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  • Animal models  (1)
  • Cytidine deaminase  (1)
  • Key words Pyrimidine salvage pathway   (1)
  • 1
    Electronic Resource
    Electronic Resource
    New insights into the pyrimidine salvage pathway of Saccharomyces cerevisiae: requirement of six genes for cytidine metabolism (1999)
    Springer
    Current genetics 36 (1999), S. 130-136 
    Details
    ISSN: 1432-0983
    Keywords: Key words Pyrimidine salvage pathway ; Cytidine deaminase ; Cytidine metabolism ; CDD1 ; Uridine/cytidine kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Cytidine metabolism in the yeast Saccharomyces cerevisiae was analyzed by genetic and biochemical approaches. Disruption of a unique ORF (Genbank accession No. U 20865) bearing homology with eucaryotic or bacterial cytidine deaminases abolished cytidine deaminase activity and resulted in 5-fluorocytidine resistance. The gene encoding cytidine deaminase will be referred to as CDD1 (Genbank accession number AF080089). The ability to isolate mutants resistant to 5-fluorocytidine which mapped to five other loci demonstrated the existence of a complex cytidine metabolic network. Deciphering this network revealed several original features: (1) cytidine entry is mediated by the purine-cytosine transporter (Fcy2p), (2) cytidine is cleaved into cytosine by the uridine nucleosidase (Urh1p), (3) cytidine is phosphorylated into CMP by the uridine kinase (Urk1p), (4) a block in cytosine deaminase (Fcy1p), but not in cytidine deaminase (Cdd1p), constitutes a limiting step in cytidine utilisation as a UMP precursor.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050482
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Characterization of the Saccharomyces cerevisiae FCY1 gene encoding cytosine deaminase and its homologue FCA1 of Candida albicans (1997)
    Springer
    Current genetics 31 (1997), S. 1-6 
    Details
    ISSN: 1432-0983
    Keywords: Key words Pyrimidine salvage pathway  ;  Cytosine deaminase  ;  FCY1  ;  FCA1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract By functional complementation of a fcy1 null mutant of Saccharomyces cerevisiae, we have cloned and characterized the FCY1 gene, encoding cytosine deaminase in Saccharomyces cerevisiae, and its homologue FCA1, encoding cytosine deaminase in Candida albicans. Disruption of FCY1 resulted in high resistance to 5-fluorocytosine (10−2 M) and in total loss of cytosine deaminase activity. By contrast the transformation by FCY1 or FCA1 of the haploid FCY1-disrupted host strain restored sensitivity to 5-fluorocytosine and allowed growth on cytosine, as a source of pyrimidine, or ammonium. FCA1 as opposed to FCY1 contains an intron. FCA1 and FCY1 encode respectively 150- and 158- residue proteins of 60% identity. Both Fcy1p and Fca1p share common motifs with cytidine and CMP deaminases, but homology with cytosine deaminase of E. coli could not be detected.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002940050169
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Susceptibility of isolated rat facial nerve to anaerobic stress (1997)
    Springer
    European archives of oto-rhino-laryngology and head & neck 254 (1997), S. S64 
    Details
    ISSN: 1434-4726
    Keywords: Facial nerve paralysis ; Nerve ischemia ; Oxidative phosphorylation ; Animal models
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Ischemic lesions are presumed to be part of many facial nerve pathologies, such as Bell's palsy. The response of facial nerve to hypoxia has not been evaluated previously in an in vitro model. In the present study, the effects of transient anaerobic stress on functional parameters and their recovery were assessed. Extratemporal rat facial nerves were desheathed and incubated in an experimental chamber using solutions containing either low (5 mM) or high (25 MM)d-glucose. In some of the experiments, 40 μM phenytoin or lidocaine was added to observe the effects of membrane stabilizing drugs. Peak height of compound nerve action potential (CNAP), extracellular direct current (DC) potential and latency were measured simultaneously during and after a 40-min period of hypoxia, induced by bubbling the solutions with N2 or application of 3 mM cyanide. This resulted in a rapid decrease of CNAP and a depolarization of the DC potential with a fast and complete post hypoxic recovery. Elevated glucose concentrations led to a slower decline in CNAP and a smaller rise of membrane potential depolarization. This was accompanied by a slower change of latency. However, post-anaerobic recovery was always diminished in the high glucose solutions. In experiments with phenytoin or lidocaine longer impulse conduction during hypoxia was observed. These findings indicate that the availability of energy-rich components underlies the complex array of physiological derangements seen in ischemia. Membrane-stabilizing drugs show an effect on signal conduction during hypoxia and need further exploration.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02439727
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    Paper (German National Licenses)
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