INT37241

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Context Info
Confidence 0.13
First Reported 1987
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 7
Total Number 8
Disease Relevance 1.22
Pain Relevance 1.05

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
plasma 2
vesicles 2
reticulum 2
ITPR3 (Homo sapiens)
Pain Link Frequency Relevance Heat
lidocaine 3 99.84 Very High Very High Very High
antagonist 6 99.52 Very High Very High Very High
local anesthetic 6 99.34 Very High Very High Very High
Calcium channel 7 98.88 Very High Very High Very High
agonist 180 86.76 High High
headache 2 78.48 Quite High
adenocard 4 71.56 Quite High
Inflammation 12 69.52 Quite High
Dismenorea 3 58.72 Quite High
Inflammatory response 2 49.60 Quite Low
Disease Link Frequency Relevance Heat
Increased Venous Pressure Under Development 10 89.76 High High
Adhesions 7 82.52 Quite High
Vomiting 4 79.12 Quite High
Headache 2 78.48 Quite High
Diuresis 1 77.36 Quite High
Bordatella Infection 1 73.40 Quite High
Pulmonary Disease 4 71.76 Quite High
INFLAMMATION 15 69.52 Quite High
Convulsion 1 66.72 Quite High
Overdose 1 65.28 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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).
Negative_regulation (reduces) of Localization (release) of IP3
1) Confidence 0.13 Published 2010 Journal Journal of Korean Medical Science Section Body Doc Link PMC2908795 Disease Relevance 0.73 Pain Relevance 0.31
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].
Negative_regulation (inhibits) of Localization (release) of InsP3 receptor-mediated
2) Confidence 0.04 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].
Negative_regulation (inhibiting) of Localization (release) of IP3
3) Confidence 0.04 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0.17 Pain Relevance 0.03
S340A (Fig. 5M and N, respectively) yielded efficient [Ca2+]i mobilization and IP3 generation in response to primary stimulation, signalling by TP?
Negative_regulation (yielded) of Localization (generation) of IP3
4) Confidence 0.04 Published 2007 Journal Biochim Biophys Acta Section Body Doc Link PMC2680961 Disease Relevance 0 Pain Relevance 0.04
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.
Negative_regulation (inhibits) of Localization (release) of IP3 in reticulum associated with antagonist
5) Confidence 0.03 Published 2010 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2861440 Disease Relevance 0.17 Pain Relevance 0.11
The inhibition of IP3-induced Ca2+ release from these membrane vesicles by various agents was examined.
Negative_regulation (inhibition) of Spec (examined) Localization (release) of IP3 in vesicles
6) Confidence 0.01 Published 1987 Journal Biochem. Pharmacol. Section Abstract Doc Link 3499904 Disease Relevance 0 Pain Relevance 0.03
Of the plasma membrane Ca2+ channel blockers, cinnarizine and flunarizine were found to be potent inhibitors of IP3-induced Ca2+ release while having no effect on ATP-dependent Ca2+ uptake.
Negative_regulation (inhibitors) of Localization (release) of IP3 in plasma
7) Confidence 0.01 Published 1987 Journal Biochem. Pharmacol. Section Abstract Doc Link 3499904 Disease Relevance 0 Pain Relevance 0.15
The local anesthetics benzocaine and lidocaine weakly inhibited the IP3-induced Ca2+ release with IC50 values of approximately 5 and 50 microM, respectively, whereas other local anesthetics tested were less potent inhibitors.
Negative_regulation (inhibited) of Localization (release) of IP3 associated with lidocaine and local anesthetic
8) Confidence 0.01 Published 1987 Journal Biochem. Pharmacol. Section Abstract Doc Link 3499904 Disease Relevance 0 Pain Relevance 0.34

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