Table 1.

Effect of PKC activation and inhibition on the AVP- or thapsigargin-induced IP3R1 redistribution

ConditionPerinucleary localized IP3R1 (% of cells)
Control 74.3±3.1 
AVP (3 μM) 21.3±1.3* 
OAG (50 μM) 31.0±8.1* 
Staurosporine (200 nM) 84.0±2.0 
Staurosporine (200 nM) + AVP (3 μM) 75.7±4.5 
Staurosporine (200 nM) + thapsigargin (1 μM) 78.7±3.5 
Bisindolylmaleimide I hydrochloride (100 nM) 71.3±2.4 
Bisindolylmaleimide I hydrochloride (100 nM) + AVP (3 μM) 52.7±0.9* 
Gö-6976 (0.5 μM) 74.7±3.7 
Gö-6976 (0.5 μM) + AVP (3 μM) 53.3±1.8* 
ConditionPerinucleary localized IP3R1 (% of cells)
Control 74.3±3.1 
AVP (3 μM) 21.3±1.3* 
OAG (50 μM) 31.0±8.1* 
Staurosporine (200 nM) 84.0±2.0 
Staurosporine (200 nM) + AVP (3 μM) 75.7±4.5 
Staurosporine (200 nM) + thapsigargin (1 μM) 78.7±3.5 
Bisindolylmaleimide I hydrochloride (100 nM) 71.3±2.4 
Bisindolylmaleimide I hydrochloride (100 nM) + AVP (3 μM) 52.7±0.9* 
Gö-6976 (0.5 μM) 74.7±3.7 
Gö-6976 (0.5 μM) + AVP (3 μM) 53.3±1.8* 

A7r5 cells were incubated for 5 hours with the PKC activator OAG alone or with different PKC inhibitors in the presence of AVP (3 μM) or thapsigargin(1 μM). The percentages of cells with IP3R1 localized in the perinuclear region are shown. Each result is the mean±s.e.m. from three independent experiments.

*

Significantly different from the control.

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