Discovery of InsP6-kinases as InsP6-dephosphorylating enzymes provides a new mechanism of cytosolic InsP6 degradation driven by the cellular ATP/ADP ratio

2014 ◽  
Vol 462 (1) ◽  
pp. 173-184 ◽  
Author(s):  
Torsten Wundenberg ◽  
Nicole Grabinski ◽  
Hongying Lin ◽  
Georg W. Mayr
Keyword(s):  
Energy Charge ◽  
Inositol Hexakisphosphate ◽  
Cellular Energy

Inositol hexakisphosphate (InsP6) kinases are identified as InsP6 phosphorylating and dephosphorylating enzymes synthesizing either 5PP-InsP5 or Ins(2,3,4,5,6)P5. Their respective activity for InsP6 is dependent on the ATP/ADP ratio, thus acting as a cellular energy charge sensor.

Experimental study of the cellular energy charge in pig kidney transplants from non–heart-beating donors

1999 ◽  
Vol 31 (6) ◽  
pp. 2352-2353 ◽  
Author(s):  
P Luque ◽  
R Alvarez-Vijande ◽  
A Alcaraz ◽  
A Aguilar ◽  
J Alcoberro ◽  
...  
Keyword(s):  
Experimental Study ◽  
Energy Charge ◽  
Kidney Transplants ◽  
Cellular Energy ◽  
Pig Kidney ◽  
Heart Beating

scholarly journals AMP-activated protein kinase: an ultrasensitive system for monitoring cellular energy charge

1999 ◽  
Vol 338 (3) ◽  
pp. 717 ◽  
Author(s):  
D. Grahame HARDIE ◽  
Ian P. SALT ◽  
Simon A. HAWLEY ◽  
Stephen P. DAVIES
Keyword(s):  
Protein Kinase ◽  
Energy Charge ◽  
Cellular Energy ◽  
Amp Activated Protein Kinase

scholarly journals AMP-activated protein kinase: an ultrasensitive system for monitoring cellular energy charge

1999 ◽  
Vol 338 (3) ◽  
pp. 717-722 ◽  
Author(s):  
D. Grahame HARDIE ◽  
Ian P. SALT ◽  
Simon A. HAWLEY ◽  
Stephen P. DAVIES
Keyword(s):  
Protein Kinase ◽  
Energy Charge ◽  
Fold Increase ◽  
Maximal Activity ◽  
Hill Coefficient ◽  
Intact Cells ◽  
Cellular Energy ◽  
Critical Range ◽  
Kinase Cascade ◽  
Amp Activated Protein Kinase

The AMP-activated protein kinase cascade is activated by elevation of AMP and depression of ATP when cellular energy charge is compromised, leading to inhibition of anabolic pathways and activation of catabolic pathways. Here we show that the system responds in intact cells in an ultrasensitive manner over a critical range of nucleotide concentrations, in that only a 6-fold increase in activating nucleotide is required in order for the maximal activity of the kinase to progress from 10% to 90%, equivalent to a co-operative system with a Hill coefficient (h) of 2.5. Modelling suggests that this sensitivity arises from two features of the system: (i) AMP acts at multiple steps in the cascade (multistep sensitivity); and (ii) the upstream kinase is initially saturated with the downstream kinase (zero-order ultrasensitivity).

AMP-activated protein kinase regulates gene expression by direct phosphorylation of nuclear proteins

2003 ◽  
Vol 31 (1) ◽  
pp. 224-227 ◽  
Author(s):  
T. Leff
Keyword(s):  
Gene Expression ◽  
Transcription Factors ◽  
Protein Kinase ◽  
Gene Transcription ◽  
Metabolic Pathways ◽  
Energy Charge ◽  
Nuclear Proteins ◽  
Cellular Energy ◽  
Ampk Activity ◽  
Amp Activated Protein Kinase

One of the primary functions of AMP-activated protein kinase (AMPK) is to regulate the metabolic pathways in response to reduced cellular energy charge. Most of the known targets of the kinase are cytoplasmic enzymes involved in both catabolic and anabolic metabolism. In addition, activation of AMPK in many cells results in changes in the pattern of gene expression. Although some of these effects are undoubtedly secondary responses to modified cellular metabolism, it is possible that in addition to its well-characterized function in the cytoplasm, AMPK also directly phosphorylates and regulates proteins involved in gene transcription. There are now several examples of transcription factors, cofactors and components of the transcriptional core machinery that are directly phosphorylated and regulated by AMPK. Here I review these examples and discuss the significance of AMPK activity in the nucleus.

scholarly journals Ultraweak photon emission in strawberry fruit during ripening and aging is related to energy level

2017 ◽  
Vol 12 (1) ◽  
pp. 393-398 ◽  
Author(s):  
Jinli Guo ◽  
Guanyu Zhu ◽  
Lianguo Li ◽  
Huan Liu ◽  
Shuang Liang
Keyword(s):  
Energy Source ◽  
Energy Level ◽  
Energy Levels ◽  
Energy Charge ◽  
Photon Emission ◽  
Adenosine Monophosphate ◽  
Adenosine Diphosphate ◽  
Strawberry Fruit ◽  
Cellular Energy ◽  
Living Organisms

AbstractBackgroundUltra-weak photon emission (UPE), or biophoton emission, is a phenomenon observed in various living organisms, including plants. In this study, we analyzed the UPE from ripening strawberry fruits, to elucidate its source and association with cellular energy.MethodsFreshly harvested and stored strawberry fruits were measured for levels of UPE and energy molecules adenosine triphosphate (ATP), adenosine monophosphate (AMP) and adenosine diphosphate (ADP). The associations between them were calculated.ResultsIn ripening fruit, a decrease in UPE positively correlated with declining levels of ATP, AMP, and energy charge. In harvested fruits, levels of UPE, ATP, and energy charge declined, but ADP and AMP increased.ConclusionChanges in UPE levels synchronized with changes in ATP and energy charge, which reflect cellular energy levels. Thus, cellular energy may be related to UPE, and may be an energy source for UPE.

Energy status and cytochromes in isolated endophytic vesicle clusters of red alder root nodules

1983 ◽  
Vol 13 (5) ◽  
pp. 921-928 ◽  
Author(s):  
Te May Ching ◽  
Philip A. Monaco ◽  
Kim K. Ching
Keyword(s):  
Oxygen Uptake ◽  
Nitrogenase Activity ◽  
Root Nodules ◽  
Energy Charge ◽  
Energy Status ◽  
Red Alder ◽  
Cellular Energy ◽  
Adenylate Pool ◽  
39 B 22 ◽  
Cytochrome P 450

Anaerobically isolated endophytic vesicle clusters from root nodules of Alnusrubra Bong. were low in cellular energy charge (0.4 to 0.5), total adenylate pool (0.4 to 0.9 nmolùmg protein−1), and nitrogenase activity (0.1 to 0.3 nmolùmg protein−1). Upon addition of substrate (glucose, sucrose, isocitrate + isocitrate dehydrogenase + NADP), energy charge decreased by 2 to 20%, total adenylate pool increased by 3- to 11-fold, and nitrogenase activity increased by 50 to 500%. Only ATP and dithionite supported substantial nitrogenase activity and greatly elevated energy status. Treating vesicle clusters with macerase and cellulase to remove the host capsule facilitated substrate and oxygen uptake, resulting in a 240% increase in total adenylate pool, a 60% increase in energy charge, and a 730% increase in nitrogenase activity. Isolated vesicle clusters contained about 320 nmol cytochromes•g protein−1, with an average molar distribution of 17% cytochrome a-a3, 39% b, 22% c, and 21% o. No cytochrome P 450 was observed in vesicle clusters. The presence of cytochromes a-a3 and o may be a mechanism of oxygen tolerance whereby the nitrogenase in Frankia spp. can operate in an environment without the protection of leghaemoglobin.

scholarly journals Mitochondrial Dysfunction Is the Focus of Quaternary Ammonium Surfactant Toxicity to Mammalian Epithelial Cells

2013 ◽  
Vol 57 (6) ◽  
pp. 2631-2639 ◽  
Author(s):  
Ângela S. Inácio ◽  
Gabriel N. Costa ◽  
Neuza S. Domingues ◽  
Maria S. Santos ◽  
António J. M. Moreno ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Quaternary Ammonium ◽  
Mammalian Cells ◽  
Energy Charge ◽  
Critical Micellar Concentration ◽  
Common Mechanism ◽  
Cellular Energy ◽  
Toxicological Studies ◽  
Complete Breakdown

ABSTRACTSurfactants have long been known to have microbicidal action and have been extensively used as antiseptics and disinfectants for a variety of general hygiene and clinical purposes. Among surfactants, quaternary ammonium compounds (QAC) are known to be the most useful antiseptics and disinfectants. However, our previous toxicological studies showed that QAC are also the most toxic surfactants for mammalian cells. An understanding of the mechanisms that underlie QAC toxicity is a crucial first step in their rational use and in the design and development of more effective and safer molecules. We show that QAC-induced toxicity is mediated primarily through mitochondrial dysfunction in mammalian columnar epithelial cell culturesin vitro. Toxic effects begin at sublethal concentrations and are characterized by mitochondrial fragmentation accompanied by decreased cellular energy charge. At very low concentrations, several QAC act on mitochondrial bioenergetics through a common mechanism of action, primarily by inhibiting mitochondrial respiration initiated at complex I and, to a lesser extent, by slowing down coupled ADP phosphorylation. The result is a reduction of cellular energy charge which, when reduced below 50% of its original value, induces apoptosis. The lethal effects are shown to be primarily a result of this process. At higher doses (closer to the critical micellar concentration), QAC induce the complete breakdown of cellular energy charge and necrotic cell death.

Sign in / Sign up

Export Citation Format

Share Document