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Akt1myr (RIPp)

eagle-i ID


Resource Type

  1. Mus musculus


  1. Resource Description
    Rat insulin II promoter drives expression in pancreatic beta cells of a form of Akt1 rendered constitutively active by the addition of an N-terminal myristoylation sequence (myr-Akt1). The transgene product is smaller than the endogenous Akt1 due to the mutant protein's deletion of its pleckstrin homology domain. In the pancreas, the transgene was expressed exclusively in the endocrine cells as assessed by immunohistochemistry using an antibody against the epitope tag.
  2. Additional Name
  3. Related Disease
  4. Related Disease
    diabetes mellitus
  5. Related Disease
    type 2 diabetes mellitus
  6. Related Publication or Documentation
    Constitutively active Akt1 expression in mouse pancreas requires S6 kinase 1 for insulinoma formation
  7. Related Publication or Documentation
    Regulation of pancreatic beta-cell growth and survival by the serine/threonine protein kinase Akt1/PKBalpha
  8. Parental Strain Name
  9. Genetic Alteration(s)
    Akt1myr (rat insulin II promoter)
  10. Phenotype Findings
    Upregulation of S6k activity
  11. Phenotype Findings
    Increased fasting insulin levels and hypoglycemia
  12. Phenotype Findings
    Hypertrophic pancreatic beta-cells
  13. Phenotype Findings
    Normal alpha and delta cells and pancreatic glucagon
  14. Phenotype Findings
  15. Phenotype Findings
    Normal hypoglycemic response and insulin responsiveness
  16. Phenotype Findings
    Resistance to streptozotocin-induced diabetes
  17. Phenotype Findings
    Elevated basal apoptosis in beta-cells
  18. Phenotype Findings
  19. Phenotype Findings
    Increased PTEN protein levels in islets
  20. Location
    Birnbaum Laboratory
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The eagle-i Consortium is supported by NIH Grant #5U24RR029825-02 / Copyright 2016