Author(s): Tschopp O, Yang ZZ, Brodbeck D, Dummler BA, HemmingsMieszczak M,
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Abstract Protein kinase B is implicated in many crucial cellular processes, such as metabolism, apoptosis and cell proliferation. In contrast to Pkb(alpha) and Pkb(beta)-deficient mice, Pkb(gamma)(-/-) mice are viable, show no growth retardation and display normal glucose metabolism. However, in adult Pkb(gamma)mutant mice, brain size and weight are dramatically reduced by about 25\%. In vivo magnetic resonance imaging confirmed the reduction of Pkb(gamma)(-/-) 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 Pkb(gamma)(-/-) 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 Pkb(gamma) and suggest a crucial role in postnatal brain development.
This article was published in Development
and referenced in Journal of Neonatal Biology