Spatial control of AMPK signaling at subcellular compartments

被引：30

作者：

Chauhan, Anoop Singh ^{[1
,2
]}

Zhuang, Li ^{[1
]}

Gan, Boyi ^{[1
,3
,4
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Expt Radiat Oncol, Houston, TX 77030 USA

[2] Univ Birmingham, Inst Canc & Genom Sci, Birmingham, W Midlands, England

[3] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, Houston, TX 77030 USA

[4] Univ Texas MD Anderson UT, Hlth Grad Sch Biomed Sci, Houston, TX USA

来源：

CRITICAL REVIEWS IN BIOCHEMISTRY AND MOLECULAR BIOLOGY | 2020年 / 55卷 / 01期

基金：

美国国家卫生研究院;

关键词：

AMPK; LKB1; CaMKK2; lysosome; endoplasmic reticulum; mitochondria; nucleus; cell junction; ACTIVATED PROTEIN-KINASE; ENDOPLASMIC-RETICULUM STRESS; NUTRIENT-SENSING MECHANISMS; MITOCHONDRIAL FISSION; DIRECT PHOSPHORYLATION; ENERGY SENSOR; CELL-GROWTH; AUTOPHAGY; LYSOSOME; PATHWAY;

D O I：

10.1080/10409238.2020.1727840

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

AMP-activated protein kinase (AMPK) is a master regulator of energy homeostasis that functions to restore the energy balance by phosphorylating its substrates during altered metabolic conditions. AMPK activity is tightly controlled by diverse regulators including its upstream kinases LKB1 and CaMKK2. Recent studies have also identified the localization of AMPK at different intracellular compartments as another key mechanism for regulating AMPK signaling in response to specific stimuli. This review discusses the AMPK signaling associated with different subcellular compartments, including lysosomes, endoplasmic reticulum, mitochondria, Golgi apparatus, nucleus, and cell junctions. Because altered AMPK signaling is associated with various pathologic conditions including cancer, targeting AMPK signaling in different subcellular compartments may present attractive therapeutic approaches for treatment of disease.

引用

页码：17 / 32

页数：16

共 128 条

[21] Hypoxic activation of AMPK is dependent on mitochondrial ROS but independent of an increase in AMP/ATP ratio [J].

Emerling, Brooke M. ;

Weinberg, Frank ;

Snyder, Colleen ;

Burgess, Zach ;

Mutlu, Goekhan M. ;

Viollet, Benoit ;

Budinger, G. R. Scott ;

Chandel, Navdeep S. .

FREE RADICAL BIOLOGY AND MEDICINE, 2009, 46 (10) :1386-1391

[22]

Fennelly C, 2017, METHODS MOL BIOL, V1594, P293, DOI 10.1007/978-1-4939-6934-0_19

[23] Metformin: From Mechanisms of Action to Therapies [J].

Foretz, Marc ;

Guigas, Bruno ;

Bertrand, Luc ;

Pollak, Michael ;

Viollet, Benoit .

CELL METABOLISM, 2014, 20 (06) :953-966

[24] AMPK: Mechanisms of Cellular Energy Sensing and Restoration of Metabolic Balance [J].

Garcia, Daniel ;

Shaw, Reuben J. .

MOLECULAR CELL, 2017, 66 (06) :789-800

[25]

Goodman M., 2014, Pharm Regul Aff, V3, DOI [10.4172/2167-7689.1000118, DOI 10.4172/2167-7689.1000118]

[26] AMP Is a True Physiological Regulator of AMP-Activated Protein Kinase by Both Allosteric Activation and Enhancing Net Phosphorylation [J].

Gowans, Graeme J. ;

Hawley, Simon A. ;

Ross, Fiona A. ;

Hardie, D. Grahame .

CELL METABOLISM, 2013, 18 (04) :556-566

[27] AMPK phosphorylation of raptor mediates a metabolic checkpoint [J].

Gwinn, Dana M. ;

Shackelford, David B. ;

Egan, Daniel F. ;

Mihaylova, Maria M. ;

Mery, Annabelle ;

Vasquez, Debbie S. ;

Turk, Benjamin E. ;

Shaw, Reuben J. .

MOLECULAR CELL, 2008, 30 (02) :214-226

[28] AMPK: An Energy-Sensing Pathway with Multiple Inputs and Outputs [J].

Hardie, D. Grahame ;

Schaffer, Bethany E. ;

Brunet, Anne .

TRENDS IN CELL BIOLOGY, 2016, 26 (03) :190-201

[29] AMPK-Sensing Energy while Talking to Other Signaling Pathways [J].

Hardie, D. Grahame .

CELL METABOLISM, 2014, 20 (06) :939-952

[30] AMPK: A Target for Drugs and Natural Products With Effects on Both Diabetes and Cancer [J].

Hardie, D. Grahame .

DIABETES, 2013, 62 (07) :2164-2172

← 1 2 3 4 5 6 7 8 9 10 →