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Страница 1 од 54 резултати
Activity of several S-adenosylhomocysteine hydrolase inhibitors against African swine fever virus replication in Vero cells.
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Several inhibitors of S-adenosylhomocysteine (AdoHcy) hydrolase have been found to selectively suppress the replication of African swine fever virus (ASFV) in Vero cells. Of the compounds tested, 3-deazaneplanocin A proved to be the most potent and selective inhibitor of ASFV replication. Its
Structure of a Nudix hydrolase (MutT) in the Mg(2+)-bound state from Bartonella henselae, the bacterium responsible for cat scratch fever.
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Cat scratch fever (also known as cat scratch disease and bartonellosis) is an infectious disease caused by the proteobacterium Bartonella henselae following a cat scratch. Although the infection usually resolves spontaneously without treatment in healthy adults, bartonellosis may lead to severe
The g5R (D250) gene of African swine fever virus encodes a Nudix hydrolase that preferentially degrades diphosphoinositol polyphosphates.
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The African swine fever virus (ASFV) g5R gene encodes a protein containing a Nudix hydrolase motif which in terms of sequence appears most closely related to the mammalian diadenosine tetraphosphate (Ap4A) hydrolases. However, purified recombinant g5R protein (g5Rp) showed a much wider range of
Effects of hyperthermia on Tetrahymena. I. Localization of acid hydrolases and changes in cell ultrastructure.
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Treatment of lethal Ebola virus infection in mice with a single dose of an S-adenosyl-L-homocysteine hydrolase inhibitor.
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Ebola Zaire virus causes lethal hemorrhagic fever in humans, for which there is no effective treatment. A variety of adenosine analogues inhibit the replication of Ebola virus in vitro, probably by blocking the cellular enzyme, S-adenosyl-L-homocysteine hydrolase, thereby indirectly limiting
Molecular characterization of Borrelia persica, the agent of tick borne relapsing fever in Israel and the Palestinian Authority.
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The identification of the Tick Borne Relapsing Fever (TBRF) agent in Israel and the Palestinian Authority relies on the morphology and the association of Borrelia persica with its vector Ornithodoros tholozani. Molecular based data on B. persica are very scarce as the organism is still
Mapping of the familial Mediterranean fever gene to chromosome 16.
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Familial Mediterranean fever (FMF) is an autosomal recessive disease characterized by recurrent attacks of fever, synovitis, peritonitis, or pleurisy. Some patients eventually develop systemic amyloidosis. The biochemical cause of the disease is unknown. We have conducted a genome-wide search for
Characterization of the African swine fever virus decapping enzyme during infection.
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African swine fever virus (ASFV) infection is characterized by a progressive decrease in cellular protein synthesis with a concomitant increase in viral protein synthesis, though the mechanism by which the virus achieves this is still unknown. Decrease of cellular mRNA is observed during ASFV
Use of the yellow fever virus vaccine strain 17D for the study of strategies for the treatment of yellow fever virus infections.
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We have employed the attenuated vaccine strain 17D of yellow fever virus (YFV) to evaluate the inhibitory effect of a selected series of compounds on YFV in Vero cells. Use of the vaccine strain does not require high-level microbiological containment facilities and should allow extensive screening.
Recurrent fever of unknown origin: An overlooked symptom of Fabry disease
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Objective: Fabry disease (FD) is a rare X-linked lysosomal storage disorder due to the absent or deficient activity of lysosomal hydrolase a-galactosidase A (α-Gal A), which leads to the accumulation of its substrates in various organs
Nucleoside triphosphate phosphohydrolase activities in African swine fever virus.
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African swine fever virus contains nucleoside triphosphate phosphohydrolase activity which releases 32P phosphate from gamma-32P ATP at a rate of about 1 mumol/h mg of virus protein. The hydrolase activity is slightly stimulated by adding nucleic acids to the reaction mixture and under conditions of
Genetic and environmental factors that regulate cytosolic epoxide hydrolase activity in normal human lymphocytes.
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To determine whether genetic mechanisms control large variations in cytosolic epoxide hydrolase (cEH) activity of unstimulated lymphocytes from normal human subjects, cEH activity was measured in (a) 6 sets of monozygotic (MZ) twins and 6 sets of dizygotic (DZ) twins; (b) 100 unrelated male
John Montgomery's legacy: carbocyclic adenosine analogues as SAH hydrolase inhibitors with broad-spectrum antiviral activity.
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Ever since the S-adenosylhomocysteine (AdoHcy, SAH) hydrolase was recognized as a pharmacological target for antiviral agents (J. A. Montgomery et al., J. Med. Chem. 25:626-629, 1982), an increasing number of adenosine, acyclic adenosine, and carbocyclic adenosine analogues have been described as
Characterization of transgenic mice with neuron-specific expression of soluble epoxide hydrolase.
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Soluble epoxide hydrolase (sEH) is the major enzyme responsible for the metabolism and inactivation of epoxyeicosatrienoic acids (EETs). EETs are produced by the cytochrome P450 (CYP) epoxygenase pathway of arachidonic acid (AA) metabolism and tend to be anti-hypertensive, anti-inflammatory and
Two qualitatively different effects of hyperthermia on acid phosphatase staining in mouse spleen, dependent on the severity of the treatment.
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Heating the lower body of the mouse for up to 1.5 hours at temperatures above 41.0 degrees C causes an increase in splenic lysosomal acid phosphatase activity. For mouse temperatures up to 42.3 degrees C the change is probably due to enzyme activation, which reaches a maximum 1.5 hours after heating
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