INT249176

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Context Info
Confidence 0.02
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 0
Pain Relevance 0

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

transmembrane transport (ITPR3, TRPC1) nucleoplasm (ITPR3) small molecule metabolic process (ITPR3)
endoplasmic reticulum (ITPR3) cytoplasm (ITPR3) signal transduction (ITPR3)
Anatomy Link Frequency
B lymphocytes 1
platelets 1
ITPR3 (Homo sapiens)
TRPC1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 16 5.00 Very Low Very Low Very Low
agonist 8 5.00 Very Low Very Low Very Low
addiction 6 5.00 Very Low Very Low Very Low
TRP channel 4 5.00 Very Low Very Low Very Low
Inflammatory response 4 5.00 Very Low Very Low Very Low
antagonist 4 5.00 Very Low Very Low Very Low
cytokine 2 5.00 Very Low Very Low Very Low
cINOD 2 5.00 Very Low Very Low Very Low
fibrosis 2 5.00 Very Low Very Low Very Low
Inflammatory mediators 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 22 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
Targeted Disruption 6 5.00 Very Low Very Low Very Low
Pulmonary Disease 4 5.00 Very Low Very Low Very Low
Neutrophil Disorders 4 5.00 Very Low Very Low Very Low
Stress 4 5.00 Very Low Very Low Very Low
Respiratory Syncytial Virus 2 5.00 Very Low Very Low Very Low
Toxicity 2 5.00 Very Low Very Low Very Low
Prostate Cancer 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
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].
InsP3 Binding (interaction) of TRPC1 in B lymphocytes
1) Confidence 0.02 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].
InsP3 Binding (interaction) of TRPC1 in platelets
2) 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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