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  • Adenylate cyclase activity  (1)
  • CA-repeat marker  (1)
  • 1
    ISSN: 1432-136X
    Schlagwort(e): Melanosome aggregation ; Signal transduction ; Adenylate cyclase activity ; Second messenger ; Fish, Carassius auratus
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin
    Notizen: Abstract The signal-transduction system that mediates the melanosome-aggregating response in melanophores of the black-moor goldfish, Carassius auratus, was investigated by examining the inhibition of adenylate cyclase activity mediated by α-adrenoceptors in cultured cells. When the melanophores were incubated with 1 mmol·l-1 3-isobutyl-1-methylxanthine for 5 min, the intracellular level of cyclic adenosine-3′,5′-monophosphate increased two- to three-fold. Norepinephrine at 100 nmol·l-1 and naphazoline at 1 μmol·l-1 inhibited the 3-isobutyl-1-methylxanthine-induced accumulation of cyclic adenosine-3′,5′-monophosphate in the cells in both the presence and the absence of isoproterenol, a β-adrenergic agonist. Methoxamine and phenylephrine also reduced the extent of accumulation of cyclic adenosine-3′,5′-monophosphate, but only when they were present at relatively high concentrations (above 100 μmol·l-1). The range of concentrations at which norepinephrine inhibited the accumulation of cyclic adenosine-3′,5′-monophosphate was consistent with the range at which it induced the aggregation of melanosomes. Pretreatment of the cells with pertussis toxin (1 μg·ml-1) for 15 h or treatment with 100 nmol·l-1 yohimbine (an α2-adrenergic antagonist) inhibited the effects of the α-adrenergic agonists on both the aggregation of melanosomes and the 3-isobutyl-1-methylxanthine-induced accumulation of cyclic adenosine-3′,5′-monophosphate, but prazosin (an α1adrenergic antagonist) at 100 nmol·l-1 was not inhibitory. These results indicate that the melanosome-aggregating response of the goldfish melanophore is induced mainly via inhibition of the activity of adenylate cyclase, which occurs as result of stimulation of a pathway that involves α1adrenergic and a inhibitory GTP-binding protein.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    ISSN: 1435-232X
    Schlagwort(e): Key words Mesomelic dysplasia Kantaputra type ; CA-repeat marker ; Linkage analysis ; Logarithm of odds (lod) score ; Haplotype analysis ; Human HOXD genes
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Biologie , Medizin
    Notizen: Abstract Mesomelic dysplasia Kantaputra type (MDK) (MIM *156232) is a new autosomal dominant skeletal dysplasia characterized by dwarfism, shortening of the forearms/lower-legs, carpal/tarsal synostosis, and dorsolateral foot deviation. We studied a Thai family in which 15 members in 3 generations were affected with MDK. With reference to the breakpoints of a balanced translocation [t(2;8)(q31;p21)] in patients from a previously reported Italian family with a skeletal dysplasia that appears similar to MDK, a linkage analysis was performed in the Thai family using 50 CA-repeat markers mapped to nearby regions (2q22-q34 and 8p24-p21) of the translocation breakpoints. The results clearly ruled out a linkage of MDK to marker loci at the 8p24-p21 region, whereas all nine affected members available for the study shared a haplotype at four loci (D2S2284, D2S326, D2S2188, and D2S2314) spanning about 22.7 cM in the 2q24-q32 region. The computer-assisted two-point linkage analysis revealed maximum logarithm of odds (lod) scores of 4.82, 4.21, 4.82, and 4.21 (θ = 0) at these loci, respectively. These data indicated that the MDK locus is in the vicinity of D2S2284 and D2S2188 loci that are most likely mapped to 2q24-q32.
    Materialart: Digitale Medien
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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