| First Author | Tschopp O | Year | 2005 |
| Journal | Development | Volume | 132 |
| Issue | 13 | Pages | 2943-54 |
| PubMed ID | 15930105 | Mgi Jnum | J:98804 |
| Mgi Id | MGI:3579958 | Doi | 10.1242/dev.01864 |
| Citation | Tschopp O, et al. (2005) Essential role of protein kinase B{gamma} (PKB{gamma}/Akt3) in postnatal brain development but not in glucose homeostasis. Development 132(13):2943-54 |
| abstractText | Protein kinase B is implicated in many crucial cellular processes, such as metabolism, apoptosis and cell proliferation. In contrast to Pkbalpha and Pkbbeta-deficient mice, Pkbgamma(-/-) mice are viable, show no growth retardation and display normal glucose metabolism. However, in adult Pkbgammamutant mice, brain size and weight are dramatically reduced by about 25%. In vivo magnetic resonance imaging confirmed the reduction of Pkbgamma(-/-) brain volumes with a proportionally smaller ventricular system. Examination of the major brain structures revealed no anatomical malformations except for a pronounced thinning of white matter fibre connections in the corpus callosum. The reduction in brain weight of Pkbgamma(-/-) mice is caused, at least partially, by a significant reduction in both cell size and cell number. Our results provide novel insights into the physiological role of PKBgamma and suggest a crucial role in postnatal brain development. |
