INT107456

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Context Info
Confidence 0.46
First Reported 2003
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 7
Disease Relevance 1.18
Pain Relevance 3.10

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

mRNA processing (Smn1) nucleolus (Smn1) RNA binding (Smn1)
nucleus (Smn1) cytoplasm (Smn1)
Anatomy Link Frequency
SMN 2
Smn1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Neurotransmitter 24 100.00 Very High Very High Very High
Calcitonin gene-related peptide 234 99.98 Very High Very High Very High
qutenza 84 99.00 Very High Very High Very High
antagonist 246 98.76 Very High Very High Very High
agonist 132 97.44 Very High Very High Very High
Bioavailability 6 94.24 High High
cerebral cortex 2 89.12 High High
TRP channel 6 84.00 Quite High
anesthesia 1 79.80 Quite High
ischemia 6 77.28 Quite High
Disease Link Frequency Relevance Heat
Cardiovascular Disease 18 98.16 Very High Very High Very High
Brain Injury 6 94.28 High High
Increased Venous Pressure Under Development 18 93.36 High High
Injury 1 91.56 High High
Death 1 78.64 Quite High
Cv Unclassified Under Development 6 77.28 Quite High
INFLAMMATION 12 76.24 Quite High
Shock 1 70.08 Quite High
Disease 24 62.24 Quite High
Pain 6 33.92 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In summary (Fig. 7), CGRP released from SMN promotes the dissociation of the ET-1/ETA-receptor complexes that are responsible for the long-lasting effects of the peptide.
Localization (released) of SMN associated with calcitonin gene-related peptide
1) Confidence 0.46 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2879375 Disease Relevance 0 Pain Relevance 0.57
We could not demonstrate that this mechanism acts as a negative feedback under normal conditions because desensitization of SMN and presence of CGRP-receptor antagonists do not alter the sensitivity to ET-1 ([33] and this study).
Localization (desensitization) of SMN associated with antagonist and calcitonin gene-related peptide
2) Confidence 0.43 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2879375 Disease Relevance 0.22 Pain Relevance 0.69
The effects of SMN-stimuli were reduced by CGRP-receptor antagonists and mimicked by exogenous CGRP, a neurotransmitter that can be released from peri-arterial SMN [27], [36], [40].
Localization (released) of SMN associated with neurotransmitter, antagonist and calcitonin gene-related peptide
3) Confidence 0.40 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2879375 Disease Relevance 0 Pain Relevance 0.55
Capsaicin, rutaecarpine and allyl isothiocyanate stimulate release of several neurotransmitters from SMN[27], [36], [37], [38], [39], [40].
Localization (release) of SMN associated with neurotransmitter and qutenza
4) Confidence 0.40 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2879375 Disease Relevance 0 Pain Relevance 0.55
We discovered that calcitonin-gene related peptide (CGRP) released from peri-arterial SMN terminates long-lasting vasoconstrictor effects of ET by promoting dissociation of ET-1/ETA-receptor complexes.


Localization (released) of SMN in SMN associated with calcitonin gene-related peptide
5) Confidence 0.40 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2879375 Disease Relevance 0.13 Pain Relevance 0.28
ET-1 can also promote activity of transient receptor potential (TRP) cation channels that stimulate release of vasodilator neurotransmitters from peri-arterial sensory-motor nerves (SMN)[27], [28].
Localization (release) of SMN in SMN associated with neurotransmitter
6) Confidence 0.40 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2879375 Disease Relevance 0.19 Pain Relevance 0.23
These include up-regulated transcription factors (SOCS-3, JAK-2, STAT-3, CREM, IRF-1, SMN, silencer factor-B, ANIA-3, ANIA-4, and HES-1) and signal transduction pathways (cpg21, Narp, and CRBP) and down-regulated transmitter release mechanisms (CITRON, synaptojanin II, ras-related rab3, neurexin-1beta, and SNAP25A and -B), kinases (IP-3-kinase, Pak1, Ca(2+)/CaM-dependent protein kinases), and ion channels (K(+) channels TWIK, RK5, X62839, and Na(+) channel I).
Localization (release) of SMN
7) Confidence 0.22 Published 2003 Journal J. Neurosci. Res. Section Abstract Doc Link 12503083 Disease Relevance 0.64 Pain Relevance 0.23

General Comments

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