TY - JOUR
T1 - Inhibition of phosphatases and increased Ca2+ channel activity by inositol hexakisphosphate
AU - Larsson, Olof
AU - Barker, Christopher J.
AU - Sjöholm, Åke
AU - Carlqvist, Håkan
AU - Michell, Robert H.
AU - Bertorello, Alejandro
AU - Nilsson, Thomas
AU - Honkanen, Richard E.
AU - Mayr, Georg W.
AU - Zwiller, Jean
AU - Berggren, Per Olof
PY - 1997/10/17
Y1 - 1997/10/17
N2 - Inositol hexakisphosphate (InsP6), the dominant inositol phosphate in insulin-secreting pancreatic β cells, inhibited the serine-threonine protein phosphatases type 1, type 2A, and type 3 in a concentration-dependent manner. The activity of voltage-gated L-type calcium channels is increased in cells treated with inhibitors of serine-threonine protein phosphatases. Thus, the increased calcium channel activity obtained in the presence of InsP6 might result from the inhibition of phosphatase activity. Glucose elicited a transient increase in InsP6 concentration, which indicates that this inositol polyphosphate may modulate calcium influx over the plasma membrane and serve as a signal in the pancreatic β cell stimulus-secretion coupling.
AB - Inositol hexakisphosphate (InsP6), the dominant inositol phosphate in insulin-secreting pancreatic β cells, inhibited the serine-threonine protein phosphatases type 1, type 2A, and type 3 in a concentration-dependent manner. The activity of voltage-gated L-type calcium channels is increased in cells treated with inhibitors of serine-threonine protein phosphatases. Thus, the increased calcium channel activity obtained in the presence of InsP6 might result from the inhibition of phosphatase activity. Glucose elicited a transient increase in InsP6 concentration, which indicates that this inositol polyphosphate may modulate calcium influx over the plasma membrane and serve as a signal in the pancreatic β cell stimulus-secretion coupling.
UR - http://www.scopus.com/inward/record.url?scp=0030667979&partnerID=8YFLogxK
U2 - 10.1126/science.278.5337.471
DO - 10.1126/science.278.5337.471
M3 - Article
C2 - 9334307
AN - SCOPUS:0030667979
SN - 0036-8075
VL - 278
SP - 471
EP - 474
JO - Science
JF - Science
IS - 5337
ER -