By. Kim et al., pp60(v-src) reactivation inhibits serum-induced accumulation of inositol phosphates and phosphatidylethanol in tsNRK, IUBMB LIFE, 48(1), 1999, pp. 85-89
In tsRSV-infected NRK (tsNRK) cells, pp60(v-src) reactivation bytemperature
-shift from a nonpermissive temperature, 39 degrees C, to a permissive one,
32 degrees C, induced the production of inositol phosphates (IPt) and phos
phatidylethanol (PEt), This was accompanied by an increase in membrane-asso
ciated protein kinase C (PKC) activity in the absence of exogenous growth f
actors. However, with serum-stimulation, the amounts of IPt and PEt at 32 d
egrees C were less than those at 39 degrees C, Pretreatment with PKC inhibi
tors, Re-31-8220 and staurosporine, enhanced the accumulation of IPt but no
t of PEt at 32 degrees C. The tyrosine phosphorylation of phospholipase C g
amma 1 (PLC gamma 1) was increased either by serum or by pp60(v-src) reacti
vation. These results suggest that serum transduces its signal through PLC
gamma 1 mediation, and that pp60(v-src), possibly through the PKC mediation
, negatively affects serum-induced PLC gamma 1 activation.