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Human CaR trafficking is dependent on COPII transport pathway
Author(s) -
Zhuang Xiaolei,
Northup John K,
Ray Kausik
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.2_supplement.291
Subject(s) - copii , endoplasmic reticulum , microbiology and biotechnology , secretion , hek 293 cells , receptor , gtpase , transmembrane protein , chemistry , secretory pathway , biology , golgi apparatus , biochemistry
The mechanism(s) of human calcium‐sensing receptor (hCaR) trafficking from the endoplasmic reticulum (ER) to the cell surface is largely unknown. Here we show that export of hCaR from the ER is regulated by the conventional coat protein complex II (COPII) via Sar1 and Rab1 GTPases in HEK 293 cells. Surprisingly, disruption of putative COPII export motifs DxE or truncation of C‐tail containing DxE motifs do not block COPII‐dependent ER export of the hCaR. It suggested there may be other selective mechanism in the ER export. A truncated receptor with the ECD and the first transmembrane portion of the receptor sufficiently transport to the cell surface in a COPII‐dependent manner. Additionally, the hCaR ECD without transmembrane portions is secreted in the culture media. Secreted ECD forms with disrupted disulfide‐linked dimerization and N‐glysosylation failed to secrete efficiently, suggesting that both modifications are pre‐requisites for hCaR transport. This work was supported in part by the Intramural Research program of the NIDCD, National Institutes of Health.