Effects of Adenophostin-A and Inositol-1,4,5-trisphosphate on Cl − Currents in Xenopus laevis Oocytes
Molecular Pharmacology, ISSN: 0026-895X, Vol: 51, Issue: 4, Page: 683-692
1997
- 30Citations
- 8Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations30
- Citation Indexes30
- 30
- CrossRef27
- Captures8
- Readers8
Article Description
Adenophostin-A, a novel compound isolated from cultures of Penicillium brevicompactum, has been shown to stimulate Ca 2+ release from inositol-1,4,5-trisphosphate (IP 3 )-sensitive Ca 2+ stores in microsomal preparations, permeabilized cells, and lipid vesicles containing purified IP 3 receptor. The purpose of the current study was to compare the effects of adenophostin-A and IP 3 on Ca 2+ release from stores and Ca 2+ influx in intact Xenopus laevis oocytes. Ca 2+ influx though store-operated Ca 2+ channels and Ca 2+ release from stores were monitored by measuring two Ca 2+ -activated Cl − currents that can be used as real-time indicators of Ca 2+ release and Ca 2+ influx (I Cl-1 and I Cl-2, respectively). We find that high concentrations (final intraoocyte concentrations of 5–10 μ m ) of adenophostin-A and IP 3 stimulate a large Ca 2+ release from stores (as measured by I Cl-1 ) followed by Ca 2+ influx (as measured by I Cl-2 ). Low concentrations (∼50 n m ) of IP 3 stimulate oscillations in Ca 2+ release without stimulating Ca 2+ influx. In contrast, low concentrations of adenophostin-A can stimulate Ca 2+ influx without stimulating a large Ca 2+ release. However, Ca 2+ influx did not occur in the complete absence of Ca 2+ release. Therefore, it is unlikely that adenophostin-A directly stimulates store-operated Ca 2+ channels. We hypothesize that adenophostin-A releases Ca 2+ from a subpopulation of stores that is tightly coupled to store-operated Ca 2+ channels.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0026895X2413516X; http://dx.doi.org/10.1124/mol.51.4.683; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=0030972573&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/9106635; https://linkinghub.elsevier.com/retrieve/pii/S0026895X2413516X; https://dx.doi.org/10.1124/mol.51.4.683; https://molpharm.aspetjournals.org/content/51/4/683
Elsevier BV
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