The genetic manipulation of mice has become an essential and elegant method for studying the function of proteins in physiology, and for testing the veracity of information obtained from cell culture experiments. During the past few years, a variety of transgenic and knockout mouse models of PKB (protein kinase B)/Akt have been generated and investigated. In this paper, we focus on the phenotypes of these PKB/Akt overexpression and mutant mice that may help to elucidate the functions exerted by PKB/Akt in mammals.
- gene knockout
- protein kinase B
- transgenic mouse model
PI-3 Kinase in Signalling and Disease, a Biochemical Society Focused Meeting held at Novartis Horsham Research Centre, U.K., 11–12 November 2003
Abbreviations used: DKO, double knockout, GBM, glioblastoma multiforme; α-MHC, α-myosin heavy chain; PKB, protein kinase B; PPAR, peroxisome proliferator-activated receptor; PTEN, phosphatase and tensin homologue deleted on chromosome 10.
- © 2004 Biochemical Society