| First Author | Zhao Y | Year | 2017 |
| Journal | Biochem Biophys Res Commun | Volume | 483 |
| Issue | 1 | Pages | 617-623 |
| PubMed ID | 27998771 | Mgi Jnum | J:241789 |
| Mgi Id | MGI:5903659 | Doi | 10.1016/j.bbrc.2016.12.094 |
| Citation | Zhao Y, et al. (2017) Deficiency in ubiquitin-like protein Ubl4A impairs migration of fibroblasts and macrophages. Biochem Biophys Res Commun 483(1):617-623 |
| abstractText | Ubiquitin-like protein Ubl4A is a small, multi-functional protein with no ubiquitination activity. We have previously demonstrated that Ubl4A directly interacts with actin-related protein 2/3 complex (Arp2/3) and promotes Arp2/3-dependent actin branching, thereby accelerating plasma membrane translocation of protein kinase Akt upon insulin stimulation. Here, we show that Ubl4A is critical for plasma membrane protrusion and cell migration. Ubl4A, F-actin and Arp2/3 are co-localized at the cell leading edges during wound closure. Knockout of Ubl4A significantly reduces actin-mediated membrane protrusion and delays wound healing by primary mouse embryonic fibroblasts. Consistently, the ability of fibroblasts to migrate out of corneal tissue ex vivo is also impaired in Ubl4A-deficient mice. Furthermore, cell motility, but not phagocytosis, is significantly decreased in Ubl4A-deficient macrophages compared with wild-type controls. These results imply an important role for Ubl4A in cell migration-associated pathophysiological processes. |
