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本文引用的文献

1
Dosage-dependent effects of Akt1/protein kinase Balpha (PKBalpha) and Akt3/PKBgamma on thymus, skin, and cardiovascular and nervous system development in mice.Akt1/蛋白激酶Bα（PKBα）和Akt3/PKBγ对小鼠胸腺、皮肤、心血管及神经系统发育的剂量依赖性影响。
Mol Cell Biol. 2005 Dec;25(23):10407-18. doi: 10.1128/MCB.25.23.10407-10418.2005.
2
Essential role of protein kinase B gamma (PKB gamma/Akt3) in postnatal brain development but not in glucose homeostasis.蛋白激酶Bγ（PKBγ/Akt3）在出生后脑发育中起关键作用，但在葡萄糖稳态中并非如此。
Development. 2005 Jul;132(13):2943-54. doi: 10.1242/dev.01864. Epub 2005 Jun 1.
3
Role for Akt3/protein kinase Bgamma in attainment of normal brain size.Akt3/蛋白激酶Bγ在实现正常脑容量中的作用。
Mol Cell Biol. 2005 Mar;25(5):1869-78. doi: 10.1128/MCB.25.5.1869-1878.2005.
4
Advances in protein kinase B signalling: AKTion on multiple fronts.蛋白激酶B信号传导的进展：多方面的作用。
Trends Biochem Sci. 2004 May;29(5):233-42. doi: 10.1016/j.tibs.2004.03.006.
5
Glucose homeostasis and tissue transcript content of insulin signaling intermediates in four inbred strains of mice: C57BL/6, C57BLKS/6, DBA/2, and 129X1.四种近交系小鼠（C57BL/6、C57BLKS/6、DBA/2和129X1）中胰岛素信号中间体的葡萄糖稳态和组织转录本含量
Endocrinology. 2004 Jul;145(7):3307-23. doi: 10.1210/en.2003-1400. Epub 2004 Mar 24.
6
Role for neuronal insulin resistance in neurodegenerative diseases.神经元胰岛素抵抗在神经退行性疾病中的作用。
Proc Natl Acad Sci U S A. 2004 Mar 2;101(9):3100-5. doi: 10.1073/pnas.0308724101. Epub 2004 Feb 23.
7
Rheb fills a GAP between TSC and TOR.Rheb填补了结节性硬化症复合物（TSC）和雷帕霉素靶蛋白（TOR）之间的空白。
Trends Biochem Sci. 2003 Nov;28(11):573-6. doi: 10.1016/j.tibs.2003.09.003.
8
Isoform-specific regulation of insulin-dependent glucose uptake by Akt/protein kinase B.Akt/蛋白激酶B对胰岛素依赖性葡萄糖摄取的亚型特异性调节。
J Biol Chem. 2003 Dec 5;278(49):49530-6. doi: 10.1074/jbc.M306782200. Epub 2003 Sep 30.
9
Mechanism of enhanced cardiac function in mice with hypertrophy induced by overexpressed Akt.Akt过表达诱导的肥大小鼠心脏功能增强的机制
J Biol Chem. 2003 Nov 28;278(48):47622-8. doi: 10.1074/jbc.M305909200. Epub 2003 Sep 16.
10
Insulin receptor substrate-2 deficiency impairs brain growth and promotes tau phosphorylation.胰岛素受体底物-2缺乏会损害大脑发育并促进tau蛋白磷酸化。
J Neurosci. 2003 Aug 6;23(18):7084-92. doi: 10.1523/JNEUROSCI.23-18-07084.2003.

仅有单一Akt亚型的生活：缺乏Akt2和Akt3的小鼠能够存活，但表现出葡萄糖稳态受损和生长缺陷。

Life with a single isoform of Akt: mice lacking Akt2 and Akt3 are viable but display impaired glucose homeostasis and growth deficiencies.

作者信息

Dummler Bettina, Tschopp Oliver, Hynx Debby, Yang Zhong-Zhou, Dirnhofer Stephan, Hemmings Brian A

机构信息

Friedrich Miescher Institute for Biomedical Research, Basel CH-4058, Switzerland.

出版信息

Mol Cell Biol. 2006 Nov;26(21):8042-51. doi: 10.1128/MCB.00722-06. Epub 2006 Aug 21.

DOI:10.1128/MCB.00722-06
PMID:16923958
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1636753/
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 approximately 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.

摘要

为了在体内解决蛋白激酶Akt家族的亚型冗余和亚型特异性问题，我们培育了同时缺乏Akt2和Akt3的小鼠。在这些小鼠中，只有Akt1亚型保留下来执行Akt的基本功能，如葡萄糖稳态、增殖、分化和早期发育。令人惊讶的是，我们发现Akt2(-/-)Akt3(-/-)甚至Akt1(+/-)Akt2(-/-)Akt3(-/-)小鼠发育正常，并且尽管所有组织中的总Akt水平显著降低，但仍能以最小的功能障碍存活。Akt1的单个功能等位基因似乎足以实现成功的胚胎发育和出生后存活。这与先前描述的Akt1(-/-)Akt2(-/-)小鼠和Akt1(-/-)Akt3(-/-)小鼠的致死表型形成鲜明对比。然而，Akt2(-/-)Akt3(-/-)小鼠对葡萄糖和胰岛素不耐受，与野生型小鼠相比体重降低了约25%。此外，我们发现Akt2(-/-)Akt3(-/-)小鼠的大脑和睾丸的相对大小和重量大幅降低，这表明Akt2和Akt3在体内对整个动物大小和单个器官大小的决定中发挥作用。