INT26335

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Context Info
Confidence 0.18
First Reported 1986
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 22
Total Number 23
Disease Relevance 3.30
Pain Relevance 2.27

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

nucleoplasm (ITPR3) small molecule metabolic process (ITPR3) endoplasmic reticulum (ITPR3)
transmembrane transport (ITPR3) cytoplasm (ITPR3) signal transduction (ITPR3)
Anatomy Link Frequency
platelets 2
nose 2
reticulum 2
B lymphocytes 1
ITPR3 (Homo sapiens)
Pain Link Frequency Relevance Heat
Potency 11 98.38 Very High Very High Very High
Calcium channel 4 96.28 Very High Very High Very High
Serotonin 10 94.04 High High
agonist 41 92.84 High High
qutenza 8 92.36 High High
imagery 23 90.56 High High
Kinase C 38 85.04 High High
cva 54 79.40 Quite High
Pain 16 78.40 Quite High
Morphine 3 77.44 Quite High
Disease Link Frequency Relevance Heat
Neuroleptic Malignant Syndrome 1 99.50 Very High Very High Very High
Adhesions 22 97.16 Very High Very High Very High
Overactive Bladder 46 92.56 High High
Vibrio Infection 6 90.48 High High
Bordatella Infection 12 88.96 High High
Cv General 3 Under Development 54 79.40 Quite High
Cancer 8 79.32 Quite High
Sprains And Strains 36 76.00 Quite High
Spasticity 8 75.36 Quite High
Pain 15 75.00 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
IP3 binds to the IP3 receptor (IP3R, ?
IP3 Binding (binds) of
1) Confidence 0.18 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844426 Disease Relevance 0.07 Pain Relevance 0.04
IP3 binds to the IP3 receptor (IP3R, ?
IP3R Binding (binds) of
2) Confidence 0.18 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844426 Disease Relevance 0.07 Pain Relevance 0.04
IP3 binds to the IP3 receptor (IP3R, ?
IP3 Binding (binds) of
3) Confidence 0.18 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844426 Disease Relevance 0.07 Pain Relevance 0.04
The “control sponge” (K579Q, R582Q), is deficient in IP3 binding and therefore should not disrupt IP3 signalling, while the “super sponge” (R511C) has increased affinity for IP3.
IP3 Binding (affinity) of
4) Confidence 0.13 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2729924 Disease Relevance 0.20 Pain Relevance 0.03
To this end, we investigated whether itr-1(sy290), a gain-of-function allele [38], could rescue the defects in nose touch response that resulted from egl-8 or plc-3 RNAi. itr-1(sy290) has a mutation, R582Q, in the IP3 binding site [38], which results in a two-fold increase in IP3 binding affinity [20].
IP3 Binding (affinity) of in nose
5) Confidence 0.12 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2729924 Disease Relevance 0 Pain Relevance 0
Thus, an itr-1 mutation that increases the receptor's affinity for IP3 partially rescues the defects in nose touch response that result from knockdown of either plc-3 or egl-8, suggesting that IP3 is an important component of the downstream signal from these PLCs.
IP3 Binding (affinity) of in nose
6) Confidence 0.12 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2729924 Disease Relevance 0 Pain Relevance 0
The “control sponge” (K579Q, R582Q), is deficient in IP3 binding and therefore should not disrupt IP3 signalling, while the “super sponge” (R511C) has increased affinity for IP3.
IP3 Binding (binding) of
7) Confidence 0.11 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2729924 Disease Relevance 0.22 Pain Relevance 0.03
Given that the xanthenes contain an adenine ring identical to that of ATP, it has been postulated that they can interact competitively with the ATP binding site on the IP3 receptor [60].
IP3 receptor Binding (interact) of
8) Confidence 0.10 Published 2010 Journal International Journal of Vascular Medicine Section Body Doc Link PMC3003984 Disease Relevance 0.07 Pain Relevance 0
While DAG remains to the membrane, IP3 diffuses to the cytosol and binds to and activates the InsP3 receptor on the membrane of the endoplasmic reticulum, opening a calcium channel, resulting in the release of Ca2+ into the cytoplasm.
IP3 Binding (binds) of in reticulum associated with calcium channel
9) Confidence 0.10 Published 2010 Journal Clin Mol Allergy Section Body Doc Link PMC2949734 Disease Relevance 0 Pain Relevance 0.15
IP3 then binds to its receptor on the membrane of the sarcoplasmic reticulum (SR) to mobilize stored calcium irons (Ca2+) into the cytosol.
IP3 Binding (binds) of in reticulum
10) Confidence 0.07 Published 2009 Journal Korean Circulation Journal Section Body Doc Link PMC2801457 Disease Relevance 0.42 Pain Relevance 0.23
2 integrin-induced Ca2+ influx seems dependent on the formation of InsP3 [39].
InsP3 Binding (formation) of
11) Confidence 0.03 Published 2008 Journal J Leukoc Biol Section Body Doc Link PMC2567897 Disease Relevance 0.44 Pain Relevance 0.04
In addition to these studies, electrotransjection of a STIM1 antibody into platelets inhibited SOCE by reducing coupling between TRPC1 and InsP3-Rs [68].
InsP3 Binding (coupling) of in platelets
12) Confidence 0.03 Published 2008 Journal J Leukoc Biol Section Body Doc Link PMC2567897 Disease Relevance 0 Pain Relevance 0
Support for this hypothesis is derived from information obtained in human platelets and B lymphocytes, which suggests that TRPC1 is activated upon interaction with InsP3-Rs [57] and that it acts not only as a component of SOCs but also as a regulatory subunit of InsP3-Rs [58].
InsP3 Binding (interaction) of in B lymphocytes
13) Confidence 0.02 Published 2008 Journal J Leukoc Biol Section Body Doc Link PMC2567897 Disease Relevance 0 Pain Relevance 0
Interaction of IP3- and ryanodine-sensitive stores.
IP3 Binding (Interaction) of
14) Confidence 0.01 Published 2008 Journal American Journal of Physiology - Renal Physiology Section Body Doc Link PMC2640952 Disease Relevance 0 Pain Relevance 0
While this specific question cannot be satisfied in the present investigation, it is clear that there is interaction of IP3- and ryanodine-sensitive Ca2+ release mechanisms.


IP3 Spec (clear) Binding (interaction) of
15) Confidence 0.01 Published 2008 Journal American Journal of Physiology - Renal Physiology Section Body Doc Link PMC2640952 Disease Relevance 0.09 Pain Relevance 0.03
Most blockers of IP3-induced Ca2+ release appear not to function by way of inhibiting K+ counter-ion movements (valinomycin does not reverse the inhibition) but rather by way of direct interaction with the IP3 receptor or the Ca2+ channel that mediates the IP3-induced Ca2+ release.
IP3 Binding (interaction) of
16) Confidence 0.01 Published 1989 Journal Mol. Pharmacol. Section Abstract Doc Link 2554117 Disease Relevance 0 Pain Relevance 0
These results suggest that a novel GTP-binding protein, distinct from Ni, couples the TRH receptor to the formation of IP3.
IP3 Binding (formation) of
17) Confidence 0.01 Published 1986 Journal J. Biol. Chem. Section Abstract Doc Link 3013886 Disease Relevance 0.30 Pain Relevance 0.26
Inhibition of [3H]IP3 binding to the microsomes by phytic acid, heparin, pyrophosphate, p-chloromercuribenzoic acid, and Ca2+ could be demonstrated but not by the other substances tested.
IP3 Binding (binding) of
18) Confidence 0.01 Published 1989 Journal Mol. Pharmacol. Section Abstract Doc Link 2554117 Disease Relevance 0 Pain Relevance 0
TRH was also able to stimulate IP3 formation with a half-maximal potency of 118 +/- 10 nM in a lysed cell preparation of 7315c cells; the TRH-stimulated formation of IP3 was enhanced by GTP. 5'-Guanosine gamma-thiotriphosphate (GTP gamma S) and 5'-guanylyl imidodiphosphate (Gpp(NH)p), nonhydrolyzable analogs of GTP, stimulated IP3 formation in the absence of TRH with half-maximal potencies of 162 +/- 50 and 7500 +/- 4300 nM, respectively.
IP3 Binding (formation) of associated with potency
19) Confidence 0.01 Published 1986 Journal J. Biol. Chem. Section Abstract Doc Link 3013886 Disease Relevance 0.45 Pain Relevance 0.21
TRH was also able to stimulate IP3 formation with a half-maximal potency of 118 +/- 10 nM in a lysed cell preparation of 7315c cells; the TRH-stimulated formation of IP3 was enhanced by GTP. 5'-Guanosine gamma-thiotriphosphate (GTP gamma S) and 5'-guanylyl imidodiphosphate (Gpp(NH)p), nonhydrolyzable analogs of GTP, stimulated IP3 formation in the absence of TRH with half-maximal potencies of 162 +/- 50 and 7500 +/- 4300 nM, respectively.
IP3 Binding (formation) of associated with potency
20) Confidence 0.01 Published 1986 Journal J. Biol. Chem. Section Abstract Doc Link 3013886 Disease Relevance 0.53 Pain Relevance 0.24

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