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  • Alzheimer-disease  (1)
  • Keywords: tod pathway; monoalkylbenzenes; toluene dioxygenase; cometabolism; Pseudomonas putida F1  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of industrial microbiology and biotechnology 25 (2000), S. 163-170 
    ISSN: 1476-5535
    Keywords: Keywords: tod pathway; monoalkylbenzenes; toluene dioxygenase; cometabolism; Pseudomonas putida F1
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: The metabolism of n-alkylbenzenes (C3–C7), biphenyl, styrene and cumene by the tod pathway from Pseudomonas putida F1 was examined in terms of catabolism by the pathway enzymes and the inducibility of the tod operon. F1 cells grown on toluene exhibited oxygen consumption in the presence of the compounds examined. Toluene dioxygenase (TDO) catalyzed the formation of monol, cis-dihydrodiol and triol metabolites from the n-alkylbenzenes tested and the triol formed from n-propylbenzene was metabolized to the derivative, 2-hydroxy-6-oxohexa-2,4-dienoate (HOHD), by subsequent enzymes in the tod pathway. Biotransformation of the tested compounds with toluene-grown F1 cells resulted in the accumulation of ring cleavage HOHD derivatives; the metabolites were inefficiently metabolized by cell extracts of toluene-grown F1 cells, indicating that 6-methyl-HOHD hydrolase encoded by todF might be a determinant for the further degradation of the selected 1-substituted benzenes. The results obtained from enzyme activity assays and reverse transcription polymerase chain reaction (RT-PCR) showed that not only growth-supporting substrates, but also n-propylbenzene, styrene and cumene act as inducers of the tod operon. Journal of Industrial Microbiology & Biotechnology (2000) 25, 163–170.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-6903
    Keywords: Alzheimer-disease ; genetic risk factors ; apolipoprotein E ; alleles ; α-1-antichymotrypsin ; VLDLR ; multiple comparisons
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The Apolipoprotein E4 allele (Apo-ε4) is the major susceptibility gene for late onset Alzheimer Disease (AD) but epidemiological data suggest that the effect of this allele is modified in different individuals by genetic or environmental factors. Age and head injury are major non-genetic factors modifying the Apo-ε4 risk. There is conflicting data as to whether alleles of other chaperon proteins (such as alpha-1-antichymotrypsin (ACT)) or Apo-ε4 receptors (such as the VDRL receptor) modify the Apo-ε4 risk for AD. We analyze problems posed by genetic association studies including those of multiple comparisons and selection of controls, the latter problem exacerbated by the wide variations in Apolipoprotein E allele frequencies observed in different groups and localities.
    Type of Medium: Electronic Resource
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