INT249235

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Context Info
Confidence 0.17
First Reported 2008
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 5
Disease Relevance 0.20
Pain Relevance 0.03

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
nose 4
B lymphocytes 3
platelets 1
ITPR3 (Homo sapiens)
Pain Link Frequency Relevance Heat
Serotonin 3 51.80 Quite High
imagery 8 26.24 Quite Low
withdrawal 6 18.96 Low Low
TRP channel 19 5.00 Very Low Very Low Very Low
Inflammation 16 5.00 Very Low Very Low Very Low
nociceptor 9 5.00 Very Low Very Low Very Low
agonist 8 5.00 Very Low Very Low Very Low
Mechanosensation 6 5.00 Very Low Very Low Very Low
Pain 6 5.00 Very Low Very Low Very Low
addiction 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Sprains And Strains 27 72.08 Quite High
Helminth Infection 42 68.00 Quite High
Loss Of Sense Of Smell 3 21.16 Low Low
INFLAMMATION 22 5.00 Very Low Very Low Very Low
Targeted Disruption 12 5.00 Very Low Very Low Very Low
Adhesions 10 5.00 Very Low Very Low Very Low
Disease 10 5.00 Very Low Very Low Very Low
Heart Rate Under Development 6 5.00 Very Low Very Low Very Low
Pain 6 5.00 Very Low Very Low Very Low
Neutrophil Disorders 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The “control sponge” (K579Q, R582Q), is deficient in IP3 binding and therefore should not disrupt IP3 signalling, while the “super sponge” (R511C) has increased affinity for IP3.
Positive_regulation (increased) of IP3 Binding (affinity) of
1) Confidence 0.17 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2729924 Disease Relevance 0.20 Pain Relevance 0.03
To this end, we investigated whether itr-1(sy290), a gain-of-function allele [38], could rescue the defects in nose touch response that resulted from egl-8 or plc-3 RNAi. itr-1(sy290) has a mutation, R582Q, in the IP3 binding site [38], which results in a two-fold increase in IP3 binding affinity [20].
Positive_regulation (increase) of IP3 Binding (affinity) of in nose
2) Confidence 0.16 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2729924 Disease Relevance 0 Pain Relevance 0
Thus, an itr-1 mutation that increases the receptor's affinity for IP3 partially rescues the defects in nose touch response that result from knockdown of either plc-3 or egl-8, suggesting that IP3 is an important component of the downstream signal from these PLCs.
Positive_regulation (increases) of IP3 Binding (affinity) of in nose
3) Confidence 0.16 Published 2009 Journal PLoS Genetics Section Body Doc Link PMC2729924 Disease Relevance 0 Pain Relevance 0
Support for this hypothesis is derived from information obtained in human platelets and B lymphocytes, which suggests that TRPC1 is activated upon interaction with InsP3-Rs [57] and that it acts not only as a component of SOCs but also as a regulatory subunit of InsP3-Rs [58].
Positive_regulation (activated) of InsP3 Binding (interaction) of in B lymphocytes
4) Confidence 0.03 Published 2008 Journal J Leukoc Biol Section Body Doc Link PMC2567897 Disease Relevance 0 Pain Relevance 0
Support for this hypothesis is derived from information obtained in human platelets and B lymphocytes, which suggests that TRPC1 is activated upon interaction with InsP3-Rs [57] and that it acts not only as a component of SOCs but also as a regulatory subunit of InsP3-Rs [58].
Positive_regulation (activated) of InsP3 in platelets Binding (interaction) of in B lymphocytes
5) Confidence 0.01 Published 2008 Journal J Leukoc Biol Section Body Doc Link PMC2567897 Disease Relevance 0 Pain Relevance 0

General Comments

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