Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.3.3.1 (citrate synthase)
 4,488 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Rtg1p is a basic helix-loop-helix transcription factor in the yeast Saccharomyces cerevisiae that is required for basal and regulated expression of CIT2, the gene encoding a peroxisomal isoform of citrate synthase. In respiratory incompetent rho degree petite cells, CIT2 transcription is elevated as much as 30-fold compared with respiratory competent rho + cells. Here we provide evidence that Rtg1p interacts directly with a CIT2 upstream activation site (UASr) and that the rho degree/rho + regulation is not due to a change in the levels of Rtg1p. A fusion protein consisting of the DNA binding domain of Gal4p fused to the NH2 terminus of the full-length wild-type Rtg1p was able to transactivate an integrated LacZ reporter under control of the Gal4p-responsive GAL1 UASG in a rho degree/rho(+)-dependent manner. Other Gal4p fusions to deletions or mutations of Rtg1p indicate that the helix-loop-helix domain is essential for transactivation. Regulated expression of CIT2 also requires the RTG2 gene product. The Gal4-Rtg1p fusion was unable to transactivate the LacZ reporter gene in a strain deleted for RTG2, suggesting that the RTG2 product does not act independently of Rtg1p in the rho degree/rho + transcriptional response.
J Biol Chem 1995 Dec 08
PMID:Transactivation by Rtg1p, a basic helix-loop-helix protein that functions in communication between mitochondria and the nucleus in yeast. 749 87

A small RNA encoded within the nucleus of yeast and mammalian cells is an essential subunit of a mitochondrial RNA-processing endonuclease (RNase MRP) that generates primers for mitochondrial DNA (mtDNA) replication. We examined expression of MRP-RNA in specialized subtypes of mammalian striated muscles that differ markedly in respiratory activity and in muscles subjected to chronic stimulation via the motor nerve, a potent stimulus to mitochondrial biogenesis. MRP-RNA was more abundant in mitochondria-rich cardiac and slow-twitch skeletal muscles than in glycolytic fast-twitch skeletal muscles. Forced contractile activity resulting from nerve stimulation increased expression of MRP-RNA by 3.5-fold within the first day and by 14-fold within 14 days. Changes in abundance of MRP-RNA preceded but otherwise occurred in parallel to changes in specific activity of citrate synthase, a marker of mitochondrial proliferation shown previously to correlate with mtDNA copy number in this model. Another small RNA (U1) also was induced transiently (1-3 days) by nerve stimulation, but such changes were not sustained and were of less magnitude (< 4-fold) than changes in MRP-RNA. These findings are consistent with the hypothesis that MRP-RNA may have a regulatory function with respect to mtDNA replication and mitochondrial biogenesis.
Am J Physiol 1993 Dec
PMID:RNA subunit of mitochondrial RNA-processing enzyme is induced by contractile activity in striated muscle. 750 87

ELB rickettsiae from cat flea homogenates were recovered in tissue culture cells following sequential passage through laboratory rats and the yolk sacs of embryonated chicken eggs. Seven days after inoculation of ELB from the infected yolk sacs, Vero cells and L929 cells were observed to contain intracellular bacteria as demonstrated by Diff Quik and indirect immunofluorescence assay staining. The rickettsial and ELB identity of the cultured agent was confirmed by PCR detection of the 16S rRNA and citrate synthase genes and PCR-restriction fragment length polymorphism analysis of the 17-kDa conserved rickettsial antigen gene. The ELB rickettsiae induced plaques in Vero cells on day 11 postinfection. Rat anti-ELB serum reacted at 1:4,096 to cultured ELB and had lower reactivity to Rickettsia typhi Wilmington (1:1,024), Rickettsia akari Kaplan (1:512), and Rickettsia australis JC (1:64). Spotted fever group polyclonal sera also exhibited lower reactivity to ELB than to the homologous antigen. Coomassie blue-stained sodium dodecyl sulfate-polyacrylamide gel electrophoresis profiles of the ELB isolate and two R. typhi strains were identical.
Infect Immun 1995 Dec
PMID:Isolation, cultivation, and partial characterization of the ELB agent associated with cat fleas. 759 Nov 42

In a mountainous area in the Dinaric Beech-Fir Forest of southern Slovenia, summer nests of the European fat dormouse (Glis glis) were collected. From these dormouse nests, 180 Monopsyllus sciurorum sciurorum fleas were examined by polymerase chain reaction with primers for the Rickettsia citrate synthase gene. Samples from one nest yielded the expected 381 base pair DNA product. The origin of the DNA product was identified as Rickettsia typhi by AluI restriction fragment length polymorphism analysis. Inoculation of the triturated positive fleas into Vero cell culture resulted in the cultivation of a rickettsia which reacted with polyclonal and species-specific monoclonal antibodies for R. typhi. The widespread distribution of this sylvatic flea species in nearly all of Europe as well as in the Middle East and its presence on other mammalian and avian hosts suggests that R. typhi might exist in unrecognised enzootic cycles. Further investigations are needed to determine the extent of these cycles in Europe and the potential occurrence of human infections.
Eur J Epidemiol 1994 Dec
PMID:Identification of a natural cycle involving Rickettsia typhi infection of Monopsyllus sciurorum sciurorum fleas from the nests of the fat dormouse (Glis glis). 767 59

Restriction fragment length polymorphism (RFLP) analysis of polymerase chain reaction (PCR) amplified genes was used for genomic identification of Armenian isolates of the Spotted fever group (SFG) rickettsiae with unclear taxonomic position. Analysis was performed by using one genus-specific primer pair derived from R. prowazekii citrate synthase gene and two species-specific primer pairs derived from R. rickettsii genes for 190 K and 120 K antigens following AluI, PstI and RsaI digestion of amplicons. All tested rickettsial SFG Armenian isolates from Dermacentor marginatus were identified as R. slovaca. The geographic distribution and genetic homogeneity of R. slovaca strains are discussed.
Acta Virol 1994 Dec
PMID:Genomic identification of Rickettsia slovaca among spotted fever group rickettsia isolates from Dermacentor marginatus in Armenia. 779 55

FarR (formerly P30) has been identified as a fatty acid and fatty acyl-CoA responsive DNA-binding protein. It is encoded by the farR gene (g30) in the citric acid cycle gene cluster of E. coli (gltA-sdhCDAB-sucABCD-farR). The amplified FarR protein specifically bound to the farR promoter (PfarR) and exhibited weak binding to the citrate synthase and lipoamide dehydrogenase promoters. Binding at PfarR was abolished by long-chain fatty acids and their CoA thioesters. In DNaseI footprints, FarR binding at PfarR protected two sites, each characterised by two related 10-bp direct repeats. It is suggested that FarR autoregulates farR expression and may modulate citric acid cycle expression in response to long-chain fatty acids.
FEBS Lett 1994 Dec 19
PMID:Identification of a fatty acyl responsive regulator (FarR) in Escherichia coli. 780 34

Previous studies demonstrated that one of the most significant cellular responses of the rabbit urinary bladder to partial outlet obstruction is a 50% decrease in the activities of the mitochondrial enzymes citrate synthase and malate dehydrogenase, when calculated as either activity per unit mass or activity per mg protein. A major question arose from these studies: Are the mitochondrial enzyme activities per mitochondrion reduced, or is the number of mitochondria per unit tissue mass reduced? The current experiments were designed to study the sequential changes in the activities of mitochondrial oxidative enzymes following partial outlet obstruction. The activities of NADH-cytochrome c reductase (NCCR), cytochrome oxidase (CO), citrate synthase (CS) and malate dehydrogenase (MDH) were measured in whole tissue homogenates and in mitochondrial preparations of separated bladder mucosa and muscle, from normal bladders, and, from hypertrophied bladders at 1, 3, and 7 days following partial outlet obstruction. The results can be summarized as follows: 1) Whole tissue homogenates: Activities of all enzymes were reduced to approximately 50% of control at 1 day following partial outlet obstruction. NCCR and CO activities returned to 75 and 85% of control respectively by 7 days post-obstruction; CS activity did not show any significant recovery over the 7 day period. 2) Mucosal and smooth muscle mitochondrial preparations: Activities of all enzymes were decreased significantly by 50% or greater at 1 day following partial outlet obstruction. The cytochrome (NCCR and CO) enzyme activities returned to control levels by 7 days post-obstruction; CS activity showed only a minor recovery over this time period. These results show that mitochondrial enzyme activity is significantly impaired immediately following partial outlet outlet obstruction, and whereas the activity of the cytochrome enzymes NCCR and CO recover to control levels (in the mitochondrial preparations) within 7 days post obstruction, the Krebs cycle enzymes (CS and MD) show no significant recovery. Thus, the regulatory mechanisms for the cytochromes is significantly different from that for the enzymes of the krebs cycle.
Mol Cell Biochem 1994 Dec 07
PMID:Alterations of mitochondrial oxidative metabolism in rabbit urinary bladder after partial outlet obstruction. 787 5

Non-synaptosomal and synaptosomal mitochondrial membrane-linked enzymatic activities, NADH-cytochrome c reductase rotenone insensitive (marker of the outer membrane) and cytochrome oxidase (marker of the inner membrane), were measured in rat brain hippocampus and striatum immediately after and 1, 4 and 7 days following the induction of complete transient ischemia (15 min) by the four vessel occlusion method. Furthermore citrate synthetase activity was measured with and without Triton X-100 in order to qualitatively evaluate the membrane permeability. Non-synaptosomal mitochondrial membranes showed reduction of both activities only in the late reperfusion phase: NADH-CCRRi decreased in striatal mitochondria after 4-7 days and only after 7 days in the hippocampus. COX activity decreased only in striatal mitochondria 7 days after ischemia. Non-synaptosomal mitochondrial membrane permeability did not show changes. Synaptosomal mitochondria showed a decrease of NADH-CCRRi only at 7 days of reperfusion both in hippocampus and striatum, while COX activity decreased only during ischemia and returned to normal levels in the following days in the two areas considered. In summary, free mitochondria showed insensitiveness to ischemia but they resulted damaged in the late reperfusion phase, while mitochondria from the synaptic terminal showed ischemic damage, partially restored during reperfusion. The striatal mitochondria showed a major susceptibility to ischemia/reperfusion damage, showing changes earlier than the hippocampal ones.
Neurochem Res 1994 Dec
PMID:Changes in non-synaptosomal and synaptosomal mitochondrial membrane-linked enzymatic activities after transient cerebral ischemia. 787 28

The presence of catalase in heart mitochondria may prevent excessive H2O2 from reaching the cytosol, eventually reacting with myoglobin (R. Radi et al., 1991, J. Biol. Chem. 266, 22028-22034). In this report we investigated whether catalase was also present in the mitochondrial matrix of skeletal muscle as it also contains myoglobin which could react with H2O2 produced by mitochondria. Catalase content of skeletal muscle tissue was about 1.4% of that in liver. Simultaneous determinations of citrate synthase (a mitochondrial marker) and catalase in intact mitochondria and mitoplasts indicated that catalase is not associated with muscle mitochondria. The lack of catalase in muscle mitochondria is not due to a limited H2O2 production by these organelles. Rat skeletal muscle mitochondria generated H2O2 (0.64 +/- 0.04 nmol/(min.mg protein), approximately 40% the rate in heart mitochondria. Other groups have shown that training causes an increase in the concentration of mitochondrial electron carriers as well as an increase in the activity of mitochondrial glutathione peroxidase and mitochondrial electron carriers. The increased concentration of mitochondrial electron carriers and the sudden changes in oxygen supply may lead to increased intracellular H2O2 during exercise.
Arch Biochem Biophys 1994 Dec
PMID:Hydrogen peroxide metabolism in skeletal muscle mitochondria. 798 95

We investigated the hypothesis that one mechanism underlying fatty acid toxicity is the selective inhibition of rate-limiting and/or regulated tricarboxylic acid cycle and related enzymes by fatty acyl coenzyme A (CoA) derivatives by examining the effects of several fatty acyl CoAs on purified citrate synthase (CS) and glutamate dehydrogenase (GDH). The results indicate that, at pathophysiological levels, palmitoyl CoA, a long-chain acyl CoA, is a potent inhibitor of CS and GDH with IC50 values of 3-15 microM. At much higher levels (in the pathological and toxicological range), octanoyl and decanoyl CoA (medium-chain acyl CoAs) inhibited both enzymes with IC50 values of 0.4-1.6 mM. Butyryl CoA, a short-chain acyl CoA, inhibited CS (IC50 = 0.9 mM) at toxicological levels but inhibited GDH poorly. These results suggest that the long-chain fatty acyl CoA inhibition of CS and GDH may assume some pathophysiological importance in fatty acid toxicity and in metabolic encephalopathies in which organic acidemia is persistent. The findings also provide additional support for the original hypothesis.
Res Commun Chem Pathol Pharmacol 1993 Dec
PMID:Differential effects of fatty acyl coenzyme A derivatives on citrate synthase and glutamate dehydrogenase. 812 33


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