| Literature DB >> 24211831 |
Jing Xue1, Xiqiang Gao, Chunyan Fu, Zhe Cong, Hong Jiang, Wei Wang, Ting Chen, Qiang Wei, Chuan Qin.
Abstract
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.Entities:
Keywords: Apoptosis; Binding; CD45; DMEM; Dulbecco’s modified Eagle’s medium; Galectin-3; MW; N-Glycans; O-Glycans; PBST; SDS–PAGE; molecular weight; phosphate buffered saline with Tween 20; sodium dodecyl sulfate–polyacrylamide gel electrophoresis
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Year: 2013 PMID： 24211831 DOI： 10.1016/j.febslet.2013.10.034
Source DB: PubMed Journal: FEBS Lett ISSN： 0014-5793 Impact factor: 4.124