scholarly journals AMP-activated protein kinase is dispensable for maintaining ATP levels and for survival following inhibition of glycolysis, but promotes tumour engraftment of Ras-transformed fibroblasts

Oncotarget ◽  
2015 ◽  
Vol 6 (14) ◽  
pp. 11833-11847 ◽  
Author(s):  
Joffrey Pelletier ◽  
Danièle Roux ◽  
Benoit Viollet ◽  
Nathalie M. Mazure ◽  
Jacques Pouysségur
Keyword(s):  
Protein Kinase ◽  
Atp Levels ◽  
Transformed Fibroblasts ◽  
Inhibition Of Glycolysis ◽  
Amp Activated Protein Kinase

AMPK activation with AICAR provokes an acute fall in plasma [K+]

2008 ◽  
Vol 294 (1) ◽  
pp. C126-C135 ◽  
Author(s):  
Dan Zheng ◽  
Anjana Perianayagam ◽  
Donna H. Lee ◽  
M. Douglas Brannan ◽  
Li E. Yang ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Infusion Rate ◽  
Extracellular Fluid ◽  
Ampk Activation ◽  
Conscious Rats ◽  
Significant Fall ◽  
Ampk Phosphorylation ◽  
Atp Levels ◽  
Ampk Activity ◽  
Amp Activated Protein Kinase

AMP-activated protein kinase (AMPK), activated by an increase in intracellular AMP-to-ATP ratio, stimulates pathways that can restore ATP levels. We tested the hypothesis that AMPK activation influences extracellular fluid (ECF) K+ homeostasis. In conscious rats, AMPK was activated with 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside (AICAR) infusion: 38.4 mg/kg bolus then 4 mg·kg−1·min−1 infusion. Plasma [K+] and [glucose] both dropped at 1 h of AICAR infusion and [K+] dropped to 3.3 ± 0.04 mM by 3 h, linearly related to the increase in muscle AMPK phosphorylation. AICAR treatment did not increase urinary K+ excretion. AICAR lowered [K+] whether plasma [K+] was chronically elevated or lowered. The K+ infusion rate needed to maintain baseline plasma [K+] reached 15.7 ± 1.3 μmol K+·kg−1·min−1 between 120 and 180 min AICAR infusion. In mice expressing a dominant inhibitory form of AMPK in the muscle (Tg-KD1), baseline [K+] was not different from controls (4.2 ± 0.1 mM), but the fall in plasma [K+] in response to AICAR (0.25 g/kg) was blunted: [K+] fell to 3.6 ± 0.1 in controls and to 3.9 ± 0.1 mM in Tg-KD1, suggesting that ECF K+ redistributes, at least in part, to muscle ICF. In summary, these findings illustrate that activation of AMPK activity with AICAR provokes a significant fall in plasma [K+] and suggest a novel mechanism for redistributing K+ from ECF to ICF.

Chronic corticosterone injections induce a decrease of ATP levels and sustained activation of AMP-activated protein kinase in hippocampal tissues of male mice

2008 ◽  
Vol 1191 ◽  
pp. 148-156 ◽  
Author(s):  
Yunan Zhao ◽  
Jia Shen ◽  
Hui Su ◽  
Bonan Li ◽  
Dongming Xing ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Male Mice ◽  
Atp Levels ◽  
Amp Activated Protein Kinase ◽  
Sustained Activation

AMP-activated protein kinase and adenylate kinase prevent the ATP catastrophe and cytotoxic protein aggregation

2019 ◽  
Author(s):  
Masak Takaine ◽  
Hiromi Imamura ◽  
Satoshi Yoshida
Keyword(s):  
Protein Kinase ◽  
Protein Aggregation ◽  
Adenylate Kinase ◽  
Cytotoxic Protein ◽  
Atp Levels ◽  
Stochastic Fluctuations ◽  
Physiological Relevance ◽  
Endogenous Proteins ◽  
Amp Activated Protein Kinase ◽  
Yeast Mutants

ABSTRACTATP is the main source of chemical energy in all life and is maintained at several millimolar in eukaryotic cells. However, the mechanisms responsible for and physiological relevance of this high and stable concentration of ATP remain unclear. We herein demonstrate that AMP-activated protein kinase (AMPK) and adenylate kinase (ADK) cooperate to maintain cellular ATP levels regardless of glucose concentrations. Single cell imaging of ATP-reduced yeast mutants revealed that ATP concentrations in these mutants underwent stochastic and transient depletion of ATP repeatedly, which induced the cytotoxic aggregation of endogenous proteins and pathogenic proteins, such as huntingtin and α-synuclein. Moreover, pharmacological elevations in ATP levels in an ATP-reduced mutant prevented the accumulation of α-synuclein aggregates and its cytotoxicity. The removal of cytotoxic aggregates depended on proteasomes, and proteasomal activity cooperated with AMPK or ADK to resist proteotoxic stresses. The present results provide the first evidence to show that cellular ATP homeostasis ensures proteostasis and revealed that stochastic fluctuations in cellular ATP concentrations contribute to cytotoxic protein aggregation, implying that AMPK and ADK are important factors that prevent proteinopathies, such as neurodegenerative diseases.

Caloric restriction and CB1 blockade activate AMP-activated protein kinase and mediate cardio-protection in a model of premature cardiac senescence

2014 ◽  
Vol 62 (S 01) ◽  
Author(s):  
B. Niemann ◽  
H. Issa ◽  
L. Li ◽  
R.-E. Silber ◽  
A. Böning ◽  
...  
Keyword(s):  
Protein Kinase ◽  
Caloric Restriction ◽  
Cardio Protection ◽  
Amp Activated Protein Kinase

Activators of AMP-activated protein kinase regulate adipocyte aldosterone secretion and mineralocorticoid receptor signalling

2015 ◽  
Author(s):  
Anna White ◽  
Aurelie Nguyen Dinh Cat ◽  
Augusto Montezano ◽  
Ian Salt ◽  
Rhian Touyz
Keyword(s):  
Protein Kinase ◽  
Mineralocorticoid Receptor ◽  
Aldosterone Secretion ◽  
Receptor Signalling ◽  
Amp Activated Protein Kinase

Chronic activation of AMP-activated protein kinase increases monocarboxylate transporter 2 and 4 expression in skeletal muscle

2017 ◽  
Vol 95 (8) ◽  
pp. 3552
Author(s):  
E. M. England ◽  
H. Shi ◽  
S. K. Matarneh ◽  
E. M. Oliver ◽  
E. T. Helm ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Protein Kinase ◽  
Monocarboxylate Transporter ◽  
Chronic Activation ◽  
Amp Activated Protein Kinase
Sign in / Sign up

Export Citation Format

Share Document