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Regulation of galectin‐3‐induced apoptosis of Jurkat cells by both O ‐glycans and N ‐glycans on CD45
Author(s) -
Xue Jing,
Gao Xiqiang,
Fu Chunyan,
Cong Zhe,
Jiang Hong,
Wang Wei,
Chen Ting,
Wei Qiang,
Qin Chuan
Publication year - 2013
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2013.10.034
Subject(s) - jurkat cells , glycan , galectin , apoptosis , chemistry , microbiology and biotechnology , galectin 1 , galectin 3 , biochemistry , biology , immunology , t cell , glycoprotein , immune system
Galectin‐3 has been reported to induce apoptosis of Jurkat cells through binding receptors such as CD45. CD45RABC is heavily O ‐glycosylated and N ‐glycosylated, while CD45RO is only N ‐glycosylated. In this study, no apoptosis induced by galectin‐3 was detected in CD45RO‐transfected cells, whereas apoptosis of CD45RABC‐transfected cells was observed, implying that O ‐glycans on CD45 might play roles in galectin‐3‐induced apoptosis. O ‐Glycosylation inhibition assay further suggests the role of O ‐glycans on CD45 in regulation of galectin‐3‐induced apoptosis. We also found that deglycosylation at N327 of CD45RO resulted in increased binding to galectin‐3 without affecting apoptosis, while deglycosylation at N36 or N109 of CD45RO enhanced galectin‐3‐induced apoptosis. These data demonstrate that galectin‐3‐induced apoptosis of Jurkat cells is regulated by both O ‐glycans and N ‐glycans on CD45.