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1 ger assays (carbachol-induced stimulation of phosphatidylinositol hydrolysis).
2 but seem to differ in functional coupling to phosphatidylinositol hydrolysis.
4 lls, leading to the loss of both BCR-coupled phosphatidylinositol hydrolysis and calcium mobilization
6 sistant to internalization, mediated greater phosphatidylinositol hydrolysis and sustained Ca(2+) mob
7 e of the strength of signaling (i.e. greater phosphatidylinositol hydrolysis and sustained Ca(2+) mob
9 eta-arrestin2 reduced angiotensin-stimulated phosphatidylinositol hydrolysis but paradoxically increa
10 engage several signaling pathways, including phosphatidylinositol hydrolysis, calcium mobilization, a
11 n, via Gi (EP3 receptors); and activation of phosphatidylinositol hydrolysis (EP1 receptor), via one
12 ins of phospholipase Cy and couples FGFR1 to phosphatidylinositol hydrolysis in several cell types.
13 that the activation of FP receptors leads to phosphatidylinositol hydrolysis, intracellular calcium r
14 ch as the inhibition of carbachol-stimulated phosphatidylinositol hydrolysis, on selected analogues c
15 e M3 receptor and may consist of products of phosphatidylinositol hydrolysis, other than inositol tri
16 fferentiated cells, although ET-1 stimulated phosphatidylinositol hydrolysis to a similar degree in b
17 t the efficacy of epinephrine in stimulating phosphatidylinositol hydrolysis was reduced 35-fold at t
18 y alpha(2A)ARs and G(q/11)- or G(i)-mediated phosphatidylinositol hydrolysis was unaffected, indicati
19 class (biochemical response: stimulation of phosphatidylinositol hydrolysis), whereas the V2 vasopre
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