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  • 1
    ISSN: 1432-0983
    Keywords: Yeast ; Mutant ; Triethyltin chloride ; Protein phosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Three mutants of Saccharomyces cerevisiae resistant to triethyltin (an inhibitor of mitochondrial ATPase) on non-fermentative media, and non-resistant to this drug on fermentative media, were isolated and named TTR1, TTR2 and TTR3. Apart from triethyltin resistance, these mutants show the following common characteristics: (1) Increased intracellular cytochrome c concentration. (2) Increased respiration rate. (3) Decreased growth yield. (4) Increased growth sensitivity to several drugs inhibiting oxidative phosphorylation: namely, CCCP (permeabilizing inner mitochondrial membrane to protons), valinomycin (permeabilizing inner mitochondrial membrane to potassium) and oligomycin (inhibitor of mitochondrial ATPase). (5) Increased sensitivity to carbon source starvation. For each mutant, these characteristics appeared to be due to a single pleiotropic nuclear mutation. Mutation TTR1 causes additional phenotypic characteristics which do not appear in mutants TTR2 and TTR3: (1) Pinkish coloration of colonies which is more pronounced after a long growth period. (2) Inability of the cells to store glycogen. (3) Growth defect of the cells on a galactose-containing medium. (4) Inability of a diploid homozygote mutant strain to sporulate. All these phenotypic characteristics have already been described in yeast mutants deregulated in cAMP-dependant protein phosphorylation. Crossing of a strain bearing the TTR1 mutation with a strain mutated in the adenylate cyclase structural gene suggested that the TTR1 phenotype is due to a modification in regulation of cAPK by cAMP, making cell multiplication possible without intracellular cAMP.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0983
    Keywords: Yeast ; Mutants ; Cytochrome ; Mitochondria ; Oxidative phosphorylation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary This paper reports studies of bioenergetic modifications in a TTR1 single-nuclear mutant, isolated as resistant to triethyltin, an inhibitor of mitochondrial ATPase, and effective in cAMP-dependent protein phosphorylation. This mutant appears to have lost the wildtype cell ability to respond to a decrease of oxygen concentration in the growth medium by a decrease of cytochrome concentration in the cell. ATP synthesis rate in mutant cells in both the prestationary and stationary phase of growth appeared increased in comparison to wild-type cells, as too was respiration rate. A comparative study of mitochondria extracted from wild-type and from TTR1 mutant cells showed an increase in respiration rate, an increase in ATP synthesis rate, and an increase in TPP+ uptake in mutant mitochondria. The specific ATPase activity, as well as its sensitivity to TET, appears to be similar for mitochondria extracted from both strains. It was proposed that the modification of mitochondrial biogenesis in the TTR1 mutant may be due to a response of the cell to an increase in ATP hydrolysis caused by the mutation. It is also possible that the modification in cAMP-dependent protein kinase regulation which appeared to occur in this mutant affects protein(s) involved in mitochondrial biogenesis.
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  • 3
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: This study investigates the functioning of synaptosomal ouabain-sensitive Na+-K+-ATPase in cold-induced edema. During vasogenic brain edema development, the enzyme affinities for Na+ and K+ are progressively decreased paralleling the increase in the tissue water content, whereas maximal velocity of the reaction is not changed. On the basis of these data, it is likely that Na+-K+-ATPase impairment accounts for the intracellular uptake of water in this model of edema.
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 254 (1989), S. 199-202 
    ISSN: 0014-5793
    Keywords: (Yeast) ; ATP/O stoichiometry ; Mitochondria ; Oxidative phosphorylation
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 0014-5793
    Keywords: (Yeast) ; Energetic metabolism ; Mitochondria ; NMR ; Polyphosphate
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 256 (1989), S. 245 
    ISSN: 0014-5793
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    FEBS Letters 244 (1989), S. 255-258 
    ISSN: 0014-5793
    Keywords: (Yeast mitochondria) ; ATP synthesis ; Kinetic control ; Phosphate carrier ; Thermodynamic control ; ΔpH
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 0014-5793
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 0014-5793
    Keywords: (Saccharomyces cerevisiae) ; Fatty acid synthesis ; Lipid synthesis ; Mitochondria ; Very long-chain fatty acid
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Neurological sciences 10 (1989), S. 147-155 
    ISSN: 1590-3478
    Keywords: Membrane damage ; acute brain trauma ; ATPase function ; cryogenic injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Sommario Fra le alterazioni biochimiche che si verificano nella fase acuta degli insulti cerebrali, una delle più importanti è la distruzione dei fosfolipidi di membrana. Nell'insulto di tipo criogeno, che è considerato un modello animale di lesione contusiva cerebrale nella traumatologia umana, il primo attacco delle membrane potrebbe consistere in um danno perossidativo determinato dai composti ferrosi del sangue. Ciò determinerebbe una attivazione della fosfolipasi A2. Come conseguenza della distruzione dei fosfolipidi si verifica un grave danno di numerosi enzimi impegnati in produzione di energia all'interno dei mitocondri. Pur tuttavia il livello dell'ATP disponibile all'interno della cellula rimane normale e persino più elevato del normale. Questo dato paradossale sembra suggerire che l'utilizzazione energetica è persino più ridotta della produzione di energia. Difatti l'attività delle Na+−K+ ATPasi che normalmente utilizzano circa il 70% del totale dell'energia cellulare è notevolmente ridotta. Noi pensiamo che l'interessamento delle NA+−K+ ATPasi è direttamente responsabile della ritenzione di NA+ intracellulare associato all'acqua regolata in modo osmotico, anche se altri disturbi biochimici, tra i quali l'acidosi tissulare e la liberazione di aminoacidi stimolanti, potrebbero contribuire alla medesima conseguenza. Per ultimo una caratteristica di questi eventi biochimici è l'attivazione precoce di questi enzimi necessari per la resintesi fosfolipica. Questo sta a significare che i processi riparativi sono in atto immediatamente dopo l'insulto permettendo la ripresa funzionale della NA+−K+ ATPase, la risoluzione dell'edema e la riattivazione degli scambi cationici essenziali per l'attività cerebrale.
    Notes: Abstract Among a number of biochemical disturbances occurring in the acute phase of brain insults, the destruction of membrane phospholipids and its consequences on the function of membrane-bound proteins is likely to be one of the most important. In the cryogenic type of injury which is classically considered as a relevant animal model of brain contusive lesions in human traumatology, the initial attack of membranes could consist in a peroxidative damage triggered by blood ferrous compounds. This in turn would lead to an activation of phospholipase A2. As a consequence of phospholipid disruption a number of enzymes involved in energy production within the mitochondria are severely impaired. Nevertheless, the level of available ATP within the cell remains normal and even higher than normal. This paradoxical finding suggests that energy utilization is even more lowered than energy production. In fact, the Na+−K+-ATPase activity which normally utilizes approximately 70% of the total amount of cellular energy is severely reduced. We assume that Na+−K+-ATPase impairment is directly responsible for the retention of intracellular Na+ accompanied by osmotically driven water, though admittedly other biochemical disturbances, including tissue acidosis and liberation of excitatory amino-acids, would contribute to the same result [2, 9, 16]. Lastly, a striking feature of these biochemical events is the early activation of those enzymes necessary for phospholipid resynthesis. This should mean that repair processes are at work immediately after the insult allowing resumption of Na+−K+-ATPase function, clearing up of brain edema and restoration of cation exchanges essential for brain work.
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