INT36040

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Context Info
Confidence 0.70
First Reported 1986
Last Reported 2010
Negated 0
Speculated 4
Reported most in Abstract
Documents 21
Total Number 25
Disease Relevance 4.87
Pain Relevance 7.77

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) transport (Itpr3) endoplasmic reticulum (Itpr3)
nucleolus (Itpr3) nucleus (Itpr3) transmembrane transport (Itpr3)
Anatomy Link Frequency
neurons 4
cardiomyocytes 1
dorsal root ganglion 1
reticulum 1
Itpr3 (Mus musculus)
Pain Link Frequency Relevance Heat
bradykinin 92 99.84 Very High Very High Very High
Kinase C 75 99.76 Very High Very High Very High
Opioid 10 99.76 Very High Very High Very High
agonist 89 99.14 Very High Very High Very High
opiate 4 98.98 Very High Very High Very High
dorsal root ganglion 10 98.64 Very High Very High Very High
algogenic 4 98.46 Very High Very High Very High
Enkephalin 13 98.36 Very High Very High Very High
member 8 16 92.44 High High
Potency 7 92.24 High High
Disease Link Frequency Relevance Heat
Ganglion Cysts 12 98.64 Very High Very High Very High
Pain 100 98.28 Very High Very High Very High
Neuroblastoma 20 98.18 Very High Very High Very High
Congenital Anomalies 3 96.80 Very High Very High Very High
Disease 29 90.00 High High
Arrhythmia Under Development 22 88.88 High High
Sudden Death 3 87.64 High High
Bordatella Infection 6 87.32 High High
Malignant Hyperthermia 1 83.44 Quite High
Stress 7 80.88 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
For instance, IP3R-binding protein released with IP3 and IP3 agonistically bind to IP3Rs and determine the threshold of Ca2+ release in cerebellar neurons (Ando et al. 2003), and IP3R-associated cyclic guanonsine monophosphate kinase substrate (IRAG) binds to IP3Rs via its coiled-coil domain and regulates IP3-mediated Ca2+ release in smooth muscle cells (Schlossmann et al. 2000; Geiselhöringer et al. 2004).
Spec (determine) Localization (release) of IP3R-associated in neurons
1) Confidence 0.70 Published 2010 Journal Chemical Senses Section Body Doc Link PMC2805811 Disease Relevance 0 Pain Relevance 0.12
Immunocytochemistry showed that both constructs of Lrmp/Jaw1 were similarly colocalized with IP3R3 on the ER membrane of transfected COS7 cells, whereas immunoprecipitation experiments showed that FLAG-Lrmp/Jaw1 and FLAG-Lrmp/Jaw1?
Localization (colocalized) of IP3R3
2) Confidence 0.70 Published 2010 Journal Chemical Senses Section Body Doc Link PMC2805811 Disease Relevance 0 Pain Relevance 0
Therefore, the deletion of the coiled-coil domain did not affect subcellular localization of Lrmp/Jaw1 and IP3R3 but altered its interaction with IP3R3.
Localization (localization) of IP3R3
3) Confidence 0.66 Published 2010 Journal Chemical Senses Section Body Doc Link PMC2805811 Disease Relevance 0 Pain Relevance 0
2 to produce IP3, which induces calcium (Ca2+) release through IP3R3 located on the membrane of endoplasmic reticulum (ER).
Localization (release) of IP3R3 in reticulum
4) Confidence 0.66 Published 2010 Journal Chemical Senses Section Body Doc Link PMC2805811 Disease Relevance 0 Pain Relevance 0.18
The results suggest that histamine causes an H1 receptor-dependent increase in [Ca++]i, probably by the increased entry of extracellular Ca++, although there may be a contribution from intracellular Ca++ released by IP3(1,4,5).
Localization (released) of IP3
5) Confidence 0.62 Published 1988 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 3262737 Disease Relevance 0.07 Pain Relevance 0.07
Inositol tris-phosphate (IP3) channels are stimulated by phospolipid metabolism and the release of IP3.
Localization (release) of IP3
6) Confidence 0.61 Published 2004 Journal Eur J Pain Section Abstract Doc Link 14987625 Disease Relevance 0 Pain Relevance 0.37
A23187, a Ca2+ ionophore, produced a 37% decrease in IP3 concentration. 12-O-Tetradecanoylphorbol-13-acetate, which mimics the effects of DG and activates protein kinase C, inhibited IP3 release by 80%.
Localization (release) of IP3 associated with kinase c
7) Confidence 0.61 Published 1987 Journal J. Neurochem. Section Abstract Doc Link 3494104 Disease Relevance 0.23 Pain Relevance 0.62
Bradykinin-induced IP3 release was blocked by several novel bradykinin analogues.
Localization (release) of IP3 associated with bradykinin
8) Confidence 0.61 Published 1987 Journal J. Neurochem. Section Abstract Doc Link 3494104 Disease Relevance 0.37 Pain Relevance 0.55
For instance, IP3R-binding protein released with IP3 and IP3 agonistically bind to IP3Rs and determine the threshold of Ca2+ release in cerebellar neurons (Ando et al. 2003), and IP3R-associated cyclic guanonsine monophosphate kinase substrate (IRAG) binds to IP3Rs via its coiled-coil domain and regulates IP3-mediated Ca2+ release in smooth muscle cells (Schlossmann et al. 2000; Geiselhöringer et al. 2004).
Spec (determine) Localization (released) of IP3Rs in neurons
9) Confidence 0.61 Published 2010 Journal Chemical Senses Section Body Doc Link PMC2805811 Disease Relevance 0 Pain Relevance 0.13
For instance, IP3R-binding protein released with IP3 and IP3 agonistically bind to IP3Rs and determine the threshold of Ca2+ release in cerebellar neurons (Ando et al. 2003), and IP3R-associated cyclic guanonsine monophosphate kinase substrate (IRAG) binds to IP3Rs via its coiled-coil domain and regulates IP3-mediated Ca2+ release in smooth muscle cells (Schlossmann et al. 2000; Geiselhöringer et al. 2004).
Spec (determine) Localization (released) of IP3 in neurons
10) Confidence 0.61 Published 2010 Journal Chemical Senses Section Body Doc Link PMC2805811 Disease Relevance 0 Pain Relevance 0.13
For instance, IP3R-binding protein released with IP3 and IP3 agonistically bind to IP3Rs and determine the threshold of Ca2+ release in cerebellar neurons (Ando et al. 2003), and IP3R-associated cyclic guanonsine monophosphate kinase substrate (IRAG) binds to IP3Rs via its coiled-coil domain and regulates IP3-mediated Ca2+ release in smooth muscle cells (Schlossmann et al. 2000; Geiselhöringer et al. 2004).
Spec (determine) Localization (released) of IP3 in neurons
11) Confidence 0.61 Published 2010 Journal Chemical Senses Section Body Doc Link PMC2805811 Disease Relevance 0 Pain Relevance 0.13
In taste cells, calmyrin/CIB1 has been suggested to interact with T1r2 and modulates IP3-evoked calcium release, recently (Hennigs et al. 2008).
Localization (release) of IP3
12) Confidence 0.61 Published 2010 Journal Chemical Senses Section Body Doc Link PMC2805811 Disease Relevance 0 Pain Relevance 0
These second messengers modulated bradykinin-dependent IP3 release to varying degrees.
Localization (release) of IP3 associated with bradykinin
13) Confidence 0.53 Published 1987 Journal J. Neurochem. Section Abstract Doc Link 3494104 Disease Relevance 0.24 Pain Relevance 0.67
Maximal stimulation of [2-3H]IP3 and [2-3H]IP2 release by bradykinin in the absence of LiCl occurred at 7 (or less) and 15 s, respectively, with average levels of 5.7-(IP3) and 3.4-(IP2) fold of control values.
Localization (release) of IP3 associated with bradykinin
14) Confidence 0.53 Published 1987 Journal J. Neurochem. Section Abstract Doc Link 3494104 Disease Relevance 0.33 Pain Relevance 0.46
In the mouse neuroblastoma x dorsal root ganglion hybrid cell line F-11, bradykinin receptor stimulation induced the release of inositol-1,4,5-trisphosphate (IP3) and inositol-1,4-bisphosphate (IP2).
Localization (release) of IP3 in dorsal root ganglion associated with ganglion cysts, dorsal root ganglion, neuroblastoma and bradykinin
15) Confidence 0.53 Published 1987 Journal J. Neurochem. Section Abstract Doc Link 3494104 Disease Relevance 0.35 Pain Relevance 0.39
These results show that pain-inducing BK has a major acute stimulatory effect on receptor-phospholipase C-coupled IP3 release, the opioid peptide DADLE has no such effect and, DADLE does not block the IP3 release induced by BK.
Localization (release) of IP3 associated with algogenic, opioid and bradykinin
16) Confidence 0.38 Published 1986 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 3516143 Disease Relevance 0.23 Pain Relevance 0.79
Under these same conditions, D-Ala2-D-Leu5 enkephalin (DADLE) (10 microM), an opiate agonist with 2nM affinity, gave no stimulation of IP3 release.
Localization (release) of IP3 associated with agonist, opiate and enkephalin
17) Confidence 0.38 Published 1986 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 3516143 Disease Relevance 0.23 Pain Relevance 0.80
These results show that pain-inducing BK has a major acute stimulatory effect on receptor-phospholipase C-coupled IP3 release, the opioid peptide DADLE has no such effect and, DADLE does not block the IP3 release induced by BK.
Localization (release) of IP3 associated with algogenic, opioid and bradykinin
18) Confidence 0.34 Published 1986 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 3516143 Disease Relevance 0.23 Pain Relevance 0.81
Maximum stimulation (4-fold) of [2-3H]inositol trisphosphate (IP3) release in the absence of Li+ from NCB-20's prelabelled for 20-24 hours with [2-3H]myo-inositol (15 microCi/confluent 60mm dish) occurred after 5-10 seconds of bradykinin exposure, with an EC50 of approximately 100nM.
Localization (release) of IP3 associated with bradykinin
19) Confidence 0.34 Published 1986 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 3516143 Disease Relevance 0.17 Pain Relevance 0.44
cardiomyocytes has been proposed to result from a deficiency of a complex of ankyrin-B with the Na/K ATPase, Na/Ca exchanger, and IP3 receptor localized in a specialized microdomain in cardiomyocyte transverse-tubules [16].
Localization (localized) of IP3 receptor in cardiomyocytes
20) Confidence 0.20 Published 2007 Journal PLoS ONE Section Body Doc Link PMC2013943 Disease Relevance 1.06 Pain Relevance 0.04

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