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B6.Cg-Akt2 tm1.1Mbb/J

eagle-i ID


Resource Type

  1. Mus musculus


  1. Resource Description
    Mice with a targeted disruption in the Akt2 locus were created by homologous recombination. The targeting vector was designed to insert LoxP sites flanking the sequence containing the coding exons 4 and 5. Mice harboring the targeted allele were identified by Southern blotting and were mated to transgenic mice expressing Cre recombinase driven by a 6-kb 5′-flanking sequence from the <i>Brn/Pou3f4</i> gene to cause germ-line excision of exons 4 and 5. Exon 5 encodes the lysine residue necessary for catalytic activity. Cre recombinase-mediated deletion of exons 4 and 5 results in a frameshift mutation leading to a premature termination even if the remaining exon 3 were to splice to exon 6. The progeny carrying both the Cre transgene and the targeted allele were mated with wild-type (WT) mice to obtain offspring in which the Cre transgene was segregated away and the targeted allele was excised, as determined by the polymerase chain reaction (PCR) and Southern blotting, respectively. These mice were mated inter se to produce offspring with homozygous deletions of Akt2.
  2. Additional Name
    Akt2 KO
  3. Additional Name
  4. Related Disease
    type 2 diabetes mellitus
  5. Related Disease
  6. Related Publication or Documentation
    Insulin regulates liver metabolism in vivo in the absence of hepatic Akt and Foxo1
  7. Related Publication or Documentation
    Insulin resistance and a diabetes mellitus-like syndrome in mice lacking the protein kinase Akt2 (PKB beta)
  8. Related Publication or Documentation
    Akt2 is required for hepatic lipid accumulation in models of insulin resistance
  9. Website(s)
  10. Parental Strain Name
  11. Genetic Alteration(s)
  12. Phenotype Findings
  13. Phenotype Findings
    Mild glucose intolerance
  14. Phenotype Findings
    Insulin resistance
  15. Phenotype Findings
    Impaired insulin-stimulated glucose uptake
  16. Phenotype Findings
    Nonsuppressible hepatic glucose production
  17. Phenotype Findings
  18. Phenotype Findings
    Increased islet mass and number
  19. Phenotype Findings
    Protection from HFD induced obesity and insulin resistance
  20. Location
    Birnbaum Laboratory
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Copyright © 2016 by the President and Fellows of Harvard College
The eagle-i Consortium is supported by NIH Grant #5U24RR029825-02 / Copyright 2016