An inositol tetrakisphosphate-containing phospholipid in activated neutrophils

@article{TraynorKaplan1988AnIT,
  title={An inositol tetrakisphosphate-containing phospholipid in activated neutrophils},
  author={A. Traynor-Kaplan and Anna L. Harris and Barbara Thompson and Palmer Taylor and Larry A. Sklar},
  journal={Nature},
  year={1988},
  volume={334},
  pages={353-356}
}
Inositol (l,4,5)trisphosphate (InsP3)1 and tetrakisphosphate (InsP4)2 have been observed in a variety of cell types and have been proposed to play roles in the receptor-mediated rise in intracellular Ca2+ (refs 2, 3). Recently, they have been shown to act synergistically in the activation of a Ca2+-dependent K+ channel in lacrimal acinar cells3. InsP3 is the product of phospholipase C (PLC) action on phosphatidylinositol 4,5-bisphosphate (PtdInsP2), whereas InsP4 is believed to arise from… Expand
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Synergism of inositol trisphosphate and tetrakisphosphate in activating Ca2+-dependent K+ channels
TLDR
It is shown that neither Ins P3 alone nor Ins P4 alone can activate a sustained current, whereas inositol 1,3,4,5-tetrakisphosphate in combination in combination evoke a sustained increase in Ca2+-activated K+ current which is dependent on external Ca2+. Expand
Type I phosphatidylinositol kinase makes a novel inositol phospholipid, phosphatidylinositol-3-phosphate
TLDR
It is proposed that type I Ptdlns kinase is responsible for the generation of PtdIns(3)P in intact cells, and that this novel phosphoinositide could be important in the transduction of mitogenic and oncogenic signals. Expand
The inositol tris/tetrakisphosphate pathway—demonstration of Ins(l,4,5)P3 3-kinase activity in animal tissues
TLDR
It is suggested that an inositol tris/tetrakisphosphate pathway exists as an alternative route to the dephosphorylation10,11 of Ins(l,4,5)P3 3-kinase and the function of this novel pathway is unknown. Expand
Release of Ca2+ from a nonmitochondrial intracellular store in pancreatic acinar cells by inositol-1,4,5-trisphosphate
TLDR
It is reported here that micromolar concentrations of Ins1,4,5P3 release Ca2+ from a nonmitochondrial intracellular Ca2- store in pancreatic acinar cells, and the results strongly suggest that this is the same Ca1+ store that is released by acetylcholine. Expand
L-myo-inositol 1,4,5,6-tetrakisphosphate is present in both mammalian and avian cells.
TLDR
The data are consistent with rapid PAF-sensitive synthesis of D-myo-[3H]inositol 1,3,4,5-tetrakisphosphate in macrophages, and demonstrate that L- myo-inositoli 1, 4,5,6-tentrakisPhosphate is synthesized in both mammalian and avian cells. Expand
Inositol tetrakis- and pentakisphosphates in GH4 cells.
TLDR
Here it is confirmed the existence of InsP4 in a pituitary cell line (GH4 cells) and described, in addition, the exist of both inositol pentakisphosphate (InsPs) and inositols hexakisph phosphate (insP6, phytic acid) and changes in these various inositl phosphates following stimulation with thyrotropin-releasing hormone (TRH). Expand
Metabolism of inositol 1,3,4-trisphosphate to a new tetrakisphosphate isomer in angiotensin-stimulated adrenal glomerulosa cells.
TLDR
The results have demonstrated that the dephosphorylation sequence of Ins-1,4,5-P3 metabolism is accompanied by a complex cycle of higher phosphorylations with formation of new intermediates of potential significance in cellular regulation. Expand
Micro-injection of inositol 1,3,4,5-tetrakisphosphate activates sea urchin eggs by a mechanism dependent on external Ca2+.
TLDR
Results show that inositol 1,3,4,5-tetrakisphosphate is an intracellular second messenger, and suggest that its function is to control cellular Ca2+ homoeostasis at the plasma membrane. Expand
Receptor-mediated activation of electropermeabilized neutrophils. Evidence for a Ca2+- and protein kinase C-independent signaling pathway.
TLDR
Results suggest that a third signaling pathway, distinct from changes in [Ca2+]i and activation of protein kinase C, is involved in the response of neutrophils to chemoattractants. Expand
Comparison of the roles of calmodulin and protein kinase C in activation of the human neutrophil respiratory burst.
TLDR
The inability of TFP and W-7 to inhibit superoxide anion generation in response to submaximal stimulatory doses of FMLP or PMA suggests that calmodulin-independent processes may be involved in activation of the respiratory burst. Expand
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