INT26334

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Context Info
Confidence 0.49
First Reported 1986
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 39
Total Number 42
Disease Relevance 2.53
Pain Relevance 5.07

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
reticulum 5
brain 2
plasma 1
chief cells 1
spike 1
ITPR3 (Homo sapiens)
Pain Link Frequency Relevance Heat
lidocaine 7 99.56 Very High Very High Very High
agonist 490 99.20 Very High Very High Very High
Opioid 2 99.16 Very High Very High Very High
local anesthetic 27 99.06 Very High Very High Very High
antagonist 147 99.02 Very High Very High Very High
Calcium channel 17 97.84 Very High Very High Very High
Kinase C 37 93.64 High High
imagery 60 92.88 High High
bradykinin 75 90.24 High High
Inflammation 41 85.48 High High
Disease Link Frequency Relevance Heat
Cancer 7 99.52 Very High Very High Very High
Neuroblastoma 4 98.24 Very High Very High Very High
Glioma 14 97.44 Very High Very High Very High
Overactive Bladder 161 95.60 Very High Very High Very High
Increased Venous Pressure Under Development 27 94.88 High High
Bordatella Infection 10 93.52 High High
Vibrio Infection 4 85.76 High High
INFLAMMATION 47 85.48 High High
Adhesions 12 81.32 Quite High
Vomiting 5 79.12 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In this metabotropic model, PLC activation would lead to the production of IP3, which in turn would activate the IP3 receptor causing release of Ca2+ from the ER [15].
Localization (release) of IP3 receptor
1) Confidence 0.49 Published 2010 Journal BMC Complement Altern Med Section Body Doc Link PMC3002894 Disease Relevance 0.09 Pain Relevance 0.08
We tested for the possible involvement of the IP3 receptor in the Echinacea-induction of intracellular Ca2+ release by evaluating the effect of 2-aminoethoxydiphenyl borate (2-APB), an IP3 receptor antagonist, on Echinacea-induced cytosolic Ca2+ increase.
Localization (release) of IP3 receptor associated with antagonist
2) Confidence 0.46 Published 2010 Journal BMC Complement Altern Med Section Body Doc Link PMC3002894 Disease Relevance 0 Pain Relevance 0.05
Echinacea-induced [Ca2+]i increases in HEK293 cells appear to be associated with release of Ca2+ from IP3-sensitive intracellular stores, and this process may involve PLC activation
Localization (release) of IP3
3) Confidence 0.40 Published 2010 Journal BMC Complement Altern Med Section Body Doc Link PMC3002894 Disease Relevance 0 Pain Relevance 0.03
The effect of opioids on phosphatidylinositol (PI) turnover to release inositol triphosphate (IP3) as second messenger was examined in mouse neuroblastoma X rat glioma hybrid cells NG108-15 (delta-receptors) and human neuroblastoma cells, SK-N-SH (predominantly mu-receptors).
Localization (release) of IP3 in SK-N-SH associated with neuroblastoma, opioid and glioma
4) Confidence 0.33 Published 1986 Journal Neurosci. Lett. Section Abstract Doc Link 3024076 Disease Relevance 0.37 Pain Relevance 0.42
IP3 releases internal calcium in endothelial cells, therefore triggering the calcium cascade and its associated biological process, such as vasoconstriction (18).
Localization (releases) of IP3 in endothelial cells associated with increased venous pressure under development
5) Confidence 0.27 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2908795 Disease Relevance 0.23 Pain Relevance 0.23
In addition, caffeine also acts on the other primary endoplasmic reticulum calcium release channel, the inositol triphosphate receptor (IP3R), over the same concentration range.
Localization (release) of IP3R in reticulum
6) Confidence 0.22 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2525814 Disease Relevance 0 Pain Relevance 0.06
Second, propofol reduces the production of IP3 and calcium release from intracellular stores (16, 17), but aminophylline induced Ca2+ release from intracellular stores, occurs via increased production of IP3 through G-protein-mediated activation (21, 25).
Localization (release) of IP3
7) Confidence 0.21 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2908795 Disease Relevance 0.73 Pain Relevance 0.31
However, after such a store is full, the subsequent accumulation of calcium in the cytoplasm can then activate a rapid calcium-induced calcium release from the same IP3-insensitive store, which produces the onset of the calcium spike.
Localization (release) of IP3 in spike
8) Confidence 0.08 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2693427 Disease Relevance 0 Pain Relevance 0.11
In this model, an agonist-induced increase in IP3 stimulates the release of calcium from an IP3-sensitive intracellular calcium storage site into the cytoplasm.
Localization (release) of IP3 associated with agonist
9) Confidence 0.08 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2693427 Disease Relevance 0 Pain Relevance 0.08
PI3K has been found to mediate phosphorylation and translocation of phospholipase C-gamma and resultant IP3 production in response to activation of P2Y purinergic receptors - this could be one mechanism by which PI3 kinase inhibitors inhibit both the initial response to ATP and the resensitization of P2Y purinergic receptors [38].
Localization (translocation) of IP3
10) Confidence 0.07 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC2955562 Disease Relevance 0 Pain Relevance 0.39
Although increased levels of OT are not evident during labor, the uterine contractile effect of oxytocin relies on activated OT receptors in the presence of increased estrogen and PG production.74 Atosiban is a nonapeptide, desamino-OT analogue, and a competitive vasopressin/oxytocin receptor antagonist (VOTra).75–78 Atosiban inhibits the OT-mediated release of IP3 from the myometrial cell membrane.75 As a result, there is reduced release of intracellular, stored calcium from the sacroplasmic reticulum of myometrial cells, and reduced influx of Ca2+ from the extracellular space through voltage gated channels.
Localization (release) of IP3 in reticulum associated with antagonist
11) Confidence 0.06 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2861440 Disease Relevance 0.17 Pain Relevance 0.11
S340A (Fig. 5M and N, respectively) yielded efficient [Ca2+]i mobilization and IP3 generation in response to primary stimulation, signalling by TP?
Localization (generation) of IP3
12) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.04
S331A yielded efficient [Ca2+]i mobilization and IP3 generation (Fig. 5D and F).
Localization (mobilization) of IP3
13) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.09
activation leading to increases in IP3 generation and mobilization of [Ca2+]i.
Localization (generation) of IP3
14) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.12
eliminating two potential target phosphorylation sites at Thr337 and Ser340, yielded efficient [Ca2+]i mobilization and IP3 generation in response to U46619 (Fig. 5G and I, respectively).
Localization (generation) of IP3
15) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.11
For example, 2-ABP has been shown to potentiate and block Ca2+ entry into cells [180], and it inhibits InsP3 receptor-mediated Ca2+ release [181].
Localization (release) of InsP3 receptor-mediated
16) Confidence 0.06 Published 2008 Journal J Leukoc Biol Section Body Doc Link PMC2567897 Disease Relevance 0.14 Pain Relevance 0.03
Amongst the key molecular targets of NO-regulated PKG thus far identified is the IP3 receptor [71], thereby inhibiting PLC activation and IP3-evoked Ca2+ release from intracellular stores [72], IP3 receptor-associated cGMP kinase substrate or IRAG [73,74], myosin binding substrate [75] and the vasodilator-stimulated phosphoprotein or VASP [76].
Localization (release) of IP3
17) Confidence 0.06 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0.17 Pain Relevance 0.03
Evidence that carbachol was acting through the IP3 signal transduction pathway to release Ca2+ was provided by experiments using drugs to interfere with various stages of the pathway.
Localization (release) of IP3
18) Confidence 0.03 Published 2008 Journal American Journal of Physiology - Renal Physiology Section Body Doc Link PMC2640952 Disease Relevance 0 Pain Relevance 0.04
However, it is worth noting that a study on guinea pig colonic smooth muscle cells (14) presents an important caveat when interpreting data relating to IP3-mediated Ca2+ release and CICR at ryanodine receptors.
Localization (release) of IP3 in smooth muscle cells
19) Confidence 0.03 Published 2008 Journal American Journal of Physiology - Renal Physiology Section Body Doc Link PMC2640952 Disease Relevance 0 Pain Relevance 0
The contribution of Ca2+ release from IP3 intracellular stores was initially investigated using 2-APB, a drug often used to block release from IP3-sensitive stores.
Localization (release) of IP3
20) Confidence 0.03 Published 2008 Journal American Journal of Physiology - Renal Physiology Section Body Doc Link PMC2640952 Disease Relevance 0 Pain Relevance 0

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