| First Author | Vaiana CA | Year | 2016 |
| Journal | J Biol Chem | Volume | 291 |
| Issue | 3 | Pages | 1529-37 |
| PubMed ID | 26589799 | Mgi Jnum | J:230057 |
| Mgi Id | MGI:5755331 | Doi | 10.1074/jbc.M115.672220 |
| Citation | Vaiana CA, et al. (2016) MicroRNA-424 Predicts a Role for beta-1,4 Branched Glycosylation in Cell Cycle Progression. J Biol Chem 291(3):1529-37 |
| abstractText | MicroRNA regulation of protein expression plays an important role in mediating many cellular processes, from cell proliferation to cell death. The human microRNA miR-424 is up-regulated in response to anti-proliferative cytokines, such as transforming growth factor beta (TGFbeta), and directly represses cell cycle progression. Our laboratory recently established that microRNA can be used as a proxy to identify biological roles of glycosylation enzymes (glycogenes). Herein we identify MGAT4A, OGT, and GALNT13 as targets of miR-424. We demonstrate that MGAT4A, an N-acetylglucosaminyltransferase that installs the beta-1,4 branch of N-glycans, is directly regulated by miR-424 in multiple mammary epithelial cell lines and observe the loss of MGAT4A in response to TGFbeta, an inducer of miR-424. Knockdown of MGAT4A induces cell cycle arrest through decreasing CCND1 levels. MGAT4A does not affect levels of beta-1,6 branched N-glycans, arguing that this effect is specific to beta-1,4 branching and not due to gross changes in overall N-linked glycosylation. This work provides insight into the regulation of cell cycle progression by specific N-glycan branching patterns. |
