Insulin Resistance and a Diabetes Mellitus-Like Syndrome in Mice Lacking the Protein Kinase Akt2 (PKBβ)
By Han Cho, J. Mu, Jason K. Kim, J. L. Thorvaldsen, Q. Chu, E. Crenshaw, Klaus H. Kaestner, M. Bartolomei, Gerald I. Shulman, M. Birnbaum. 2001
1,723 citations recorded by the source corpus.
Subfields: Molecular Biology, Surgery
View Paper: https://www.semanticscholar.org/paper/6c90784e5246f9733e442682df2b7354c9a6b6be
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In Molecular Biology
- David M. Sabatini
- Lewis C. Cantley
- B. Manning
- T. Franke
- J. Engelman
- M. Laplante
- G. Hotamışlıgil
- Steven P. Gygi
In Surgery
Citations in the corpus
- The nuts and bolts of AGC protein kinases (2010, background): “Mouse knockout studies strikingly indicate that AKT2 plays a particularly dominant part in maintaining glucose homeostasi”
- Severe diabetes, age-dependent loss of adipose tissue, and mild growth deficiency in mice lacking Akt2/PKB beta. (2003, background): “Interestingly, Akt2-deficient mice described in a recent report (25) were diabetic but did not exhibit a growth deficiency.”
- Akt1 controls macrophage response to LPS by regulating microRNAs (2009, background): “In mammals, the Akt family consists of three isoforms, Akt1 (PKBa), Akt2 (PKBb), and Akt3 (PKBg), which are functionally distinct despite their sequence similarities (Cho et al., 2001; Easton et al., 2005; Mao et al., 2007; Maroulakou et al., 2007; Yang et al., 2005).”
- Ablation in mice of the mTORC components raptor, rictor, or mLST8 reveals that mTORC2 is required for signaling to Akt-FOXO and PKCalpha, but not S6K1. (2006, background): “Three Akt/PKB genes with redundant functions exist in mammals (Akt1/PKBa, Akt2/ PKBb, and Akt3/PKBg), and genetic disruption of any one Akt/PKB gene results in viable animals (Chen et al., 2001; Cho et al., 2001; Easton et al., 2005; Garofalo et al., 2003).”
- Targeting PI3K signalling in cancer: opportunities, challenges and limitations (2009, background): “In addition, mouse and human studies suggest a prominent role for AKT2 in insulin responsiveness, and the loss of AKT2 activity might promote a strong diabetic phenotyp”