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Mutations in Disordered Regions Can Cause Disease by Creating Dileucine Motifs.
Meyer, Katrina; Kirchner, Marieluise; Uyar, Bora; Cheng, Jing-Yuan; Russo, Giulia; Hernandez-Miranda, Luis R; Szymborska, Anna; Zauber, Henrik; Rudolph, Ina-Maria; Willnow, Thomas E; Akalin, Altuna; Haucke, Volker; Gerhardt, Holger; Birchmeier, Carmen; Kühn, Ralf; Krauss, Michael; Diecke, Sebastian; Pascual, Juan M; Selbach, Matthias.
Afiliación
  • Meyer K; Proteome Dynamics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Kirchner M; Proteome Dynamics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Uyar B; Bioinformatics Platform, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Cheng JY; Proteome Dynamics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Russo G; Molecular Pharmacology and Cell Biology, Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Hernandez-Miranda LR; Developmental Biology/Signal Transduction, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Szymborska A; Integrative Vascular Biology Laboratory, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany; DZHK (German Centre for Cardiovascular Research) partner site, 13347 Berlin, Germany.
  • Zauber H; Proteome Dynamics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Rudolph IM; Molecular Cardiovascular Research, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Willnow TE; Molecular Cardiovascular Research, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Akalin A; Bioinformatics Platform, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Haucke V; Molecular Pharmacology and Cell Biology, Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Gerhardt H; Integrative Vascular Biology Laboratory, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany; DZHK (German Centre for Cardiovascular Research) partner site, 13347 Berlin, Germany; Berlin Institute of Health (BIH), 10178 Berlin,
  • Birchmeier C; Developmental Biology/Signal Transduction, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Kühn R; Berlin Institute of Health (BIH), 10178 Berlin, Germany; Core Facility Transgenics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Krauss M; Molecular Pharmacology and Cell Biology, Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Robert-Rössle-Str. 10, 13125 Berlin, Germany.
  • Diecke S; DZHK (German Centre for Cardiovascular Research) partner site, 13347 Berlin, Germany; Berlin Institute of Health (BIH), 10178 Berlin, Germany; Core Facility Pluripotent Stem Cells, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Ger
  • Pascual JM; Department of Neurology and Neurotherapeutics, UT Southwestern Medical Center, 5323 Harry Hines Blvd. Dallas, TX 75390, USA.
  • Selbach M; Proteome Dynamics, Max Delbrück Center for Molecular Medicine in the Helmholtz Association (MDC), Robert-Rössle-Str. 10, 13125 Berlin, Germany; Charité-Universitätsmedizin Berlin, 10117 Berlin, Germany. Electronic address: matthias.selbach@mdc-berlin.de.
Cell ; 175(1): 239-253.e17, 2018 09 20.
Article en En | MEDLINE | ID: mdl-30197081
Many disease-causing missense mutations affect intrinsically disordered regions (IDRs) of proteins, but the molecular mechanism of their pathogenicity is enigmatic. Here, we employ a peptide-based proteomic screen to investigate the impact of mutations in IDRs on protein-protein interactions. We find that mutations in disordered cytosolic regions of three transmembrane proteins (GLUT1, ITPR1, and CACNA1H) lead to an increased clathrin binding. All three mutations create dileucine motifs known to mediate clathrin-dependent trafficking. Follow-up experiments on GLUT1 (SLC2A1), the glucose transporter causative of GLUT1 deficiency syndrome, revealed that the mutated protein mislocalizes to intracellular compartments. Mutant GLUT1 interacts with adaptor proteins (APs) in vitro, and knocking down AP-2 reverts the cellular mislocalization and restores glucose transport. A systematic analysis of other known disease-causing variants revealed a significant and specific overrepresentation of gained dileucine motifs in structurally disordered cytosolic domains of transmembrane proteins. Thus, several mutations in disordered regions appear to cause "dileucineopathies."
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transportador de Glucosa de Tipo 1 / Proteínas Intrínsecamente Desordenadas Límite: Animals / Humans Idioma: En Revista: Cell Año: 2018 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Transportador de Glucosa de Tipo 1 / Proteínas Intrínsecamente Desordenadas Límite: Animals / Humans Idioma: En Revista: Cell Año: 2018 Tipo del documento: Article País de afiliación: Alemania Pais de publicación: Estados Unidos