Phospholipid signaling

@article{Divecha1995PhospholipidS,
  title={Phospholipid signaling},
  author={Nullin Divecha and Robin F. Irvine},
  journal={Cell},
  year={1995},
  volume={80},
  pages={269-278}
}
Ten years ago, describing what is new in phospholipid signaling in ten pages of Cell would have been easy; it would have been essentially a summary of the phosphoinositidase C (PIC) story: phosphatidylinositol(4,5)bisphosphate (Ptdlns(4,5)P2) hydrolysis to inositiol(1,4,5)trisphosphate (Ins(1",4,5)P3), with the synergistic action of Ca 2÷ (mobilized by Ins(1,4,5)P3) and diacylglycerol (DAG) on protein kinase C (PKC) (Table 1). As will become obvious below, the involvement of phospholipids in… Expand
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TLDR
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TLDR
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TLDR
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TLDR
The structural organization, enzymatic properties and molecular diversity of PLC splicing variants are discussed and functional and physiological roles of each isozyme are studied. Expand
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The results suggest that PIS accelerates G1 progression and stimulates growth by increasing cellular levels of cyclins D1 and E. Expand
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TLDR
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References

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PtdIns(4,5)P2 serves as a precursor of a diverse family of signalling molecules, including diacylglycerol (and hence phosphatidic acid), Ins(1,4,5)P3 [and hence Ins(1,3,4,5)P4] and PtdIns(3,4,5)P3.Expand
Phosphatidylinositol 3,4,5-trisphosphate is formed from phosphatidylinositol 4,5-bisphosphate in thrombin-stimulated platelets.
TLDR
Findings point to the activation of phosphoinositide 3-kinase as a critical receptor-regulated step in thrombin-stimulated platelets. Expand
Characterization of a phosphatidylinositol-specific phosphoinositide 3-kinase from mammalian cells
TLDR
A distinct PtdIns-specific phosphoinositide 3-kinase activity in mammalian cells is characterized, which is resistant to the drug wortmannin and uses only PTDIns as a substrate in vitro; it therefore has the capacity to generate Ptdins 3-phosphate specifically. Expand
Pathway for the formation of D-3 phosphate containing inositol phospholipids in intact human platelets.
TLDR
During 32P labeling and after thrombin stimulation of human platelets, as much as 60% of the total radioactivity present in PtdIns(3,4)P2 was found in the D-4 phosphate and only 35% in theD-3 phosphate indicating that Ptd insurance(3)P is the precursor of Ptd Insurance (3, 4)P 2, which defines the predominant pathway for synthesis of these lipids in platelets. Expand
Phosphatidylinositol 3‐kinase
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  • Biology, Medicine
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TLDR
The homology of the yeast vps34 with the mammalian phosphatidylinositol 3‐kinase has suggested a role for this pathway in vesicular trafficking, and the 3‐phosphoinositide pathway has been implicated in growth factor‐dependent mitogenesis, membrane ruffling and glucose uptake. Expand
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Cell locomotion and changes in cell structure initiated by the binding of extracellular ligands to transmembrane receptors are generally accompanied by a transient increase in cytoplasmic Ca2+Expand
Specific interaction between phosphatidylinositol 4,5-bisphosphate and profilactin
TLDR
It is demonstrated here that isolated profilin, as well as the profilactin complex, interacts with anionic phospholipids, suggesting the possibility of a relationship between the induction of actin filament formation and the increased activity in the phosphatidylinositol cycle seen as a result of ligand–receptor interactions in various systems. Expand
Platelet-derived growth factor stimulates synthesis of Ptdlns(3,4,5)P3 by activating a Ptdlns(4,5)P2 3-OH kinase
TLDR
It is shown that the key step in the synthesis of 3-phosphorylated inositol lipids in 3T3 cells stimulated by platelet-derived growth factor is the activation of a phosphatidylinositol(4,5)-bisphosphate (3)-hydroxy (PtdIns( 4,5)P2 3-OH) kinase. Expand
Activation of phosphoinositide 3-kinase is required for PDGF-stimulated membrane ruffling
TLDR
It is argued strongly that phosphatidylinositol (3,4,5)-trisphosphate synthesis is required for growth-factor-stimulated membrane ruffling in porcine aortic endothelial cells, and synthesis of this lipid may be part of a signalling pathway leading to direct or indirect activation of the small GTP-binding protein Rac. Expand
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TLDR
It is shown that neomycin, a drug which has a high affinity for phosphoinositides and in vivo interferes with the PI cycle, inhibits the polymerization of actin in platelets induced either by thrombin or by ADP. Expand
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