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1 binan of LAM is not capped or is capped with inositol phosphate.
2 ed a significantly decreased accumulation of inositol phosphate.
3 yze the conversion of glucose 6-phosphate to inositol phosphate.
4 pairment of signal generation of cAMP and/or inositol phosphate.
5 2)-InsP(4) synthesis without affecting other inositol phosphates.
6 scribed here as a unified approach to access inositol phosphates.
7 (AT(1)) receptor-stimulated accumulation of inositol phosphates.
8 iciently modulate intercellular signaling by inositol phosphates.
9 CH(3) and were accompanied by an increase in inositol phosphates.
10 nd the synthesis and functions of the higher inositol phosphates.
11 yme that generates a series of water-soluble inositol phosphates.
12 interference decreases the amounts of these inositol phosphates.
13 tive activity allowing for its regulation by inositol phosphates.
14 udies into the cellular activities of higher inositol phosphates.
15 e and utilized as affinity ligands to entrap inositol phosphates.
16 ponsive to hCG with respect to production of inositol phosphates.
17 icity for the phosphate at the 3 position of inositol phosphates.
18 , including bilayers containing phosphatidyl inositol phosphates.
19 ly generates PIP(3) as well as water soluble inositol phosphates.
20 ls by determining the accumulation of [(3)H]-inositol phosphates ([(3)H]-IPs) by anion-exchange chrom
21 Rab1 significantly attenuated AT1R-mediated inositol phosphate accumulation and ERK1/2 activation an
22 alphaq/11 protein dissociation and increased inositol phosphate accumulation and GPCR-kinase interact
23 ) receptor agonist, decreased DOI-stimulated inositol phosphate accumulation and increased the phosph
25 kinase, and epidermal growth factor-induced inositol phosphate accumulation and phosphorylation/dese
26 increases such agonist signaling pathways as inositol phosphate accumulation as assessed by either cl
28 reover, PLC-epsilon-dependent stimulation of inositol phosphate accumulation by activation of the epi
30 TPDase1 fusion protein, we quantitated basal inositol phosphate accumulation in cells stably expressi
31 ll GTPases activate PLC-epsilon, we measured inositol phosphate accumulation in COS-7 cells expressin
32 RhoA, RhoB, and RhoC all markedly stimulated inositol phosphate accumulation in PLC-epsilon-expressin
33 ty of either carbachol or AC-42 to stimulate inositol phosphate accumulation or intracellular calcium
34 ned previously in studies of P2Y1-R-promoted inositol phosphate accumulation or platelet aggregation.
35 n COS-7 cells resulted in G protein-promoted inositol phosphate accumulation that was partially rever
36 onhydrolyzable agonist ADPbetaS to stimulate inositol phosphate accumulation was similar, and the EC(
37 ximately 82% impairment) from stimulation of inositol phosphate accumulation while the capacity to in
38 tely 67% desensitization of agonist-promoted inositol phosphate accumulation without significantly af
39 s-encoded US28 GPCR in its ability to induce inositol phosphate accumulation, activate NF-kappaB, and
40 apidly induces signaling events resulting in inositol phosphate accumulation, Ca(2+) mobilization, in
50 es also showed that agonist-stimulated [(3)H]inositol phosphate accumulations were more sustained in
53 ation-dependent increase on both total [(3)H]inositol phosphate and intracellular calcium, and to ind
58 an essential precursor for the production of inositol phosphates and inositol phospholipids in all eu
60 ms involving receptor-mediated generation of inositol phosphates and phosphorylated phosphatidylinosi
62 t as a regulator--potentially explaining why inositol phosphates and their kinases have been found to
63 hexose residue, one hexuronic acid residue, inositol phosphate, and a ceramide moiety with a C18 tri
69 mutation or phosphorylation at this site on inositol phosphate as compared to cAMP signaling was fou
71 yme also accepts a variety of alkyl and aryl inositol phosphates as substrates, making it a suitable
72 ubstrates and monomeric water-soluble cyclic inositol phosphates as well as long-chain PI in bilayer
73 orpromazine significantly lowered all higher inositol phosphates, as well as DIPs, whereas the calmod
74 ic cleavage of aryl and nonhydrophobic alkyl inositol phosphates (beta(lg) = -0.58) indicates that th
75 -fold decrease in the K(m) of the IMPase for inositol phosphates between 75 and 85 degrees C (for l-I
76 lical scaffold in the C-lobe constitutes the inositol phosphate-binding site, which, along with the p
79 ikinase (IPMK) is a central component of the inositol phosphate biosynthetic routes, playing essentia
81 he kindlin-1 PH domain is most likely not an inositol phosphate but another phosphorylated species.
85 , the minerals, total alpha-galactosides and inositol phosphates contents were reduced (>25%) in both
86 l requirements for binding and activation by inositol phosphates, demonstrating that activation requi
89 acid binding affinity of the RSV MA domain, inositol phosphates do not regulate RSV Gag-facilitated
90 f the yeast and plant enzymes, without bound inositol phosphates, do not structurally rationalize HsI
91 2-monophosphate (Ins(2)P1), a member of the inositol phosphate family of compounds, which are import
95 Rab8 expression attenuates mGluR1a-mediated inositol phosphate formation and calcium release from mo
96 the maximum efficacy for 5-HT2AR-stimulated inositol phosphate formation and that the deletion of th
97 rho-TIA reduced maximal NE-stimulated [(3)H]inositol phosphate formation in HEK293 cells expressing
98 for inhibition of norepinephrine-stimulated inositol phosphate formation showed a single low-affinit
100 the alpha1D-AR C terminus markedly decreased inositol phosphate formation stimulated by norepinephrin
104 chromatography step to separate radiolabeled inositol phosphates from radiolabeled inositol, making t
105 with Galpha(q), vav2 impaired G(q)-mediated inositol phosphate generation but not G(s)-mediated cAMP
106 Moreover, the benefit for PTHR-mediated inositol phosphate generation in the absence of vav2 req
109 differences in receptor levels, magnitude of inositol phosphate generation, and dynamics of inositol
110 F-2 in LPA-induced cell migration, invasion, inositol phosphate generation, and nuclear factor-kappaB
115 These data indicate that binding to the inositol phosphate head group is necessary but may not b
117 62, on M1-muscarinic receptor stimulation of inositol phosphate hydrolysis, consistent with a direct
118 exakisphosphate (InsP6) is the most abundant inositol phosphate in cells, yet it remains the most eni
119 hosphate or Ins P6, is the most abundant myo-inositol phosphate in plant cells, but its biosynthesis
120 action, and either inositol in eukaryotes or inositol phosphate in prokaryotes as the acceptor alcoho
121 aling pathway to induce high levels of total inositol phosphates in an agonist-independent manner.
122 stigations aimed at elucidating the roles of inositol phosphates in cellular growth and development i
125 AGS4/G18.1b did not alter the generation of inositol phosphates in COS7 cells cotransfected with the
126 ) domains to bind inositol lipids or soluble inositol phosphates in vitro and to localize to cellular
130 and many recent studies point to a role for inositol phosphates, including InsP(5), InsP(6), and ino
132 Remarkably, high concentrations of soluble inositol phosphates induce dissociation of myo1c(IQ-tail
135 A method for the detection and speciation of inositol phosphates (InsP(n)) in sediment samples was te
136 e for phytase) and appearance of lower-order inositol phosphates (InsP5 -InsP1 ), the hydrolysis prod
139 traction and measurement of all six forms of inositol phosphates (InsPs) in almond meal and brown ski
141 nserved protein that initiates production of inositol phosphate intracellular messengers (IPs), which
143 radioligand-binding and functional assays of inositol phosphate (IP) accumulation and Ca(2+) mobiliza
144 T2A receptors, we found that IL-6 attenuates inositol phosphate (IP) accumulation in response to the
146 t in stimulating 5-HT2C-receptor-coupled [3H]inositol phosphate (IP) formation and calcium mobilizati
148 tution, assays for hormone binding, cAMP and inositol phosphate (IP) induction, and photoaffinity lab
150 The effects of some of these drugs on the inositol phosphate (IP) levels in ciliary processes were
151 erved when pilocarpine was used to stimulate inositol phosphate (IP) metabolism, but not when acetylc
153 d-type (WT) NK3R, with near complete loss of inositol phosphate (IP) signaling, implicating these dom
155 erine myometrial smooth muscle cells induced inositol phosphate (IP) turnover, which was abolished by
157 ing assembly, MA specifically interacts with inositol phosphate (IP)-containing lipids in the plasma
159 CS1, which are involved in the generation of inositol phosphates (IP4, IP5, and inositol pyrophosphat
160 ablished that IP(3) is converted to numerous inositol phosphates (IPs) and pyrophosphates (PP-IPs) th
162 cofactors are added; either nucleic acid or inositol phosphates (IPs) can promote particle assembly.
164 te kinases (IPKs) sequentially phosphorylate inositol phosphates (IPs) to yield a group of small sign
165 mpetition assays confirmed that RSV MA binds inositol phosphates (IPs), but in contrast to HIV-1 GagD
166 g, but the apparent affinity for the soluble inositol phosphate is substantially lower than that for
167 inositol is blocked, and the mass of soluble inositol phosphates is a quantitative readout of recepto
172 witch, inhibiting or stimulating Akt via its inositol phosphate kinase or PI3-kinase activities, resp
174 inase (ITPK1) is a reversible, poly-specific inositol phosphate kinase that has been implicated as a
175 uction of PI(4,5)P(2) by type 1 phosphatidyl inositol phosphate kinase type 1gamma (PIPK1gamma) is th
177 ) through the action of up to six classes of inositol phosphate kinases (IPKs), it is not clear that
178 n mammals and fungi, two distinct classes of inositol phosphate kinases mediate biosynthesis of inosi
181 Plc inhibitor U73122 prevented increases in inositol phosphate levels and blocked progression of cel
182 n this study, we investigated the changes in inositol phosphate levels in alpha-factor-treated S. cer
185 LCbeta2 suppresses elevated basal [Ca2+] and inositol phosphates levels and the sustained agonist-ind
186 tillation proximity assay to measure soluble inositol phosphate mass in cell extracts, thus obviating
187 anonical Galphaq signaling via production of inositol phosphates mediated by each receptor was also r
189 These results contribute to our knowledge of inositol phosphate metabolism and will lay a foundation
190 evelopment for COPD and asthma (genes in the inositol phosphate metabolism pathway and CHRM3) and des
191 ella to stimulate Rho GTPases signalling and inositol phosphate metabolism through alternative mechan
192 Using several yeast mutants with defects in inositol phosphate metabolism, we identify dramatic memb
196 etermined the crystal structure of the yeast inositol phosphate multikinase Ipk2 in the apoform and i
197 monstrated that the human homolog of the rat inositol phosphate multikinase is an inositol 1,3,4,6-te
198 ists of three subgroups, inositol 3-kinases, inositol phosphate multikinases, and inositol hexakispho
199 ly or completely lost the ability to produce inositol phosphate or diacylglycerol messengers after st
200 irions were obtained in vitro by addition of inositol phosphates or phosphatidylinsitol phosphates to
201 ven polyphosphoinositol lipids, more than 30 inositol phosphates), or by the number of functions for
203 tabolism, proteins of the diacylglycerol and inositol phosphate pathways, mitochondrial proteins, his
212 yrotropin-releasing hormone (TRH)-stimulated inositol phosphate production and accelerated internaliz
213 1)gamma(2) inhibits Gbeta(1)gamma(2)-induced inositol phosphate production and Akt activation in COS-
214 e observations, PAR1 and PAR2 stimulation of inositol phosphate production and RhoA activation was bl
215 hat basal and agonist-induced AA release and inositol phosphate production as well as expression of P
216 iased agonist exhibiting partial agonism for inositol phosphate production but essentially full agoni
217 genous beta-arrestins reduced TRH-stimulated inositol phosphate production by 48% (beta-arrestin-1),
218 five-fold higher levels of Ang II-stimulated inositol phosphate production compared to E1,2,3 express
219 urenic acid elicits calcium mobilization and inositol phosphate production in a GPR35-dependent manne
220 in an activation-dependent manner, stimulate inositol phosphate production in a receptor-independent
223 RH) receptor (GnRHR) progressively decreases inositol phosphate production in response to agonist, va
224 or did not elevate cytosolic free calcium or inositol phosphate production in response to angiotensin
225 ion of the LPA(1) or PAR1 receptor increased inositol phosphate production in response to LPA or SFLL
226 t increases in intracellular free Ca(2+) and inositol phosphate production in these cells but did not
227 dent constitutive activity, assessed through inositol phosphate production in transiently or stably t
228 ositide-specific phospholipase C pathway but inositol phosphate production is stimulated by growth-re
229 intact HEK293 cells and completely inhibited inositol phosphate production stimulated by H1HR, wherea
232 was measured by radioimmunoassay, [(3)H]myo-inositol phosphate production was measured by ion-exchan
233 F(2alpha) > CCh > ET-1; and their effects on inositol phosphate production were in the following orde
234 also significantly attenuated H1HR-mediated inositol phosphate production, as did an N-terminal frag
235 q)4Q failed to couple activated receptors to inositol phosphate production, it was able to bind betag
236 binding and internalization, stimulation of inositol phosphate production, or activation of Pyk2 and
237 ssed in hepatic C9 cells markedly stimulated inositol phosphate production, phosphorylation of the pr
238 ion did not reduce global agonist-stimulated inositol phosphate production, suggesting a requirement
245 gents used to antagonize PLC (U73122) or the inositol phosphate receptor (Xestospongin C) inhibited F
246 this substrate in an assay, we purified the inositol phosphate-regulated protein kinase and determin
248 hibition of Galpha(q)-Q152A-R183C-stimulated inositol phosphate release is reduced in comparison to G
250 or but had no effect on the agonist-promoted inositol phosphate response of the M1 or P2Y(2) receptor
253 s bearing a 5-phosphate and 54 water-soluble inositol phosphates reveals that SP-synaptojanin and SHI
256 n also enhances the increase in the level of inositol phosphates seen upon G protein stimulation, sug
257 localisation studies that suggest that these inositol phosphates serve to anchor a portion of cellula
258 the enzymatic cleavage of hydrophobic alkyl inositol phosphates showed low negative Bronsted coeffic
259 e relative coupling to G(s) (cAMP) and G(q) (inositol phosphates) signal transduction pathways during
260 nisms involving Shp2, desensitizes PDGFRbeta inositol phosphate signaling and enhances PDGFRbeta-trig
263 alterations in its coupling to both cAMP and inositol phosphate signaling pathways relative to the wi
267 GRK5-mediated desensitization of PDGFRbeta inositol phosphate signaling was diminished by Shp2 knoc
268 nt impairs G protein-dependent activation of inositol phosphate signaling while enhancing beta-arrest
269 tors does not alter 5-HT2C Galphaq-dependent inositol phosphate signaling, 5-HT2A or 5-HT2B receptor-
270 while failing to recruit arrestin, activate inositol phosphate signaling, or internalize CB2 recepto
271 Finally, in contrast to the results with inositol phosphate signaling, we provide evidence that t
272 uirement for intracellular Ca(2+) stores and inositol phosphate signaling, whereas Pep/PEPR signaling
278 e InoEFGK (TM0418-TM0421) transporter to myo-inositol-phosphate suggests that the novel pathway in Th
281 pentakisphosphate (IP(7)), are water-soluble inositol phosphates that contain high energy diphosphate
284 cell rounding and stimulate the formation of inositol phosphates to the same extent as PGF2alpha in c
285 ayed high-affinity MCH binding, resulting in inositol phosphate turnover and release of intracellular
286 id not prevent the receptor from stimulating inositol phosphate turnover but almost completely preven
287 lular PLC with an inhibitor (U73122) reduced inositol phosphate turnover in all of the HNSCC cell lin
288 onstrates that BQCA requires M(1) to promote inositol phosphate turnover in primary neurons and to in
289 ositol phosphate generation, and dynamics of inositol phosphate turnover occurred in the different ce
290 g system involving calcium ions, calmodulin, inositol phosphates, ubiquitin, cyclin, and GTP-binding
291 lyzed T. brucei extracts for the presence of inositol phosphates using polyacrylamide gel electrophor
295 ric channels are selectively permeable among inositol phosphates, whereas the corresponding homomeric
296 complexes has been shown to be regulated by inositol phosphates, which bind in a pocket sandwiched b
297 array of kinases and phosphatases into other inositol phosphates with diverse and critical cellular a
299 tion on the selectivity, the permeability of inositol phosphates with one to four phosphate groups th
300 d striking differences in permeability among inositol phosphates with three or four phosphate groups
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