NDLI: Life with a Single Isoform of Akt: Mice Lacking Akt2 and Akt3 Are Viable but Display Impaired Glucose Homeostasis and Growth Deficiencies▿ †

Content Provider	PubMed Central
Author	Dummler, Bettina Tschopp, Oliver Hynx, Debby Yang, Zhong-zhou Dirnhofer, Stephan Hemmings, Brian A.
Copyright Year	2006
Abstract	To address the issues of isoform redundancy and isoform specificity of the Akt family of protein kinases in vivo, we generated mice deficient in both Akt2 and Akt3. In these mice, only the Akt1 isoform remains to perform essential Akt functions, such as glucose homeostasis, proliferation, differentiation, and early development. Surprisingly, we found that Akt2 −/− Akt3 −/− and even Akt1 +/− Akt2 −/− Akt3 −/− mice developed normally and survived with minimal dysfunctions, despite a dramatic reduction of total Akt levels in all tissues. A single functional allele of Akt1 appears to be sufficient for successful embryonic development and postnatal survival. This is in sharp contrast to the previously described lethal phenotypes of Akt1 −/− Akt2 −/− mice and Akt1 −/− Akt3 −/− mice. However, Akt2 −/− Akt3 −/− mice were glucose and insulin intolerant and exhibited an ∼25% reduction in body weight compared to wild-type mice. In addition, we found substantial reductions in relative size and weight of the brain and testis in Akt2 −/− Akt3 −/− mice, demonstrating an in vivo role for both Akt2 and Akt3 in the determination of whole animal size and individual organ sizes.
Related Links	http://dx.doi.org/10.1128/mcb.00722-06
Ending Page	8051
Page Count	10
Starting Page	8042
File Format	PDF
ISSN	02707306
e-ISSN	10985549
Journal	Molecular and Cellular Biology
Issue Number	21
Volume Number	26
Language	English
Publisher	American Society for Microbiology
Publisher Date	2006-11-01
Access Restriction	Open
Rights Holder	American Society for Microbiology
Subject Keyword	Cell Biology Molecular Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Biology

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