INT65832

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Context Info
Confidence 0.07
First Reported 1996
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 7
Disease Relevance 0.83
Pain Relevance 1.42

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

Anatomy Link Frequency
sensory neurons 1
neuron 1
embryonic kidney 1
reticulum 1
PIRT (Homo sapiens)
Pain Link Frequency Relevance Heat
qutenza 13 100.00 Very High Very High Very High
hyperexcitability 12 98.48 Very High Very High Very High
Potency 1 92.72 High High
addiction 28 90.52 High High
Pain 60 78.96 Quite High
antagonist 2 78.60 Quite High
Root ganglion neuron 5 75.00 Quite High
agonist 1 75.00 Quite High
guanethidine 2 59.64 Quite High
potassium channel 2 50.00 Quite Low
Disease Link Frequency Relevance Heat
Erythermalgia 100 93.68 High High
Pain 60 77.76 Quite High
Ganglion Cysts 5 75.00 Quite High
Tinnitus 1 60.12 Quite High
Congenital Pain Insensitivity 4 23.16 Low Low
Channelopathies 4 21.44 Low Low
Somatoform Disorder 8 18.08 Low Low
Non-diabetic Peripheral Neuropathy 4 16.72 Low Low
Nociception 12 5.00 Very Low Very Low Very Low
Epilepsy 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The midpoint of current activation of both channels was shifted to hyperpolarized potentials.
Positive_regulation (activation) of channels
1) Confidence 0.07 Published 2006 Journal Otol. Neurotol. Section Body Doc Link 16371858 Disease Relevance 0.06 Pain Relevance 0
The first system provides a fast relaxation in response to low frequency of stimulation and may involve the action of a transmitter(s) (possibly ATP) which mobilizes intracellular Ca2+ from sarcoplasmic reticulum leading to the activation of apamin-sensitive K+ channels.
Positive_regulation (activation) of channels in reticulum
2) Confidence 0.02 Published 1996 Journal J Auton Pharmacol Section Abstract Doc Link 8884460 Disease Relevance 0 Pain Relevance 0.07
In contrast, resiniferatoxin and its analog, phorbol 12-phenylacetate 13-acetate 20-homovanillate, was more potent in activating the CAP-activated channels in cultured sensory neurons than VR1.
Positive_regulation (activating) of channels in sensory neurons associated with qutenza
3) Confidence 0.01 Published 2001 Journal Neurosci. Lett. Section Abstract Doc Link 11166956 Disease Relevance 0.07 Pain Relevance 0.93
Remaining available channels were activated by a 20 ms test pulse to -10 mV.
Positive_regulation (activated) of channels
4) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2262064 Disease Relevance 0 Pain Relevance 0
Computer simulations of the effect of mutant NaV1.7 channels in model DRG neurons have in fact shown that the hyperpolarized shift in the activation of channels is the key factor in inducing neuron hyperexcitability, whereas slow inactivation modulates the effect on the firing frequency of these neurons [22].
Positive_regulation (activation) of channels in neuron associated with hyperexcitability
5) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2262064 Disease Relevance 0.34 Pain Relevance 0.21
Steady-state fast inactivation was achieved with a series of 500-ms prepulses (-140 to 10 mV in 10 mV increments) and the remaining non-inactivated channels were activated by a 20 ms step depolarization to -10 mV.
Positive_regulation (activated) of channels
6) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2262064 Disease Relevance 0 Pain Relevance 0
Human embryonic kidney cells (HEK293) stably expressing either wild-type (NaV1.7R) or mutant (I136V) channels were generated as described before [21].


Positive_regulation (generated) of channels in embryonic kidney
7) Confidence 0.01 Published 2008 Journal Mol Pain Section Body Doc Link PMC2262064 Disease Relevance 0.36 Pain Relevance 0.21

General Comments

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