| First Author | Clemen CS | Year | 2003 |
| Journal | Exp Cell Res | Volume | 291 |
| Issue | 2 | Pages | 406-14 |
| PubMed ID | 14644162 | Mgi Jnum | J:86832 |
| Mgi Id | MGI:2682149 | Doi | 10.1016/j.yexcr.2003.07.012 |
| Citation | Clemen CS, et al. (2003) The lack of annexin A7 affects functions of primary astrocytes. Exp Cell Res 291(2):406-14 |
| abstractText | Annexin A7 is a Ca(2+)- and phospholipid-binding protein, which is thought to function in membrane organization and Ca(2+)-dependent signaling processes. It localizes to different cellular compartments and exists in a 47- and 51-kDa isoform with the large isoform being expressed in brain, skeletal, and heart muscle. In human temporal brain annexin A7 was found exclusively in astroglial cells. As astrocytes are thought to play key roles in several processes of the brain we focused on Ca(2+)-dependent signaling processes and astrocyte proliferation. Primary astrocytes from an anxA7(-/-) mouse exhibited an increased velocity of mechanically induced astrocytic Ca(2+) waves as compared to wild type. We also observed a remarkably increased proliferation rate in cultured mutant astrocytes. A search for annexin A7 binding partners with advanced biochemical methods confirmed sorcin as the major binding protein. However, in vivo GFP-tagged annexin A7 and sorcin appeared to redistribute mainly independently from each other in wild type and in mutant astrocytes. Our results favor an involvement of annexin A7 in Ca(2+)-dependent signaling or Ca(2+) homeostasis in astrocytes. |
