Membrane traffic fuses with cartilage development.
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.
Sacher
Michael
M
Biotechnology Research Institute, 6100 Royalmount Avenue, Montreal, QC, Canada H4P 2R2. michael.sacher@bri.nrc.ca
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
D002352:Carrier Proteins; D026901:Membrane Transport Proteins; C120759:TRAPPC2 protein, human; D014157:Transcription Factors