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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Signaling pathway other than phosphatidylinositol turnover is responsible for constant expression of c-myc gene in primary cultures of rat hepatocytes.

We investigated signal transduction pathways involved in c-myc activation, using rat hepatocytes in primary culture. c-Myc mRNA was constantly expressed in the cultured hepatocytes regardless of the conditions present. When the expression was examined in the presence of various agents modulating intracellular signals, isoflavonoids (genistein, psi-tectorigenin, and orobol) significantly decreased c-myc mRNA levels, in a dose dependent manner. However, genistein did not decrease Li+ induced inositol phosphate accumulation using [3H]inositol-labeled cultured hepatocytes. In addition, we have shown that these isoflavonoids increase cytoplasmic free Ca2+, when measured using aequorin-loaded hepatocytes. In light of these observations, the persistent basal level of c-myc expression seems to be maintained by mechanisms other than phosphatidylinositol turnover.[1]

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