INT120505

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Context Info
Confidence 0.27
First Reported 2004
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 6
Total Number 7
Disease Relevance 1.46
Pain Relevance 1.68

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
platelet 2
external 1
ITPR3 (Homo sapiens)
Pain Link Frequency Relevance Heat
antidepressant 38 97.32 Very High Very High Very High
Kinase C 27 96.12 Very High Very High Very High
qutenza 5 92.92 High High
5HT 282 92.28 High High
agonist 32 87.76 High High
Potency 2 84.04 Quite High
Pain 13 83.60 Quite High
cytokine 4 72.60 Quite High
Serotonin 5 49.68 Quite Low
Cannabinoid 8 32.40 Quite Low
Disease Link Frequency Relevance Heat
Neuroleptic Malignant Syndrome 1 99.78 Very High Very High Very High
Anxiety Disorder 178 96.60 Very High Very High Very High
Pain 12 83.60 Quite High
Apoptosis 4 82.28 Quite High
Stress 3 73.64 Quite High
Sprains And Strains 9 69.96 Quite High
Helminth Infection 14 65.88 Quite High
Disease 14 54.08 Quite High
Motor Neuron Diseases 62 50.00 Quite Low
Repression 3 41.20 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To examine whether thapsigargin- and Echinacea-induced Ca2+ entry pathways are pharmacologically similar in the HEK model, 2-APB was applied in the continued presence of external Ca2+. 2-APB is considered the most potent and consistent compound in blocking SOCE, acting as a potent SOCE inhibitor independent of, and in addition to, its ability to inhibit the IP3 receptor [17]. 2-APB has no effect on voltage-operated Ca2+ channels [18] or on non-voltage-activated Ca2+ entry pathways [19].
Negative_regulation (inhibit) of IP3 receptor in external
1) Confidence 0.27 Published 2010 Journal BMC Complement Altern Med Section Body Doc Link PMC3002894 Disease Relevance 0 Pain Relevance 0
activity, and this in conjunction with the downregulation of IP3R, predicts a reduction in calcium release from the ER.
Negative_regulation (downregulation) of IP3R
2) Confidence 0.21 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844426 Disease Relevance 0.27 Pain Relevance 0.04
In a second approach, to disrupt IP3R function rather than IP3 signalling, we used the unc-119 promoter to control expression of an itr-1 dsRNAi “snapback” construct [34].
Negative_regulation (disrupt) of IP3R
3) Confidence 0.16 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2729924 Disease Relevance 0.25 Pain Relevance 0
This could be a possible consequence of a reduction in the platelet levels of IP3, an intracellular product of the 5HT2 receptor-mediated phosphoinositide hydrolysis stimulating PKC, before returning to normal values after an eight-week SRI treatment (Delorme et al 2004).
Spec (possible) Negative_regulation (reduction) of IP3 in platelet associated with kinase c
4) Confidence 0.06 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2416754 Disease Relevance 0.28 Pain Relevance 0.41
This decrease in the platelet IP3 content was positively correlated with a reduction in the number of 5HT2A receptor binding sites (Delorme et al 2004), which could be reflective of postsynaptic receptor down-regulation caused by SRI administration (Maes and Meltzer 1995; Duman 1999).
Negative_regulation (decrease) of IP3 in platelet
5) Confidence 0.06 Published 2005 Journal Neuropsychiatric Disease and Treatment Section Body Doc Link PMC2416754 Disease Relevance 0.22 Pain Relevance 0.44
The ATP-induced [Ca2+]i rise was attenuated by applications of either a phospholipase C inhibitor, or inhibitors for IP3 or ryanodine receptors.
Negative_regulation (inhibitors) of IP3
6) Confidence 0.01 Published 2004 Journal FASEB J. Section Abstract Doc Link 15289444 Disease Relevance 0.08 Pain Relevance 0.08
NMS and PDBu, repressors of IP3 formation, drastically inhibited both the components of Ca2+ response. 4.
Negative_regulation (repressors) of IP3 associated with neuroleptic malignant syndrome
7) Confidence 0.00 Published 2005 Journal Cell. Mol. Neurobiol. Section Abstract Doc Link 16133936 Disease Relevance 0.37 Pain Relevance 0.72

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