed_authors><pubmed_authors>Strack S</pubmed_authors><pubmed_authors>Gasch A</pubmed_authors><pubmed_authors>Wild F</pubmed_authors><pubmed_authors>Brohm K</pubmed_authors></additional><is_claimable>false</is_claimable><name>Role of autophagy, SQSTM1, SH3GLB1, and TRIM63 in the turnover of nicotinic acetylcholine receptors.</name><description>Removal of ubiquitinated targets by autophagosomes can be mediated by receptor molecules, like SQSTM1, in a mechanism referred to as selective autophagy. While cytoplasmic protein aggregates, mitochondria, and bacteria are the best-known targets of selective autophagy, their role in the turnover of membrane receptors is scarce. We here showed that fasting-induced wasting of skeletal muscle involves remodeling of the neuromuscular junction (NMJ) by increasing the turnover of muscle-type CHRN (cholinergic receptor, nicotinic/nicotinic acetylcholine receptor) in a TRIM63-dependent manner. Notably, this process implied enhanced production of endo/lysosomal carriers of CHRN, which also contained the membrane remodeler SH3GLB1, the E3 ubiquitin ligase, TRIM63, and the selective autophagy recepto</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jan</publication><modification>2025-04-04T07:30:30.023Z</modification><creation>2019-03-27T01:49:36Z</creation></dates><accession>S-EPMC4389866</accession><cross_references><pubmed>24220501</pubmed><doi>10.4161/auto.26841</doi></cross_references></HashMap>