Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P10636 (tau protein)
 5,110 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The entry of Theileria parva sporozoites into bovine lymphocytes occurs rapidly and involves a defined series of events. In the present study the role of calcium in sporozoite entry was examined. Depletion of Ca2+ from the external medium had little effect on sporozoite entry suggesting that the initial sporozoite-host cell interaction is a Ca(2+)-independent process. Sporozoite entry could, however, be inhibited by a range of Ca2+ channel blockers (verapamil, nicardipine, diltiazem) and calmodulin antagonists (TPF, chloropromazine, W7 and calmidazolium). Evidence is also presented that demonstrates that sporozoite entry is dependent on changes in sporozoite cytosolic Ca2+ caused by the release of Ca2+ from intrasporozoite stores. First, reagents that produced an influx of Ca2+ into the parasite (A23187) blocked entry. Second, depletion of intrasporozoite Ca2+ levels (10 microM A23187 + 1.0 mM EGTA) or an increase in the cytoplasmic buffering capacity of the sporozoite cytoplasm (by preloading sporozoites with MAPT/AM) inhibited invasion. Third, sporozoite entry was inhibited by TMB-8 which blocks the release of Ca2+ from intracellular stores. Lastly, treatment of sporozoites with the Ca(2+)-mobilizing agents thapsigargin, cyclopiazonic acid but not InsP3 prevented sporozoite entry. In these cases the premature release of intrasporozoite Ca2+ inhibited sporozoite binding to the host cell surface; sporozoites that bound became internalized at rates comparable to the controls. In contrast, treatment of lymphocytes with these reagents had no significant effect on sporozoite entry. Collectively these results demonstrate that the mobilization of Ca2+ from intrasporozoite stores following sporozoite binding to the host cell surface is essential for successful parasite invasion.
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PMID:Mobilization of intrasporozoite Ca2+ is essential for Theileria parva sporozoite invasion of bovine lymphocytes. 854 93

Nitric oxide (NO.) can induce transient [Ca2+] changes in endothelial cells not different from receptor mediated signalling. Whether this Ca2+ signal may provide a link with IL-8 secretion induced by NO. donors was investigated in human endothelial cells. Sodium nitroprusside (SNP) and S-nitroso-N-acetyl-DL-penicillamine (SNAP) dose dependently increased IL-8 production in this cell type. Additive IL-8 secretion was found with TNFalpha. Buffering intracellular Ca2+ with MAPT/AM suppressed NO. induced [Ca2+]i changes and reduced subsequent IL-8 secretion. The additive effect of both NO. donors on TNFalpha induced IL-8 secretion was completely blocked in the presence of MAPT/AM. SKF 96365, which has been shown to block receptor mediated Ca2+ entry, and TMB-8, which blocks intracellular Ca2+ release, both inhibited IL-8 secretion, particularly when TNFalpha was used as a costimulator, indicating that [Ca2+]i changes are important components of IL-8 induction by NO..
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PMID:Intracellular Ca2+ dependence of nitric oxide mediated enhancement of interleukin-8 secretion in human endothelial cells. 935 Sep 89