Severe diabetes, age-dependent loss of adipose tissue, and mild growth deficiency in mice lacking Akt2/PKB beta.

By R. Garofalo, S. J. Oreña, K. Rafidi, A. J. Torchia, J. Stock, Audrey L Hildebrandt, Timothy M. Coskran, S. Black, D. Brees, J. Wicks and 2 more. Journal of Clinical Investigation, 2003

769 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/c583f3f51ce842012322f51b594be89939575215

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In Molecular Biology

1. David M. Sabatini
2. B. Manning
3. C. Thoreen
4. G. Hotamışlıgil
5. M. Laplante
6. D. Guertin
7. C. R. Kahn
8. E. Rosen

Citations in the corpus

• From mice to men: insights into the insulin resistance syndromes. (2006, background): “Akt2 knockout mice also have increased serum triglycerides (113) and under some conditions develop β-cell failure and diabetes (113).”
• Macrophage plasticity and polarization: in vivo veritas. (2012, neutral): “However, in a number of pathological conditions, such as neurodegenerative disorders (140), this is not the case, and macrophage populations express mixed or unique phenotypes.”
• Akt stimulates hepatic SREBP1c and lipogenesis through parallel mTORC1-dependent and independent pathways (2011, background): “Genetic mouse models have demonstrated that both of these responses to insulin occur, at least in part, downstream of the protein kinase Akt2 (Cho et al., 2001; Garofalo et al., 2003; Leavens et al., 2009).”
• Molecular Mechanisms That Influence the Macrophage M1–M2 Polarization Balance (2014, background): “Indeed, macrophages with combinations of M1 and M2 markers can be found in neurodegenerative disorders (108), atherosclerotic plaques (109), and some murine tumors (110).”
• 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).”
• Adipocyte differentiation from the inside out (2006, background): “Mice that lack both Akt1 and Akt2 are lipoatrophic, and MEFs from these animals cannot undergo differentiatio”