| First Author | Muramatsu A | Year | 2015 |
| Journal | Biochem Biophys Res Commun | Volume | 463 |
| Issue | 4 | Pages | 999-1005 |
| PubMed ID | 26072378 | Mgi Jnum | J:228692 |
| Mgi Id | MGI:5708468 | Doi | 10.1016/j.bbrc.2015.06.049 |
| Citation | Muramatsu A, et al. (2015) Potential involvement of kinesin-1 in the regulation of subcellular localization of Girdin. Biochem Biophys Res Commun 463(4):999-1005 |
| abstractText | Girdin is an actin-binding protein that has multiple functions in postnatal neural development and cancer progression. We previously showed that Girdin is a regulator of migration for neuroblasts born from neural stem cells in the subventricular zone (SVZ) and the dentate gyrus of the hippocampus in the postnatal brain. Despite a growing list of Girdin-interacting proteins, the mechanism of Girdin-mediated migration has not been fully elucidated. Girdin interacts with Disrupted-In-Schizophrenia 1 and partitioning-defective 3, both of which have been shown to interact with the kinesin microtubule motor proteins. Based on this, we have identified that Girdin also interacts with kinesin-1, a member of neuronal kinesin proteins. Although a direct interaction of Girdin and kinesin-1 has not been determined, it is of interest to find that Girdin loss-of-function mutant mice with the mutation of a basic amino acid residue-rich region (Basic mut mice) exhibit limited interaction with kinesin-1. Furthermore, expression of a kinesin-1 mutant with motor defects, leads to Girdin mislocalization. Finally, consistent with previous studies on the role of kinesin proteins in trafficking a cell-cell adhesion molecule N-cadherin, Basic mut mice showed an aberrant expression pattern of N-cadherin in migrating SVZ neuroblasts. These findings suggest a potential role of Girdin/kinesin-1 interaction in the regulation of neuroblast migration in the postnatal brain. |
