LKB1 and AMPK and the cancer-metabolism link - ten years after

被引：252

作者：

Hardie, D. Grahame ^{[1
]}

Alessi, Dario R. ^{[2
]}

机构：

[1] Univ Dundee, Coll Life Sci, Div Cell Signalling & Immunol, Dundee DD1 5EH, Scotland

[2] Univ Dundee, Coll Life Sci, MRC, Prot Phosphorylat Unit, Dundee DD1 5EH, Scotland

来源：

BMC BIOLOGY | 2013年 / 11卷

基金：

英国医学研究理事会; 英国惠康基金;

关键词：

ACTIVATED PROTEIN-KINASE; ACETYL-COA CARBOXYLASE; PEUTZ-JEGHERS-SYNDROME; TUMOR-SUPPRESSOR LKB1; GLUCOSE-UPTAKE; YEAST SNF1; LKB1-AMPK PATHWAY; DIABETIC-PATIENTS; UPSTREAM KINASES; CELLULAR-ENERGY;

D O I：

10.1186/1741-7007-11-36

中图分类号：

Q [生物科学];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The identification of a complex containing the tumor suppressor LKB1 as the critical upstream kinase required for the activation of AMP-activated protein kinase (AMPK) by metabolic stress was reported in an article in Journal of Biology in 2003. This finding represented the first clear link between AMPK and cancer. Here we briefly discuss how this discovery came about, and describe some of the insights, especially into the role of AMPK in cancer, that have followed from it.

引用

页数：11

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