| First Author | Schmalzigaug R | Year | 2007 |
| Journal | J Histochem Cytochem | Volume | 55 |
| Issue | 10 | Pages | 1039-48 |
| PubMed ID | 17565117 | Mgi Jnum | J:126878 |
| Mgi Id | MGI:3762265 | Doi | 10.1369/jhc.7A7207.2007 |
| Citation | Schmalzigaug R, et al. (2007) Differential expression of the ARF GAP genes GIT1 and GIT2 in mouse tissues. J Histochem Cytochem 55(10):1039-48 |
| abstractText | GIT1 and GIT2 belong to the family of ADP-ribosylation factor GTPase-activating proteins (ARF-GAP) and have been implicated in the regulation of G protein-coupled receptor sequestration, cell migration, T-cell activation, neuronal spine formation, and aggregate formation in Huntington's disease. Examination of endogenous GIT protein expression in tissues, however, has been hampered by the lack of GIT2-specific antibodies. To visualize GIT1 and GIT2 gene expression in mouse tissues, we created mice with beta-galactosidase (beta-Gal) reporters inserted into the two GIT genes. beta-Gal staining confirmed the broad tissue distribution of GIT1 and GIT2 in the mouse but also revealed striking differences. GIT2 is expressed in most cells of the body, whereas GIT1 is restricted to only a subset of cells. For example, GIT2 is uniformly expressed throughout lung and liver, whereas GIT1 is restricted to cells lining blood vessels, bronchi, and bile ducts. Expression of GIT1 and GIT2 is mutually exclusive in the testes, where a developmental expression shift occurs, with GIT2 present in spermatogonia but GIT1 in mature spermatids. In conclusion, analysis of endogenous GIT expression revealed a nearly ubiquitous distribution of GIT2, whereas GIT1 is restricted to specific cell types even in tissues with apparently high GIT1 expression and is entirely absent from some tissues. |
