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CMTM5-v1, a four-transmembrane protein, presents a secreted form released via a vesicle-mediated secretory pathway

  • Li, Henan (Center for Human Disease Genomics, Department of Immunology, School of Basic Medical Sciences, Health Science Center, Peking University) ;
  • Guo, Xiaohuan (Center for Human Disease Genomics, Department of Immunology, School of Basic Medical Sciences, Health Science Center, Peking University) ;
  • Shao, Luning (Center for Human Disease Genomics, Department of Immunology, School of Basic Medical Sciences, Health Science Center, Peking University) ;
  • Plate, Markus (Center for Human Disease Genomics, Department of Immunology, School of Basic Medical Sciences, Health Science Center, Peking University) ;
  • Mo, Xiaoning (Center for Human Disease Genomics, Department of Immunology, School of Basic Medical Sciences, Health Science Center, Peking University) ;
  • Wang, Yu (Center for Human Disease Genomics, Department of Immunology, School of Basic Medical Sciences, Health Science Center, Peking University) ;
  • Han, Wenling (Center for Human Disease Genomics, Department of Immunology, School of Basic Medical Sciences, Health Science Center, Peking University)
  • Published : 2010.03.31

Abstract

family (CMTM) is a novel family of proteins linking classical chemokines and the transmembrane 4 superfamily (TM4SF). Our earlier studies indicated several CMTM members (such as CKLF1 and CMTM2) have a secreted form. This is the first report of the secreted form of CMTM5-v1, the major RNA splicing form of CMTM5, which is produced as small vesicles (<100 nm diameter) and floats at a peak density of 1.19 g/ml on continuous sucrose gradients. CMTM5-v1 has no obvious co-localization with CD63 or Golgi complex. In addition, brefeldin A but not wortmannin can inhibit the secretion of CMTM5-v1. Our results suggest that CMTM5-v1 might be secreted via a different vesicle-mediated secretory pathway, which will be helpful for the studies of vesicle-mediated secretion and MARVEL domain-containing proteins.

Keywords

References

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