<HashMap><database>biostudies-literature</database><scores/><additional><submitter>McLendon JM</submitter><funding>American Heart Association</funding><funding>NHLBI NIH HHS</funding><funding>National Institutes of Health</funding><funding>Roy J. and Lucille A. Carver College of Medicine, University of Iowa</funding><pagination>56-69</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12465015</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>201</volume><pubmed_abstract>Centrosomes localize to perinuclear foci where they serve multifunctional roles, arranging the microtubule organizing center (MTOC) and anchoring ubiquitin proteasome system (UPS) machinery, as suggested by prior studies. In mature cardiomyocytes, centrosomal proteins redistribute into a specialized perinuclear cage-like structure, and a potential centrosomal-UPS interface has not been studied, despite established roles for UPS in cardiomyopathy. In addition, there have been no reports citing cardiomyocyte UPS dysfunction upon or after manipulation of centrosomal proteins. Taxilin-beta (Txlnb), a cardiomyocyte-enriched protein, belongs to a family of centrosome adapter proteins implicated in protein quality control. We hypothesize that Txlnb is part of the perinuclear centrosomal cage and </pubmed_abstract><journal>Journal of molecular and cellular cardiology</journal><pubmed_title>Gain and loss of the centrosomal protein taxilin-beta influences cardiac proteostasis and stress.</pubmed_title><pmcid>PMC12465015</pmcid><funding_grant_id>R01-HL150557</funding_grant_id><funding_grant_id>R01-HL144717</funding_grant_id><funding_grant_id>R01 HL148796</funding_grant_id><funding_grant_id>R01 HL144717</funding_grant_id><funding_grant_id>T32-HL007121</funding_grant_id><funding_grant_id>R01-HL148796</funding_grant_id><funding_grant_id>19POST34380640</funding_grant_id><funding_grant_id>R01 HL150557</funding_grant_id><funding_grant_id>T32 HL007121</funding_grant_id><pubmed_authors>Baehr LM</pubmed_authors><pubmed_authors>Boudreau RL</pubmed_authors><pubmed_authors>McLendon JM</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Bodine SC</pubmed_authors><pubmed_authors>Stein CS</pubmed_authors></additional><is_claimable>false</is_claimable><name>Gain and loss of the centrosomal protein taxilin-beta influences cardiac proteostasis and stress.</name><description>Centrosomes localize to perinuclear foci where they serve multifunctional roles, arranging the microtubule organizing center (MTOC) and anchoring ubiquitin proteasome system (UPS) machinery, as suggested by prior studies. In mature cardiomyocytes, centrosomal proteins redistribute into a specialized perinuclear cage-like structure, and a potential centrosomal-UPS interface has not been studied, despite established roles for UPS in cardiomyopathy. In addition, there have been no reports citing cardiomyocyte UPS dysfunction upon or after manipulation of centrosomal proteins. Taxilin-beta (Txlnb), a cardiomyocyte-enriched protein, belongs to a family of centrosome adapter proteins implicated in protein quality control. We hypothesize that Txlnb is part of the perinuclear centrosomal cage and </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Apr</publication><modification>2026-07-09T10:24:57.986Z</modification><creation>2026-07-09T10:18:22.272Z</creation></dates><accession>S-EPMC12465015</accession><cross_references><pubmed>40010430</pubmed><doi>10.1016/j.yjmcc.2025.02.008</doi></cross_references></HashMap>