| First Author | Li YL | Year | 2008 |
| Journal | PLoS One | Volume | 3 |
| Issue | 12 | Pages | e3841 |
| PubMed ID | 19048108 | Mgi Jnum | J:144374 |
| Mgi Id | MGI:3830798 | Doi | 10.1371/journal.pone.0003841 |
| Citation | Li YL, et al. (2008) Cell surface sialylation and fucosylation are regulated by L1 via phospholipase Cgamma and cooperate to modulate neurite outgrowth, cell survival and migration. PLoS One 3(12):e3841 |
| abstractText | BACKGROUND: Cell surface glycosylation patterns are markers of cell type and status. However, the mechanisms regulating surface glycosylation patterns remain unknown. METHODOLOGY/PRINCIPAL FINDINGS: Using a panel of carbohydrate surface markers, we have shown that cell surface sialylation and fucosylation were downregulated in L1(-/y) neurons versus L1(+/y) neurons. Consistently, mRNA levels of sialyltransferase ST6Gal1, and fucosyltransferase FUT9 were significantly reduced in L1(-/y) neurons. Moreover, treatment of L1(+/y) neurons with L1 antibodies, triggering signal transduction downstream of L1, led to an increase in cell surface sialylation and fucosylation compared to rat IgG-treated cells. ShRNAs for both ST6Gal1 and FUT9 blocked L1 antibody-mediated enhancement of neurite outgrowth, cell survival and migration. A phospholipase Cgamma (PLCgamma) inhibitor and shRNA, as well as an Erk inhibitor, reduced ST6Gal1 and FUT9 mRNA levels and inhibited effects of L1 on neurite outgrowth and cell survival. CONCLUSIONS: Neuronal surface sialylation and fucosylation are regulated via PLCgamma by L1, modulating neurite outgrowth, cell survival and migration. |
