ArticleThe Biochemical journal2000
Rapid activation and partial inactivation of inositol trisphosphate receptors by adenophostin A.
Article in The Biochemical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Reliable measurement of free CaCell calcium · 2020Article
- Inositol 1,4,5-trisphosphate receptor 1 degradation in mouse eggs and impact on [Ca2+]i oscillations.Journal of cellular physiology · 2010Article
- Inositol trisphosphate receptor and ion channel models based on single-channel data.Chaos (Woodbury, N.Y.) · 2009Article
- A kinetic model of the inositol trisphosphate receptor based on single-channel data.Biophysical journal · 2009Article
- Regulation of single inositol 1,4,5-trisphosphate receptor channel activity by protein kinase A phosphorylation.The Journal of physiology · 2008Article
- Inositol trisphosphate receptor Ca2+ release channels.Physiological reviews · 2007Review
- Graded recruitment and inactivation of single InsP3 receptor Ca2+-release channels: implications for quantal [corrected] Ca2+release.The Journal of physiology · 2006Article
- Determinants of adenophostin A binding to inositol trisphosphate receptors.The Biochemical journal · 2002Article
- Regulation of nuclear pore complex conformation by IP(3) receptor activation.Biophysical journal · 2002Article
- Adenophostin A and ribophostin, but not inositol 1,4,5-trisphosphate or manno-adenophostin, activate the Ca2+ release-activated Ca2+ current, I(CRAC), in weak intracellular Ca2+ buffer.The Biochemical journal · 2002Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Adenophostin A, the most potent known agonist of inositol 1,4, 5-trisphosphate (InsP(3)) receptors, stimulated (45)Ca(2+) release from the intracellular stores of permeabilized hepatocytes. The concentration of adenophostin A causing the half-maximal effect (EC(50)) was 7.1+/-0.5 nM, whereas the EC(50) for InsP(3) was 177+/-26 nM; both responses were positively co-operative. In rapid superfusion analyses of (45)Ca(2+) release from the intracellular stores of immobilized hepatocytes, maximal concentrations of adenophostin A or InsP(3) evoked indistinguishable patterns of Ca(2+) release. The Ca(2+) release evoked by both agonists peaked at the same maximal rate after about 375 ms and the activity of the receptors then decayed to a stable, partially (60%) inactivated state with a half-time (t(1/2)) of 318+/-29 ms for adenophostin A and 321+/-22 ms for InsP(3). Dissociation rates were measured by recording rates of InsP(3)-receptor channel closure after rapid removal of agonist. The rate of adenophostin A dissociation (t(1/2), 840+/-195 ms) was only 2-fold slower than that of InsP(3) (t(1/2), 436+/-48 ms). We conclude that slow dissociation of adenophostin A from InsP(3) receptors does not underlie either its high-affinity binding or the reported differences in the Ca(2+) signals evoked by InsP(3) and adenophostin A in intact cells.
Indexed as
Identifiers
11104705PMC1221536What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.