AMP‐activated protein kinase: the energy charge hypothesis revisited

By D. Hardie, S. Hawley. Bioessays, 2001

821 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Surgery

View Paper: https://www.semanticscholar.org/paper/ccc9f7ab9f60c09c7615e1cf0ebc4b9ddf6a6774

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. D. Hardie
2. K. Guan
3. K. Inoki
4. Tianqing Zhu
5. Inna M. Sokolova
6. G. S. Olsen
7. Anne E. Gadalla
8. S. Hawley

In Molecular Biology

1. D. Hardie
2. David M. Sabatini
3. K. Guan
4. R. Shaw
5. Bruce E. Kemp
6. J. Blenis
7. K. Inoki
8. S. Hawley

In Surgery

1. D. Hardie
2. S. Hawley
3. K. Guan
4. Bruce E. Kemp
5. K. Inoki
6. Fiona A. Ross
7. Tianqing Zhu
8. Inna M. Sokolova

Citations in the corpus

• TSC2 mediates cellular energy response to control cell growth and survival. (2003, methodology): “25 mM 2DG-activated AMPK as TSC2 Is Required to Mediate indicatedby thedramatic increaseof T172phosphoryla-the Cellular Energy Response tion in AMPK (Figure 1D) (Hardie and Hawley, 2001).”
• CBS domains form energy-sensing modules whose binding of adenosine ligands is disrupted by disease mutations. (2004, background): “AMPK exists as heterotrimeric complexes comprising catalytic α subunits and regulatory β and γ subunits (14).”
• The AMP-activated protein kinase pathway – new players upstream and downstream (2004, background): “However, if the reaction catalysed by adenylate kinase (2ADP ↔ ATP + AMP) is maintained close to equilibrium (which appears to be the case in most eukaryotic cells), one can easily show that the AMP:ATP ratio varies as the square of the ADP:ATP ratio (Hardie and Hawley, 2001).”
• Functional diversity of protein phosphatase-1, a cellular economizer and reset button. (2004, background): “Activated Snf1/ AMPK in turn promotes 1) glucose import; 2) gluconeogenesis; 3) respiration; 4) the use of alternative sugars and other carbon sources like fatty acids, ethanol, glycerol, pyruvate, and lactate; and 5) the downregulation of anabolic pathways (72, 158).”
• Complexes between the LKB1 tumor suppressor, STRADα/β and MO25α/β are upstream kinases in the AMP-activated protein kinase cascade (2003, background): “longer-term effects on gene expression [1,2].”
• Intrasteric control of AMPK via the γ1 subunit AMP allosteric regulatory site (2004, background): “…multiple steps; fatty acid synthesis by phosphorylation of acetyl-CoA carboxylase- , cholesterol synthesis by phosphorylation of HMG-CoA reductase, triglyceride synthesis by phosphorylation of GPAT (glycerol-phosphate acyl transferase), and hormone-sensitive lipase (Hardie and Hawley 2001).”
• The AMP-activated protein kinase AAK-2 links energy levels and insulin-like signals to lifespan in C. elegans. (2004, background): “Similarly, senescent human fibroblasts have a higher AMP:ATP ratio, a sensitive measure of energy levels, than do young fibroblasts (Hardie and Hawley 2001; Wang et al. 2003).”
• Regulation of the TSC pathway by LKB1: evidence of a molecular link between tuberous sclerosis complex and Peutz-Jeghers syndrome. (2004, background): “Under such conditions, AMPK is activated and phosphorylates numerous substrates to suppress anabolism and enhance catabolism, thereby regulating cellular energy homeostasis (Hardie and Hawley 2001).”
• Energy-limited tolerance to stress as a conceptual framework to integrate the effects of multiple stressors. (2013, background): “…energetic status of cells (such as adenylate energy charge [AEC] or ADP:ATP ratios) have been proposed as biomarkers of stress in a variety of organisms although their physiological implications for cellular metabolism are debated (Isani et al. 1997; Thebault et al. 2000; Hardie and Hawley 2001).”
• Target of rapamycin (TOR): an integrator of nutrient and growth factor signals and coordinator of cell growth and cell cycle progression (2004, background): “AMPK is activated under states of low cellular energy (high AMP/ATP ratio) and acts to reduce ATP expenditure by inhibiting key enzymes of biosynthetic pathways and to increase the ATP supply by activating pathways producing ATP (reviewed in Hardie and Hawley, 2001).”
• Use of Cells Expressing γ Subunit Variants to Identify Diverse Mechanisms of AMPK Activation (2010, methodology): “To obtain a quantitative measure of energy stress, we therefore measured the ADP:ATP ratio and used it as a surrogate for AMP:ATP (which, assuming that adenylate kinase reaction is at equilibrium, will vary as the square of ADP:ATP [Hardie and Hawley, 2001]).”