Influence of choline and ethanolamine administration on choline and ethanolamine phosphorylating activities of mouse liver and kidney

1979 ◽  
Vol 57 (7) ◽  
pp. 981-985 ◽  
Author(s):  
R. K. Upreti
Keyword(s):  
Substrate Concentration ◽  
Mouse Liver ◽  
Kinase Activity ◽  
De Novo ◽  
Choline Kinase ◽  
Male Mice ◽  
De Novo Synthesis ◽  
Ethanolamine Kinase ◽  
Liver And Kidney

The administration of ethanolamine to adult male mice resulted in a significant increase in ethanolamine kinase activity in liver and kidney. Similarly, choline administration resulted in a significant increase in choline kinase activity in liver and kidney. The administration of ethanolamine resulted in enhancement of choline kinase activity concomitantly with ethanolamine kinase activity in liver and kidney. The administration of choline, however, did not result in any significant increase in ethanolamine kinase activity in liver or kidney. Cycloheximide administration along with choline–ethanolamine prevented the increase in kinase activity in liver and kidney. The results obtained have been discussed in relation to the regulatory role of choline kinase and ethanolamine kinase by de novo synthesis in response to enhanced substrate concentration, the secondary nature of choline kinase induction on ethanolamine administration, and possible distinction between choline kinase and ethanolamine kinase.

The role of glycolysis in aflatoxin biosynthesis

1981 ◽  
Vol 27 (12) ◽  
pp. 1276-1282 ◽  
Author(s):  
Jaya Sivaswami Tyagi ◽  
T. A. Venkitasubramanian
Keyword(s):  
Kinase Activity ◽  
Aspergillus Parasiticus ◽  
De Novo ◽  
Specific Activity ◽  
De Novo Synthesis ◽  
Pyruvate Kinase Activity ◽  
Toxigenic Strain ◽  
Glycolytic Intermediates ◽  
Pyruvic Acids

In resting mycelia of Aspergillus parasiticus NRRL 3240, all the glycolytic intermediates with the exception of glucose and phosphoenolpyruvate stimulated the de novo synthesis of aflatoxin from exogenous acetate. Intracellular levels of glycolytic intermediates were measured in the toxigenic strain, A. parasiticus NRRL 3240, and the nontoxigenic strain, A. flavus NRRL 3537. In 48-h cultures, the concentrations of the intermediates beyond the phosphofructokinase reaction were higher in toxigenic mycelial extracts than in nontoxigenic cultures. There was a marked reduction in the specific activity of phosphofructokinase with increasing age in the toxigenic strain. The specific activity of this enzyme was two- to four-fold lower in zinc-deficient mycelia of A. parasiticus. In resting cultures, the uptake rate of labeled glucose was considerably lower in zinc-deficient mycelia than in zinc-replete or nontoxigenic cultures. On the basis of the results obtained, it can be said that intense formation of aflatoxin is associated with a sharp fall in the level of phosphoenolpyruvic and pyruvic acids. This was accompanied by a significantly higher pyruvate kinase activity.

scholarly journals The Role of Mitochondrial Dysfunction in the Progression of Alzheimer’s Disease

2019 ◽  
Vol 25 (40) ◽  
pp. 5578-5587 ◽  
Author(s):  
Claus Desler ◽  
Meryl S. Lillenes ◽  
Tone Tønjum ◽  
Lene Juel Rasmussen
Keyword(s):  
Alzheimer’S Disease ◽  
Reactive Oxygen Species ◽  
Alzheimer's Disease ◽  
Mitochondrial Dysfunction ◽  
De Novo ◽  
Oxygen Species ◽  
De Novo Synthesis ◽  
Atp Production ◽  
Essential Phospholipids

The current molecular understanding of Alzheimer’s disease (AD) has still not resulted in successful interventions. Mitochondrial dysfunction of the AD brain is currently emerging as a hallmark of this disease. One mitochondrial function often affected in AD is oxidative phosphorylation responsible for ATP production, but also for production of reactive oxygen species (ROS) and for the de novo synthesis of pyrimidines. This paper reviews the role of mitochondrial produced ROS and pyrimidines in the aetiology of AD and their proposed role in oxidative degeneration of macromolecules, synthesis of essential phospholipids and maintenance of mitochondrial viability in the AD brain.

The role of particulate carbon in the de-novo synthesis of polychlorinated dibenzodioxins and-furans in fly-ash

Chemosphere ◽  
1990 ◽  
Vol 20 (10-12) ◽  
pp. 1953-1958 ◽  
Author(s):  
L. Stieglitz ◽  
G. Zwick ◽  
J. Beck ◽  
H. Bautz ◽  
W. Roth
Keyword(s):  
Fly Ash ◽  
De Novo ◽  
De Novo Synthesis ◽  
Particulate Carbon ◽  
Polychlorinated Dibenzodioxins

scholarly journals NAD+-Dependent Deacetylase Hst1p Controls Biosynthesis and Cellular NAD+ Levels in Saccharomyces cerevisiae

2003 ◽  
Vol 23 (19) ◽  
pp. 7044-7054 ◽  
Author(s):  
Antonio Bedalov ◽  
Maki Hirao ◽  
Jeffrey Posakony ◽  
Melisa Nelson ◽  
Julian A. Simon
Keyword(s):  
De Novo ◽  
Critical Role ◽  
Salvage Pathway ◽  
De Novo Synthesis ◽  
Array Analysis ◽  
Binding Partner ◽  
Dependent Protein ◽  
New Protein

ABSTRACT Nicotine adenine dinucleotide (NAD+) performs key roles in electron transport reactions, as a substrate for poly(ADP-ribose) polymerase and NAD+-dependent protein deacetylases. In the latter two processes, NAD+ is consumed and converted to ADP-ribose and nicotinamide. NAD+ levels can be maintained by regeneration of NAD+ from nicotinamide via a salvage pathway or by de novo synthesis of NAD+ from tryptophan. Both pathways are conserved from yeast to humans. We describe a critical role of the NAD+-dependent deacetylase Hst1p as a sensor of NAD+ levels and regulator of NAD+ biosynthesis. Using transcript arrays, we show that low NAD+ states specifically induce the de novo NAD+ biosynthesis genes while the genes in the salvage pathway remain unaffected. The NAD+-dependent deacetylase activity of Hst1p represses de novo NAD+ biosynthesis genes in the absence of new protein synthesis, suggesting a direct effect. The known Hst1p binding partner, Sum1p, is present at promoters of highly inducible NAD+ biosynthesis genes. The removal of HST1-mediated repression of the NAD+ de novo biosynthesis pathway leads to increased cellular NAD+ levels. Transcript array analysis shows that reduction in cellular NAD+ levels preferentially affects Hst1p-regulated genes in comparison to genes regulated with other NAD+-dependent deacetylases (Sir2p, Hst2p, Hst3p, and Hst4p). In vitro experiments demonstrate that Hst1p has relatively low affinity toward NAD+ in comparison to other NAD+-dependent enzymes. These findings suggest that Hst1p serves as a cellular NAD+ sensor that monitors and regulates cellular NAD+ levels.

scholarly journals SCAP/SREBP pathway is required for the full steroidogenic response to cyclic AMP

2016 ◽  
Vol 113 (38) ◽  
pp. E5685-E5693 ◽  
Author(s):  
Masami Shimizu-Albergine ◽  
Brian Van Yserloo ◽  
Martin G. Golkowski ◽  
Shao-En Ong ◽  
Joseph A. Beavo ◽  
...  
Keyword(s):  
Cyclic Amp ◽  
Leydig Cells ◽  
De Novo ◽  
Regulatory Element ◽  
De Novo Synthesis ◽  
Intracellular Lipid ◽  
Element Binding Protein ◽  
Short Palindromic Repeat ◽  
Sterol Regulatory Element

Luteinizing hormone (LH) stimulates steroidogenesis largely through a surge in cyclic AMP (cAMP). Steroidogenic rates are also critically dependent on the availability of cholesterol at mitochondrial sites of synthesis. This cholesterol is provided by cellular uptake of lipoproteins, mobilization of intracellular lipid, and de novo synthesis. Whether and how these pathways are coordinated by cAMP are poorly understood. Recent phosphoproteomic analyses of cAMP-dependent phosphorylation sites in MA10 Leydig cells suggested that cAMP regulates multiple steps in these processes, including activation of the SCAP/SREBP pathway. SCAP [sterol-regulatory element-binding protein (SREBP) cleavage-activating protein] acts as a cholesterol sensor responsible for regulating intracellular cholesterol balance. Its role in cAMP-mediated control of steroidogenesis has not been explored. We used two CRISPR (clustered regularly interspaced short palindromic repeat)-Cas9 (CRISPR associated protein 9) knockout approaches to test the role of SCAP in steroidogenesis. Our results demonstrate that SCAP is required for progesterone production induced by concurrent inhibition of the cAMP phosphodiesterases PDE4 and PDE8. These inhibitors increased SCAP phosphorylation, SREBP2 activation, and subsequent expression of cholesterol biosynthetic genes, whereas SCAP deficiency largely prevented these effects. Reexpression of SCAP in SCAP-deficient cells restored SREBP2 protein expression and partially restored steroidogenic responses, confirming the requirement of SCAP–SREBP2 in steroidogenesis. Inhibitors of 3-hydroxy-3-methylglutaryl-Coenzyme A reductase and isoprenylation attenuated, whereas exogenously provided cholesterol augmented, PDE inhibitor-induced steroidogenesis, suggesting that the cholesterol substrate needed for steroidogenesis is provided by both de novo synthesis and isoprenylation-dependent mechanisms. Overall, these results demonstrate a novel role for LH/cAMP in SCAP/SREBP activation and subsequent regulation of steroidogenesis.

Characterization of the AMP-binding protein gene family in Arabidopsis thaliana: will the real acyl-CoA synthetases please stand up?

2000 ◽  
Vol 28 (6) ◽  
pp. 955-957 ◽  
Author(s):  
J. Shockey ◽  
J. Schnurr ◽  
J. Browse
Keyword(s):  
Protein Gene ◽  
De Novo ◽  
Functional Characterization ◽  
De Novo Synthesis ◽  
Triacylglycerol Composition ◽  
Sequence Comparisons ◽  
Triacylglycerol Metabolism ◽  
Binding Protein Gene

One of the most prominent and important topics in modern agricultural biotechnology is the manipulation of oilseed triacylglycerol composition. Towards this goal, we have sought to identify and characterize acyl-CoA synthetases (ACSs), which play an important role in both de novo synthesis and modification of existing lipids. We have identified and cloned 20 different genes that bear strong sequence homology to known ACSs from other organisms. Through sequence comparisons and functional characterization, we have identified several members of this group that encode ACSs, while the other genes fall into the broader category of genes for AMP-binding proteins (AMPBPs). Distinguishing ACSs from AMPBPs will simplify our efforts to understand the role of ACS in triacylglycerol metabolism.

scholarly journals Elevation of hepatic sulphotransferase activities in mice with resistance to cystic fibrosis

2002 ◽  
Vol 364 (1) ◽  
pp. 115-120 ◽  
Author(s):  
Josie L. FALANY ◽  
Heather GREER ◽  
Timea KOVACS ◽  
Eric J. SORSCHER ◽  
Charles N. FALANY
Keyword(s):  
Cystic Fibrosis ◽  
Mouse Liver ◽  
Northern Blot Analysis ◽  
Transmembrane Conductance Regulator ◽  
Male Mice ◽  
Transmembrane Conductance ◽  
Female Adult ◽  
Cf Transmembrane Conductance Regulator ◽  
Different Levels

The severity of intestinal disease in the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) (-/−) mice has been reported to co-segregate with gene loci which contain the genes for hydroxysteroid sulphotransferase (SULT). Because of the potential involvement of steroid hormones in CF, we investigated levels of steroid SULT activity in the livers of CFTR mice to determine whether the levels of SULT activity correlate with the occurrence or severity of CF. To elucidate the possible role of SULT activity in ameliorating the deleterious effects of CF in CFTR (-/−) mice, we determined the levels of phenol SULT (PST), hydroxysteroid SULT [dehydroepiandrosterone (DHEA)-ST] and oestrogen SULT (EST) activity in control CFTR (+/+), heterozygous CFTR (+/−) and homozygous CFTR (-/−) mice, which survive to adulthood. The level of PST activity was not significantly different between any of the groups of mice, regardless of sex or genotype. Although DHEA-ST activity was significantly higher in female mice than in male mice, there was no difference in DHEA-ST activity that could be correlated with genotype. In contrast with PST and DHEA-ST activities, we found that some male and all female adult CFTR (-/−) mice had elevated, dramatically different levels of EST from both CFTR (+/+) and CFTR (+/−) mice. Results from these SULT activity experiments were confirmed by Northern-blot analysis of mouse-liver RNA. Subsequent studies with preweanling mice revealed no differences in the levels of EST that could be correlated with genotype. Thus this study indicates that EST is elevated significantly in CFTR (-/−) mice which survive to adulthood and provides important biochemical information that EST levels may be protective in CF.

scholarly journals The role of bromine in the de novo synthesis in a model fly ash system

Chemosphere ◽  
1994 ◽  
Vol 28 (7) ◽  
pp. 1299-1309 ◽  
Author(s):  
R. Luijk ◽  
C. Dorland ◽  
P. Smit ◽  
J. Jansen ◽  
H.A.J. Govers
Keyword(s):  
Fly Ash ◽  
De Novo ◽  
De Novo Synthesis ◽  
Model Fly Ash

Fatty acid synthase is a prognostic marker and associated with immune infiltrating in gastric cancers precision medicine

2020 ◽  
Vol 14 (3) ◽  
pp. 185-199
Author(s):  
Yangying Zhou ◽  
Weiping Su ◽  
Huan Liu ◽  
Taili Chen ◽  
Naseruddin Höti ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Fatty Acid ◽  
Fatty Acid Synthase ◽  
De Novo ◽  
Survival Outcome ◽  
De Novo Synthesis ◽  
Bioinformatics Analyses ◽  
Key Enzyme ◽  
Tumor Types

Aim: Fatty acid synthase (FASN), a key enzyme for de novo synthesis of fatty acids, has been identified as an oncogene in some tumor types; however, the function of FASN in gastric cancer (GC) is poorly elucidated. Method: Integrative bioinformatics analyses were performed to unveil the role of FASN in tumor progression and cancer-associated immunology of GC. Result: FASN was overexpressed in the GC tissues and correlated with an inferior survival outcome, and largely contributed to the carcinogenesis of GC. Moreover, FASN expression was closely associated with the immune-infiltrating levels of CD8+ T, CD4+ T, neutrophils, macrophages and dendritic cells. Conclusion: FASN was closely associated with GC and may be involved in the tumorigenesis and cancer–immune interactions, and could be a promising prognostic and therapeutic biomarker in GC.

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