title: Membrane traffic fuses with cartilage development.
abstract: The ability of cells to synthesize and secrete proteins is essential for numerous cellular functions. Therefore, when mutations in one component of the secretory pathway result in a tissue-specific defect, a unique opportunity arises to examine the molecular mechanisms at play. The recent finding that a defect in the protein sedlin, whose yeast counterpart is involved in the first step of the secretory pathway, leads to a cartilage-specific disorder in humans raises numerous questions and interesting possibilities for understanding both the pathobiology involved and the role of membrane traffic in normal cartilage development.
authors.affiliation: Biotechnology Research Institute, 6100 Royalmount Avenue, Montreal, QC, Canada H4P 2R2. michael.sacher@bri.nrc.ca
authors.forename: Michael
authors.initials: M
authors.lastname: Sacher
mesh_terms: D000818:Animals; D002352:Carrier Proteins / Q000235:genetics / Q000378:metabolism; D002356:Cartilage / Q000254:growth & development*; D002462:Cell Membrane / Q000378:metabolism*; D004721:Endoplasmic Reticulum / Q000378:metabolism; D006056:Golgi Apparatus / Q000378:metabolism; D006801:Humans; D026901:Membrane Transport Proteins; D010009:Osteochondrodysplasias / Q000235:genetics; D021381:Protein Transport / Q000502:physiology*; D014157:Transcription Factors
chemical_list: D002352:Carrier Proteins; D026901:Membrane Transport Proteins; C120759:TRAPPC2 protein, human; D014157:Transcription Factors