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  • Rifamycin-resistance  (1)
  • c-met  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 204 (1986), S. 192-194 
    ISSN: 1617-4623
    Keywords: Rifamycin-resistance ; Mu-mutagenesis ; rpoB gene ; RNA polymerase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary A new class of rifamicin-resistant mutants of Escherichia coli was obtained by lysogenic insertions of bacteriophage Mu Amp DNA. Rifamycin resistance is closely linked to the ampicillin resistance conferred by the prophage. Mapping by conjugation with auxotrophic markers revealed that the rifamycin-resistant mutations are located between 28 and 37 min on the E. coli chromosome standard map, some distance from the rpoB gene at 89.5 min. The DNA-dependent RNA polymerase of these mutants is highly sensitive to rifampicin.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1573-7276
    Keywords: B16 melanoma ; c-met ; HGF/SF ; liver metastasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Metastasis to the liver is a frequent event in clinical oncology, the molecular mechanisms of which are not fully understood. We have recently reported a consistent overexpression of c-met in B16 melanoma cells selected in vivo for enhanced liver metastatic ability. In this study we address the question as to whether constitutive activation of c-met is a necessary and sufficient condition for enhanced liver colonization B16 melanoma cells. Different levels of c-met expression and/or activation in B16 cells were achieved subcloning, or by c-DNA transfection with either HGF/SF or the oncogenic form of c-met (tpr-met). Metastatic ability of the different populations was then evaluated in vivo by the lung colonization (experimental metastasis) assay. Results indicate that c-met (but not tpr-met) activation in B16 melanoma cells may increase their liver colonizing potential, probably by enhancing motility and invasion in response paracrine interactions with its ligand. C-met expres sion per se, however, is not able to change the organ specificity of the cells. C-met activation appears instead to be required at later stages of liver colonization by B16 melanoma cells, in order to enhance their site-specific metastatic ability. © Rapid Science 1998
    Type of Medium: Electronic Resource
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