INT31762

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.74
First Reported 1988
Last Reported 2009
Negated 1
Speculated 0
Reported most in Body
Documents 22
Total Number 22
Disease Relevance 1.60
Pain Relevance 4.15

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) endoplasmic reticulum (Itpr3) nucleolus (Itpr3)
nucleus (Itpr3) transmembrane transport (Itpr3) cytoplasm (Itpr3)
Anatomy Link Frequency
cardiac myocytes 2
spikes 2
smooth muscle 1
sciatic nerve 1
glial cell 1
Itpr3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Sciatic nerve 6 99.92 Very High Very High Very High
Kinase C 262 99.74 Very High Very High Very High
Kappa opioid receptor 8 99.68 Very High Very High Very High
nMDA receptor 37 99.58 Very High Very High Very High
agonist 127 99.20 Very High Very High Very High
sodium channel 8 99.08 Very High Very High Very High
tolerance 2 99.00 Very High Very High Very High
Morphine 1 98.76 Very High Very High Very High
Nav1.6 2 98.44 Very High Very High Very High
Opioid 1 98.16 Very High Very High Very High
Disease Link Frequency Relevance Heat
Nash(non-alcoholic Steatohepatitis) 36 99.00 Very High Very High Very High
Increased Venous Pressure Under Development 58 93.88 High High
Ganglion Cysts 31 92.04 High High
Anaerobic Bacterial Infections 1 91.60 High High
Glioma 4 84.44 Quite High
Neuroblastoma 7 84.08 Quite High
Natriuresis 4 83.36 Quite High
Pain 30 72.80 Quite High
Depression 4 69.92 Quite High
Stroke 8 69.16 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
IP3R3 is present in the paranodal regions of the nodes.
Gene_expression (present) of IP3R3 in nodes
1) Confidence 0.74 Published 2007 Journal Neuroreport Section Abstract Doc Link 17496801 Disease Relevance 0 Pain Relevance 0.32
Expression of IP3 receptor isoforms at the nodes of Ranvier in rat sciatic nerve.
Gene_expression (Expression) of IP3 in sciatic nerve associated with sciatic nerve
2) Confidence 0.74 Published 2007 Journal Neuroreport Section Title Doc Link 17496801 Disease Relevance 0 Pain Relevance 0.27
Inositol 1,4,5-trisphosphate (IP3) production in cardiac myocytes was determined by the IP3 binding protein assay.
Gene_expression (production) of IP3 in cardiac myocytes
3) Confidence 0.44 Published 1998 Journal Eur. J. Pharmacol. Section Abstract Doc Link 9726662 Disease Relevance 0 Pain Relevance 0
Further study is needed to determine the events that occur after the kappa-opioid receptor stimulation to production of IP3 upon the development of tolerance to a kappa-opioid.
Gene_expression (production) of IP3 associated with tolerance, kappa opioid receptor and opioid
4) Confidence 0.40 Published 1996 Journal Eur. J. Pharmacol. Section Abstract Doc Link 8836621 Disease Relevance 0 Pain Relevance 0.62
These results establish that the effect of the toxin on both intracellular Ca2+ and IP3 levels occurs via a membrane potential sensor instead of directly by Na+ flux and supports the notion of a train of action potentials being more efficient as a stimulus than sustained depolarization, suggesting that tetanus is the physiological stimulus for the IP3-dependent calcium signal involved in regulation of gene expression.
Gene_expression (levels) of IP3 associated with action potential and anaerobic bacterial infections
5) Confidence 0.33 Published 2008 Journal Cell Calcium Section Abstract Doc Link 18276006 Disease Relevance 0.09 Pain Relevance 0.27
The half-maximal concentration of isoproterenol required for [Ca2+]i mobilization and IP3 production was comparable (approximately 10(-5) M).
Gene_expression (production) of IP3
6) Confidence 0.28 Published 1988 Journal J. Biol. Chem. Section Abstract Doc Link 2900837 Disease Relevance 0 Pain Relevance 0.03
Carbachol induced a approximately 3.5-fold increase in inositol trisphosphate (IP3) production in parotid cells within 30 s. 8-Bromo-cAMP, N6,O2'-dioctanoyl-cAMP, and isoproterenol consistently induced a significant stimulation in IP3 production.
Gene_expression (production) of IP3
7) Confidence 0.28 Published 1988 Journal J. Biol. Chem. Section Abstract Doc Link 2900837 Disease Relevance 0 Pain Relevance 0.06
Carbachol induced a approximately 3.5-fold increase in inositol trisphosphate (IP3) production in parotid cells within 30 s. 8-Bromo-cAMP, N6,O2'-dioctanoyl-cAMP, and isoproterenol consistently induced a significant stimulation in IP3 production.
Gene_expression (production) of IP3
8) Confidence 0.28 Published 1988 Journal J. Biol. Chem. Section Abstract Doc Link 2900837 Disease Relevance 0 Pain Relevance 0.06
First, MeHg mobilized Ca2+ from an intracellular store sensitive to inositol-1,4,5-tris-phosphate (IP3) which was independent of IP3 generation.
Gene_expression (generation) of IP3
9) Confidence 0.23 Published 1996 Journal Neurotoxicology Section Abstract Doc Link 8784818 Disease Relevance 0 Pain Relevance 0.07
Interestingly, albeit the potentiation during DHPG application was not dependent on NMDA receptors and PKC but on PLC, IP3 receptors, NOS, CaMKII and ERK, the long-lasting property of the potentiation was disappeared by the blockades of NMDA receptors, as well as individual antagonists used to block signal transduction pathways.
Gene_expression (receptors) of IP3 associated with kinase c, antagonist and nmda receptor
10) Confidence 0.22 Published 2009 Journal Mol Pain Section Body Doc Link PMC2743647 Disease Relevance 0.07 Pain Relevance 0.42
The model described P2Y/P2X surface receptor activation (including Gq protein signaling), Phophoinositide (PI) metabolism, ATPase pumps, Na/Ca exchangers, ion leaks and IP3R channels (Fig. 1 and Table 1).
Gene_expression (channels) of IP3R
11) Confidence 0.16 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2735677 Disease Relevance 0.14 Pain Relevance 0.11
Morphine (1 microM) reduced both forskolin-stimulated cAMP levels and IP3 levels by 20 +/- 5 and 34 +/- 8% respectively in COS and CHO cell cultures expressing the cloned rat mu receptor cDNA.
Gene_expression (levels) of IP3 in CHO associated with morphine
12) Confidence 0.08 Published 1994 Journal Neuroreport Section Abstract Doc Link 8003685 Disease Relevance 0 Pain Relevance 0.38
Interestingly, FCCP did not affect the potent release induced by a high dose of UTP (data not shown), as if for long-lasting oscillatory activity to occur in the presence of low IP3 synthesis a fine regulation of cytoplasmic Ca2+ was needed to maintain IP3R channels available to open.
Gene_expression (synthesis) of IP3
13) Confidence 0.08 Published 2006 Journal Purinergic Signal Section Body Doc Link PMC2096653 Disease Relevance 0 Pain Relevance 0
In agreement with our previous data (Nash et al. 2004) such activity promotes enhanced IP3 formation, seen as spikes above the level of IP3 produced by the presence of agonist (Fig. 1b).
Gene_expression (produced) of IP3 in spikes associated with nash(non-alcoholic steatohepatitis) and agonist
14) Confidence 0.05 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0.25 Pain Relevance 0.32
4 is stimulated [66] to mediate the synthesis of IP3, which then causes liberation of Ca2+ from intracellular stores [67].
Gene_expression (synthesis) of IP3
15) Confidence 0.05 Published 2004 Journal Purinergic Signal Section Body Doc Link PMC2096562 Disease Relevance 0 Pain Relevance 0.16
Furthermore, enhanced synaptic activity in hippocampal neurons, initiated by suppression of inhibitory GABAA receptors with picrotoxin, dramatically enhances M1 mACh receptor-stimulated IP3 production and Ca2+ store release (Nash et al. 2004).
Gene_expression (production) of IP3 in neurons associated with nash(non-alcoholic steatohepatitis)
16) Confidence 0.05 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0.18 Pain Relevance 0.21
However, the picrotoxin-induced IP3 spikes normally seen in the presence of MCh (Fig. 2c) were absent following inclusion of the AMPA receptor antagonist DNQX (10 ?
Neg (absent) Gene_expression (spikes) of IP3 in spikes associated with antagonist
17) Confidence 0.05 Published 2007 Journal Journal of Neurochemistry Section Body Doc Link PMC2658029 Disease Relevance 0 Pain Relevance 0.47
The signalling cascade underlying this inhibition included activation of PLC, generation of IP3, and release of Ca2+ from intracellular stores [110].
Gene_expression (generation) of IP3
18) Confidence 0.03 Published 2004 Journal Purinergic Signal Section Body Doc Link PMC2096562 Disease Relevance 0.26 Pain Relevance 0.06
Stimulating a single glial cell leads to the production of InsP3, triggering the release of Ca2+ from internal stores in the stimulated cell as well as in adjacent cells.
Gene_expression (production) of InsP3 in glial cell
19) Confidence 0.02 Published 2005 Journal Purinergic Signal Section Body Doc Link PMC2096541 Disease Relevance 0 Pain Relevance 0.03
Vasopressin interacts with V1Rs, which are found in high density on vascular smooth muscle, through the Gq/11 pathway to stimulate phospholipase C and produce the intracellular messengers inositol trisphosphate (IP3) and diacylglycerol.
Gene_expression (produce) of IP3 in smooth muscle
20) Confidence 0.02 Published 2004 Journal Crit Care Section Body Doc Link PMC420051 Disease Relevance 0.26 Pain Relevance 0.11

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox