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RX871024 induces Ca...
RX871024 induces Ca2+ mobilization from thapsigargin-sensitive stores in mouse pancreatic beta-cells
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Efanova, IB (author)
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- Zaitsev, SV (author)
- Karolinska Institutet
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Brown, G (author)
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- Berggren, PO (author)
- Karolinska Institutet
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Efendic, S (author)
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(creator_code:org_t)
- American Diabetes Association, 1998
- 1998
- English.
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In: Diabetes. - : American Diabetes Association. - 0012-1797 .- 1939-327X. ; 47:2, s. 211-218
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https://doi.org/10.2...
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Abstract
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- The effects of RX871024, a compound with an imidazoline structure, on cytoplasmic-free Ca2+ concentration ([Ca2+]i) in mouse pancreatic β-cells were studied. RX871024 modulates [Ca2+]i; by at least two mechanisms. One mechanism involves closure ofATPregulated K+ channels, resulting in membrane depolarization, opening of voltage-gated L-type Ca2+ channels, and a subsequent increase in [Ca2+]i. Another mechanism, reported here for the first time, deals with RX871024-induced mobilization of Ca2+ from nonmitochondrial thapsigargin-sensitive intracellular stores. Reduced glutathione, inhibitors of cytochrome P-450, and monoaminooxidases A and B blocked this Ca2+ mobilization. It is concluded that the mechanism of RX871024-induced Ca2+ mobilization from intracellular stores involves changes in the oxidation/reduction state of the pancreatic β-cell and may be controlled by cytochrome P-450.
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