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- W1561566187 endingPage "2458" @default.
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- W1561566187 abstract "Abstract Deoxygenation of sickle cells is known to increase cation permeabilities (Na+, K+, and Ca2+). The possible mechanisms involved in the increased uptake of Ca2+ were investigated: activation of Ca2+ channels, involvement of the anion channel, and the formation of endocytic vacuoles. The Ca2+ channel blocker nifedipine reduced the deoxy-stimulated Ca2+ uptake by about 30% to 40%. The anion channel inhibitor DIDS (4,4′ diisothiocyanate stilbene 2,2′ disulfonate) inhibited the deoxy-stimulated Ca2+ uptake by approximately 50%. Maximal possible endocytic uptake, measured by using an impermeant marker ([3H] inuline), accounted for 6% to 9% of the total Ca2+ uptake. These data indicate that the deoxygenation-induced increase in Ca2+ permeability could result from both the activation of a Ca2+ channel and of a transport system for cations involving interactions between polymerized hemoglobin S, band 3 and other membrane components. Endocytosis appears to play only a minor role in the Ca2+ uptake of deoxygenated sickle cells." @default.
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- W1561566187 date "1990-06-15" @default.
- W1561566187 modified "2023-10-14" @default.
- W1561566187 title "Ca2+ permeability in deoxygenated sickle cells" @default.
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- W1561566187 doi "https://doi.org/10.1182/blood.v75.12.2453.2453" @default.
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