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1 hN-P-Man-Man-(EthN-P)Man-GlcN attached to an inositol phospholipid.
2 naceous matrix, cytoskeletal components, and inositol phospholipids.
3 y removing phosphate from the D3 position of inositol phospholipids.
4 ore protein with a cationic motif that binds inositol phospholipids.
5 all implicated in the remodeling of membrane inositol phospholipids.
6 anding of the regulation of such proteins by inositol phospholipids.
7 nstream of PI 3-kinase associated changes in inositol phospholipids.
8 ar signaling molecules derived from membrane inositol phospholipids.
9 s demonstrate that chemical stress activates inositol phospholipid 3-kinase and glucose transport in
10 In this study, we have investigated whether inositol phospholipid 3-kinase is activated by chemical
11 l responses of these cells the activation of inositol phospholipid 3-kinase is not responsible for th
12 ving a PtdIns-specific, wortmannin-sensitive inositol phospholipid 3-kinase may be required to suppor
13 have attempted to assess the basis by which inositol phospholipid 3-kinase may participate in the re
15 senite induced rapid activation (< 2 min) of inositol phospholipid 3-kinase with an approximately fou
16 hatase with specificity for 3-phosphorylated inositol phospholipids, accompany progression of brain t
17 tested the kinase in the presence of several inositol phospholipids and found that only low micromola
19 orm an "intermolecular" PH domain that binds inositol phospholipids and is required for ion channel l
20 in to generate a series of 3' phosphorylated inositol phospholipids and tested whether any of these l
21 ed intracellular levels of 3' phosphorylated inositol phospholipids and the induction of signaling re
23 in Dictyostelium, the hydrocarbon chains of inositol phospholipids are a highly selected subset of t
25 hatidylinositols, suggesting that endogenous inositol phospholipids are required for the activation o
27 lly ablates the ability of PTEN to recognize inositol phospholipids as a substrate, suggesting that l
28 n fluorescent protein, which translocates to inositol phospholipids at the leading edge of cells duri
29 re are several recently reported examples of inositol phospholipids binding to pleckstrin homology (P
31 ents have established that the metabolism of inositol phospholipids by phosphoinositide 3-kinases (PI
32 in 2A to mitochondria and that modulation of inositol phospholipids by synaptojanin 2A may play a rol
33 auses phospholipase C-mediated hydrolysis of inositol phospholipids, calcium mobilization, and activa
36 tide receptors (P2UR or P2Y2R) that activate inositol phospholipid hydrolysis and Ca24 mobilization i
37 adioligand binding and by agonist-stimulated inositol phospholipid hydrolysis and intracellular Ca2+
38 educed M1-muscarinic receptor stimulation of inositol phospholipid hydrolysis in 1321N1 astrocytoma c
41 Our data indicate the involvement of IP3 and inositol phospholipids in both short- and long-term resp
43 phogrin is able to dephosphorylate specific inositol phospholipids, including phosphatidylinositol (
46 gest that the production of 3-phosphorylated inositol phospholipids is involved in the activation of
47 dSer by choline, ethanolamine, glycerol, and inositol phospholipids markedly inhibits PtdSer transfer
48 This effect is accompanied by alterations in inositol phospholipid metabolism and inositol auxotrophy
49 binding proteins, heterotrimeric G proteins, inositol phospholipid metabolism, and protein serine/thr
50 gest that PI(20:4/20:4) is a novel bioactive inositol phospholipid molecule that regulates innate imm
53 that only partially inhibited hydrolysis of inositol phospholipids or release of secretory granules.
56 up of protein tyrosine phosphatases that use inositol phospholipids, rather than phosphoproteins, as
57 ns have been found to interact in vitro with inositol phospholipids; recent experiments show that the
60 c stimulation triggers activation of Src and inositol-phospholipid signalling, which polarizes in the
61 r molecules, including adenylyl cyclases and inositol-phospholipid-specific phospholipase C (PLC)1-3.
64 hospholipases of the C type, which hydrolyze inositol phospholipids to yield inositol trisphosphate a
65 n mutant syk gene failed to elicit increased inositol phospholipid turnover after EMF exposure, where
67 alanin and other galanin analogues increased inositol phospholipid turnover and intracellular calcium
68 normal EMF response, whereas no increase in inositol phospholipid turnover in response to EMF was no
69 s responsible for EMF-induced stimulation of inositol phospholipid turnover, and its SH2 domains are
72 elated to changes in both ubiquitination and inositol phospholipids, we have examined whether GLUT4 t
73 r the interaction of inositol phosphates and inositol phospholipids with syndecan-4 could regulate PK
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