Scyl1, Mutated in a Recessive Form of Spinocerebellar Neurodegeneration, Regulates COPI-mediated Retrograde Traffic

This publication has 66 references indexed in Scilit:

• Atlastin GTPases are required for Golgi apparatus and ER morphogenesis
  Human Molecular Genetics, 2008
• Novel cargo-binding site in the β and δ subunits of coatomer
  The Journal of cell biology, 2007
• Mutation in the Scyl1 gene encoding amino‐terminal kinase‐like protein causes a recessive form of spinocerebellar neurodegeneration
  EMBO Reports, 2007
• Coatomer, the Coat Protein of COPI Transport Vesicles, Discriminates Endoplasmic Reticulum Residents from p24 Proteins
  Molecular and Cellular Biology, 2006
• Clathrin-dependent Association of CVAK104 with Endosomes and theTrans-Golgi Network
  Molecular Biology of the Cell, 2006
• Role of the AP2 β-Appendage Hub in Recruiting Partners for Clathrin-Coated Vesicle Assembly
  PLoS Biology, 2006
• Maintenance of Golgi structure and function depends on the integrity of ER export
  The Journal of cell biology, 2001
• Disruptions in Golgi structure and membrane traffic in a conditional lethal mammalian cell mutant are corrected by epsilon-COP.
  The Journal of cell biology, 1994
• Short cytoplasmic sequences serve as retention signals for transmembrane proteins in the endoplasmic reticulum
  Cell, 1989
• Rapid redistribution of Golgi proteins into the ER in cells treated with brefeldin A: Evidence for membrane cycling from Golgi to ER
  Cell, 1989