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1 th an increase in the levels of its product, inositol 1,4,5-trisphosphate.
2 (PI(4,5)P(2) or PIP(2)) and the formation of inositol 1,4,5-trisphosphate.
3 nto the second messengers diacylglycerol and inositol 1,4,5-trisphosphate.
4 te also induces cytoplasmic concentration of inositol 1,4,5-trisphosphate.
5 of the second messengers, diacylglycerol and inositol-1,4,5-trisphosphate.
6 (2+)-releasing intracellular messenger d-myo-inositol 1,4,5-trisphosphate [1, Ins(1,4,5)P(3)] are imp
10 iated proteins in human platelets identified inositol 1,4,5-trisphosphate 3-kinase isoform B (IP3KB)
13 -grown 5ptase11 mutants contain increases in inositol (1,4,5) trisphosphate and an inositol bisphosph
14 hippocampal-dependent memory in part through inositol 1,4,5-trisphosphate and brain-derived neurotrop
16 y of cellular pathways through production of inositol 1,4,5-trisphosphate and diacylglycerol (DAG).
17 ts ability to generate the second messengers inositol 1,4,5-trisphosphate and diacylglycerol, PLC, un
18 ggers PLC-mediated hydrolysis of PIP(2) into inositol 1,4,5-trisphosphate and diacylglycerol, which a
21 eric G-protein coupling, and inhibits IP(3) (inositol-1,4,5-trisphosphate) and calcium mobilization,
22 hatidylinositol 4-phosphate, diacylglycerol, inositol 1,4,5-trisphosphate, and Ca(2+) upon muscarinic
23 ransient increases in intracellular calcium, inositol 1,4,5-trisphosphate, and G(q)-GTP in response t
24 (VSP), which depletes PIP2 without changing inositol 1,4,5-trisphosphate, and monitored NBCe1-mediat
25 , in particular via the second messenger myo-inositol 1,4,5-trisphosphate, and phosphoinositides comp
26 tensin II-induced cleavage is independent of inositol 1,4,5-trisphosphate- and Ca(2+)-mediated signal
28 a receptor-independent method for producing inositol (1,4,5)-trisphosphate as the heart of the model
29 escent phosphatidylinositol 4,5-bisphosphate/inositol 1,4,5-trisphosphate biosensor GFP-PLCdelta1-PH
30 cted by inhibition of the production of IP3 (inositol-1,4,5-trisphosphate) by phospholipase-C and acc
31 mechanism involving M1/M3 receptor-mediated inositol 1,4,5-trisphosphate/Ca(+2) signalling and downs
32 mechanism involving M1/M3 receptor-mediated inositol 1,4,5-trisphosphate/Ca(+2) signalling and downs
33 large cholangiocytes by activation of D-myo-inositol 1,4,5-trisphosphate/Ca(2+) /calmodulin-dependen
34 inhibit NBCe1, whereas hydrolysis of PIP2 to inositol 1,4,5-trisphosphate/Ca(2+) can stimulate the tr
36 luble inositol phosphate headgroups, such as inositol 1,4,5-trisphosphate, can compete with PtdIns(4,
38 ia L-type Ca(2+) channels and, on the other, inositol 1,4,5-trisphosphate-dependent Ca(2+) release.
39 increasing ROS production which facilitated inositol 1,4,5-trisphosphate-dependent Ca(2+) release.
40 inic acid-adenine dinucleotide phosphate- or inositol 1,4,5-trisphosphate-dependent calcium release a
41 R expression, (iii) persistent activation of inositol 1,4,5-trisphosphate-dependent cell signaling ca
42 idylinositol 4,5-bisphosphate hydrolysis and inositol 1,4,5-trisphosphate-dependent intra-acrosomal c
46 ng concentrations for intracellular calcium, inositol 1,4,5-trisphosphate, diacylglycerol, phosphatid
48 signaling under these conditions depends on inositol-1,4,5-trisphosphate generation from phospholipa
49 onse to environmental cues that promote IP3 (inositol 1,4,5-trisphosphate) generation, IP3 receptors
50 l 4,5-bisphosphate (PIP(2)) and formation of inositol 1,4,5-trisphosphate in TRPV6-expressing cells.
51 ease from the sarcoplasmic reticulum through inositol 1,4,5-trisphosphate-induced Ca release and not
52 as inhibited by blocking phospholipase C and inositol 1,4,5-trisphosphate-induced Ca(2+) release, ind
54 belongs to a family of kinases that convert inositol 1,4,5-trisphosphate (Ins(1,4,5)P3 or IP3) to in
56 butes to intracellular signaling through its inositol-1,4,5-trisphosphate (Ins(1,4,5)P3) 3-kinase and
58 4,5)P(2) levels was accompanied by increased inositol 1,4,5 trisphosphate (InsP(3)) production, and w
59 s also were reduced by selectively buffering inositol 1,4,5-trisphosphate (InsP(3)) within the nucleu
60 asticity (ITDP) in cortical input depends on inositol 1,4,5-trisphosphate (InsP(3))-sensitive Ca(2+)
62 ss that is regulated, in mammalian cells, by inositol-1,4,5-trisphosphate (InsP(3)), cyclic ADP ribos
64 to the nucleus, as well as upon formation of inositol 1,4,5,-trisphosphate (InsP3) in the nucleus, wh
67 2+) release and airway contraction evoked by inositol-1,4,5-trisphosphate (InsP3) uncaging in airway
70 crystallographic studies have emphasized PH-inositol 1,4,5-trisphosphate (IP 3) interactions, biophy
72 hatidylinositol 4,5-bisphosphate (PIP(2)) to inositol 1,4,5-trisphosphate (IP(3)) and diacylglycerol
73 y results from an increase in the potency of inositol 1,4,5-trisphosphate (IP(3)) in producing facili
76 eration, and Inpp5a overexpression decreases inositol 1,4,5-trisphosphate (IP(3)) levels and ameliora
77 gamma2 (PLCgamma2) accounts for LPS-induced inositol 1,4,5-trisphosphate (IP(3)) production and subs
78 +)](i)) by increasing the sensitivity of the inositol 1,4,5-trisphosphate (IP(3)) receptor (IP(3)R) t
79 ivation of TRPC3 channels is concurrent with inositol 1,4,5-trisphosphate (IP(3)) receptor (IP(3)R)-m
87 led receptors (GPCRs) through the binding of inositol 1,4,5-trisphosphate (IP(3)) to its receptor (IP
88 ssay in which binding of fluorescein-labeled inositol 1,4,5-trisphosphate (IP(3)) to N-terminal fragm
90 , which encompasses dramatic potentiation of inositol 1,4,5-trisphosphate (IP(3))-dependent Ca(2+) re
91 icoids inhibit downstream responses, such as inositol 1,4,5-trisphosphate (IP(3))-induced calcium sig
94 d knockout mice, we show that in addition to inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) rel
95 osolic Ca(2+) rise is primarily initiated by inositol 1,4,5-trisphosphate (IP(3))-mediated Ca(2+) rel
96 lations are initiated by Ca(2+) release from inositol 1,4,5-trisphosphate (IP(3))-sensitive intracell
97 (VGCC) and mobilization of Ca(2+) from both inositol 1,4,5-trisphosphate (IP(3))-sensitive stores an
101 otein, adenylyl cyclase, Epac-1 protein, and inositol 1,4,5-trisphosphate (IP(3))/IP(3) receptor, wer
102 efficient chemical synthesis of an analog of inositol-1,4,5-trisphosphate (IP(3)) hexakis acetoxymeth
103 d by silencing of the NBCe1-B/CFTR activator inositol-1,4,5-trisphosphate (IP(3)) receptor-binding pr
107 thway occurs at the level of hormone-induced inositol 1,4,5 trisphosphate (IP3 ) production and does
108 hate (IP), inositol 4,5-bisphosphate (IP2 ), inositol 1,4,5-trisphosphate (IP3 ), and inositol hexaki
109 on is an increase in [Ca(2+) ]i triggered by inositol 1,4,5-trisphosphate (IP3 )-induced release of C
110 d CaMKII activation is probably initiated by inositol 1,4,5-trisphosphate (IP3 )-mobilized Ca(2+) : 8
111 ly to involve downstream Ca(2+) release from inositol 1,4,5-trisphosphate (IP3 )-triggered Ca(2+) -st
112 (PLC-gamma1), with the resultant increase in inositol 1,4,5-trisphosphate (IP3) and intracellular cal
114 ausing mutant presenilins (PS) interact with inositol 1,4,5-trisphosphate (IP3) receptor (IP3R) Ca(2+
115 anisms, e.g., single channel kinetics of the inositol 1,4,5-trisphosphate (IP3) receptor Ca2+ channel
116 omain mediates interaction of Bcl-2 with the inositol 1,4,5-trisphosphate (IP3) receptor, an IP3-gate
117 ertebrate genomes code for three subtypes of inositol 1,4,5-trisphosphate (IP3) receptors (IP3R1, -2,
118 nic M3 receptors, or by direct activation of inositol 1,4,5-trisphosphate (IP3) receptors by photolys
119 ntributes to the ubiquitination of activated inositol 1,4,5-trisphosphate (IP3) receptors, and also,
120 hosphate kinase 2 (ip3k2), thereby affecting inositol 1,4,5-trisphosphate (IP3) signaling and calcium
121 holipase C-gamma (PLC-gamma) which increases inositol 1,4,5-trisphosphate (IP3) to release intracellu
124 Sigma-1 receptor (sigma-1R) agonists enhance inositol 1,4,5-trisphosphate (IP3)-dependent calcium rel
126 ition of the phospholipase C gamma 2 (PLCG2)/inositol 1,4,5-trisphosphate (IP3)/Ca(2+)/protein kinase
129 the cell and parallel fiber stimulus evoking inositol-1,4,5-trisphosphate (IP3)-meditated calcium rel
131 ntext-specific autophagy through its target, inositol 1,4,5-trisphosphate kinase 2 (ip3k2), thereby a
132 C and to the formation of diacylglycerol and inositol 1,4,5-trisphosphate, leading to the release of
133 celerating Ca(2+) clearance and exaggerating inositol 1,4,5-trisphosphate-mediated Ca(2+) liberation.
134 rial function and to involve phospholipase C/inositol 1,4,5-trisphosphate-mediated Ca(2+) mobilizatio
135 steoclast (OC) differentiation by modulating inositol 1,4,5-trisphosphate-mediated calcium oscillatio
136 slocates to the nucleus to initiate nuclear, inositol 1,4,5-trisphosphate-mediated calcium signals in
137 lus secretion coupling and its regulation by inositol 1,4,5-trisphosphate, nicotinic acid adenine din
138 or the first time that the POCKET containing inositol 1,4,5-trisphosphate on crystal structure (the "
139 ce of extracellular Ca(2+), and that the PLC-inositol 1,4,5-trisphosphate pathway, which controls the
140 egranulation by thapsigargin, which bypasses inositol 1,4,5-trisphosphate production, is also substan
141 ysis of phosphatidylinositol 4,5-biphosphate inositol 1,4,5-trisphosphate production, nuclear Ca(2+)
144 ome through phospholipase C, which catalyses inositol-1,4,5-trisphosphate production and thereby indu
145 discovered that mHtt protein binds to type 1 inositol (1,4,5)-trisphosphate receptor (InsP3R1) and in
149 The potentiation is absent in conditional inositol 1,4,5 trisphosphate receptor type 2 KO mice, wh
150 tin A (AdA) is a potent agonist of the d-myo-inositol 1,4,5-trisphosphate receptor (Ins(1,4,5)P3R).
151 ut not wild-type Atx2 specifically binds the inositol 1,4,5-trisphosphate receptor (InsP(3)R) and inc
152 (i)) by endoplasmic reticulum (ER)-localized inositol 1,4,5-trisphosphate receptor (InsP(3)R) Ca(2+)-
157 th the cytosolic C-terminal region of type 1 inositol 1,4,5-trisphosphate receptor (InsP(3)R1), an in
158 ) specifically binds to and activates type 1 inositol 1,4,5-trisphosphate receptor (InsP(3)R1), an in
159 exp) specifically associated with the type 1 inositol 1,4,5-trisphosphate receptor (InsP(3)R1), an in
160 -mediated calcium release through the type 2 inositol 1,4,5-trisphosphate receptor (InsP(3)R2) in car
162 PS1 (M146L)and PS2 (N141I) interact with the inositol 1,4,5-trisphosphate receptor (InsP3R) Ca2+ rele
163 2+ release from intracellular stores through inositol 1,4,5-trisphosphate receptor (InsP3R) channels
164 , neuronal calcium sensor 1 (NCS-1), and the inositol 1,4,5-trisphosphate receptor (InsP3R) to preven
165 er intracellular Ca(2+) channels such as the inositol 1,4,5-trisphosphate receptor (InsP3R), is neces
167 alicular membrane is mediated by the type II inositol 1,4,5-trisphosphate receptor (InsP3R2), so we i
168 mutation in ITPR2, which encodes the type 2 inositol 1,4,5-trisphosphate receptor (InsP3R2), that wa
170 lobal Ca(2+) concentration ([Ca(2+)](i)) via inositol 1,4,5-trisphosphate receptor (IP(3)R) activatio
171 poptotic activity of Bcl-2 by binding to the inositol 1,4,5-trisphosphate receptor (IP(3)R) Ca(2)(+)
172 in the channel domain that are critical for inositol 1,4,5-trisphosphate receptor (IP(3)R) channel f
173 t gating dynamics of a single, nonconducting inositol 1,4,5-trisphosphate receptor (IP(3)R) channel,
174 examethasone induces a striking elevation of inositol 1,4,5-trisphosphate receptor (IP(3)R) levels in
175 euronal Ca(2+) signaling by enhancing type-1 inositol 1,4,5-trisphosphate receptor (IP(3)R) steady-st
176 we demonstrated that PC2 interacts with the inositol 1,4,5-trisphosphate receptor (IP(3)R) to modula
177 ng a proteomics approach, we identify type 1 inositol 1,4,5-trisphosphate receptor (IP(3)R1) as a spe
179 is and the degradation of the Ca(2+) channel inositol 1,4,5-trisphosphate receptor (IP3R) affects pro
182 sm involves an interaction of Bcl-2 with the inositol 1,4,5-trisphosphate receptor (IP3R) Ca2+ channe
185 r ryanodine (400 microM), the antagonists of inositol 1,4,5-trisphosphate receptor (IP3R) or ryanodin
186 om apical Ca(2+) pools that are gated by the inositol 1,4,5-trisphosphate receptor (IP3R) types 2 and
187 n genes encoding the neuronal isoform of the inositol 1,4,5-trisphosphate receptor (ITPR1) and genes
188 ffects of NAFLD on expression of the type II inositol 1,4,5-trisphosphate receptor (ITPR2), the princ
191 rypanosoma brucei acidocalcisomes possess an inositol 1,4,5-trisphosphate receptor (TbIP(3)R) for Ca(
192 sed from these organelles through a channel, inositol 1,4,5-trisphosphate receptor (TbIP(3)R), which
193 sed phosphorylation of the ER Ca(2+) channel inositol 1,4,5-trisphosphate receptor 1 (IP3R1) in CNG c
194 , voltage-dependent Ca(2+) channels, and the inositol 1,4,5-trisphosphate receptor as well as the N-m
196 parks arise from the cooperative activity of inositol 1,4,5-trisphosphate receptor Ca(2+) channels (I
197 co/ER Ca(2+) ATPase, ryanodine receptor, and inositol 1,4,5-trisphosphate receptor channel in various
198 tributed to the differential distribution of inositol 1,4,5-trisphosphate receptor channel isoforms i
199 R Ca(2+) ATPase, ER Ca(2+) release channels, inositol 1,4,5-trisphosphate receptor channel, ryanodine
200 ized releases of calcium through clusters of inositol 1,4,5-trisphosphate receptor channels constitut
201 phate receptor (ITPR1) and genes involved in inositol 1,4,5-trisphosphate receptor degradation (ERLIN
202 phospholipase C inhibitor U73122 and by the inositol 1,4,5-trisphosphate receptor inhibitor Xestospo
203 athway in which the expression of the type-1 inositol 1,4,5-trisphosphate receptor is regulated by th
207 vation of cytosolic Ca(2+) by binding to the inositol 1,4,5-trisphosphate receptor on the endoplasmic
208 monitor conformational changes of the type I inositol 1,4,5-trisphosphate receptor protein in membran
209 ubiquitinated endoplasmic reticulum protein inositol 1,4,5-trisphosphate receptor type 1 (IP3R1), wh
210 563del] and c.7659T>G [p.Phe2553Leu]) in the inositol 1,4,5-trisphosphate receptor type 1 gene (ITPR1
211 TPase and ryanodine receptor type 2, but not inositol 1,4,5-trisphosphate receptor type 2, were requi
213 d upon activation of phospholipase C and the inositol 1,4,5-trisphosphate receptor, but not upon extr
215 n immunoprecipitation assay, we found ITPR1 (inositol 1,4,5-trisphosphate receptor, type 1) as a dire
217 espective primary tumors, include C17orf104, inositol 1,4,5-trisphosphate receptor, type 3 (ITPR3), a
218 tically, we showed that HAX-1 interacts with inositol 1,4,5-trisphosphate receptor-1 (InsP3R1) in the
219 Hg, ECs generated low-frequency (~2 min(-1)) inositol 1,4,5-trisphosphate receptor-based Ca(2+) event
220 onapoptotic necrotic cell death triggered by inositol 1,4,5-trisphosphate receptor-dependent calcium
221 l melastatin subfamily 4 channels via type 2 inositol 1,4,5-trisphosphate receptor-mediated Ca(2+) re
225 inds, deubiquitylates, and stabilizes type 3 inositol-1,4,5-trisphosphate receptor (IP3R3), modulatin
226 ed morphology and express IP3R3, which is an inositol-1,4,5-trisphosphate receptor constitutively exp
227 transients (CaTs) are due to upregulation of inositol-1,4,5-trisphosphate receptor induced Ca(2+) rel
230 to demonstrate that sensitization of type 1 inositol (1,4,5)-trisphosphate receptors by mHtt, which
234 Protein kinase A (PKA) phosphorylation of inositol 1,4,5-trisphosphate receptors (InsP(3)Rs) repre
235 ositive and negative [Ca(2+)](i) feedback on inositol 1,4,5-trisphosphate receptors (InsP(3)Rs).
239 Others, including the almost ubiquitous inositol 1,4,5-trisphosphate receptors (IP(3)R) and thei
240 stimulates formation of cAMP and sensitizes inositol 1,4,5-trisphosphate receptors (IP(3)R) to IP(3)
241 in A (AdA), the most potent agonist of d-myo-inositol 1,4,5-trisphosphate receptors (IP(3)R), is thou
242 upling of sarcoplasmic reticulum (SR) type 1 inositol 1,4,5-trisphosphate receptors (IP(3)R1) to plas
243 es of endoplasmic reticulum Ca(2+) channels, inositol 1,4,5-trisphosphate receptors (IP(3)Rs) and rya
245 A number of studies have demonstrated that inositol 1,4,5-trisphosphate receptors (IP(3)Rs) interac
247 knockdown and pharmacological inhibition of inositol 1,4,5-trisphosphate receptors (IP(3)Rs) stimula
248 pled receptors stimulates Ca(2+) release via inositol 1,4,5-trisphosphate receptors (IP(3)Rs), engagi
249 etabotropic glutamate receptors (mGluRs) and inositol 1,4,5-trisphosphate receptors (IP(3)Rs), suppor
251 ) release through the ryanodine receptors or inositol 1,4,5-trisphosphate receptors (IP3 R) and upon
257 ms, like the endoplasmic reticulum-localized inositol 1,4,5-trisphosphate receptors (IP3Rs) and the v
259 hat Bok binds strongly and constitutively to inositol 1,4,5-trisphosphate receptors (IP3Rs), proteins
260 cell lines that Bok interacts strongly with inositol 1,4,5-trisphosphate receptors (IP3Rs), suggesti
263 ly dependent on Ca2+ oscillation mediated by inositol 1,4,5-trisphosphate receptors 2 and 3 (ITPR2 an
264 ) release from the endoplasmic reticulum via inositol 1,4,5-trisphosphate receptors and by Ca(2+) ent
265 the cooperative activity of Ca(2+)-regulated inositol 1,4,5-trisphosphate receptors and ryanodine rec
266 uggests that it results from potentiation of inositol 1,4,5-trisphosphate receptors and/or phospholip
268 epletion of internal stores or inhibition of inositol 1,4,5-trisphosphate receptors but not by inhibi
269 2+) signals interact with both ryanodine and inositol 1,4,5-trisphosphate receptors during agonist st
270 iquitin E3 ligase gene RNF170, which targets inositol 1,4,5-trisphosphate receptors for degradation,
271 nd blockade of either ryanodine receptors or inositol 1,4,5-trisphosphate receptors reduced [Ca(2+)](
272 astrocytes lack mGluR5, and knockout of the inositol 1,4,5-trisphosphate receptors that release Ca(2
273 neurons, cGKII-dependent phosphorylation of inositol 1,4,5-trisphosphate receptors was decreased, re
274 activity were also blunted by inhibition of inositol 1,4,5-trisphosphate receptors with 2-aminoethox
275 reticulum membrane (ryanodine receptors and inositol 1,4,5-trisphosphate receptors) of isolated card
278 through the PKA-mediated phosphorylation of inositol-1,4,5-trisphosphate receptors (InsP(3)Rs), whic
280 d the detailed intracellular distribution of inositol-1,4,5-trisphosphate receptors (IP(3)Rs), and ry
281 s (RyRs), dihydropyridine receptors (DHPRs), inositol-1,4,5-trisphosphate receptors (IP(3)Rs), canoni
283 IRE1alpha determined the distribution of inositol-1,4,5-trisphosphate receptors at MAMs by operat
284 ryanodine receptors, increased expression of inositol-1,4,5-trisphosphate receptors, and differential
287 naptic stores (activated by spot-uncaging of inositol 1,4,5-trisphosphate) remain unaffected by GPR55
288 he lack of coupling between SP signaling and inositol 1,4,5-trisphosphate sensitive Ca(2+) stores, to
289 holipase C but is largely uncoupled from the inositol 1,4,5-trisphosphate sensitive Ca(2+) stores.
290 arise from regenerative Ca(2+) release from inositol 1,4,5-trisphosphate-sensitive stores followed b
293 trisphosphate 3-kinase B (or Itpkb) converts inositol 1,4,5-trisphosphate to inositol 1,3,4,5-tetraki
296 vely, these results support the concept that inositol-1,4,5-trisphosphate type 3 receptor signaling i
298 variety of inositol phosphates including myo-inositol 1,4,5-trisphosphate, which is a secondary messe
299 se C and the formation of diacylglycerol and inositol 1,4,5-trisphosphate, which results in the relea
300 ) to produce cAMP and via G(q/11) to produce inositol-1,4,5-trisphosphate, which is degraded to inosi