INT9555

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Context Info
Confidence 0.57
First Reported 1992
Last Reported 2007
Negated 0
Speculated 1
Reported most in Body
Documents 3
Total Number 4
Disease Relevance 0.92
Pain Relevance 0.56

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

plasma membrane (KCNQ2) transmembrane transport (KCNQ2)
Anatomy Link Frequency
nerve 1
KCNQ2 (Homo sapiens)
Pain Link Frequency Relevance Heat
Pain 2 94.96 High High
potassium channel 4 93.76 High High
dorsal root ganglion 4 84.56 Quite High
nociceptor 1 81.00 Quite High
Neuronal excitability 1 75.00 Quite High
headache 1 64.88 Quite High
Action potential 1 55.20 Quite High
local anesthetic 4 5.00 Very Low Very Low Very Low
anticonvulsant 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Pain 2 94.96 High High
Paralysis 1 93.48 High High
Ganglion Cysts 4 84.56 Quite High
Congenital Anomalies 1 74.20 Quite High
Bordatella Infection 1 68.72 Quite High
Diplopia 1 67.80 Quite High
Pharyngitis 1 65.52 Quite High
Headache 1 64.88 Quite High
Fever 1 64.28 Quite High
Convulsion 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Whole-cell voltage-clamp recordings revealed that bath application of the ligand for MrgD, beta-alanine, resulted in robust inhibition of KCNQ2/3 activity.
Negative_regulation (inhibition) of KCNQ2
1) Confidence 0.57 Published 2007 Journal J. Neurosci. Section Abstract Doc Link 17442834 Disease Relevance 0.49 Pain Relevance 0.49
RESULTS: Bupivacaine inhibited KCNQ2/Q3 channels in a concentration-dependent and reversible manner.
Negative_regulation (inhibited) of KCNQ2
2) Confidence 0.41 Published 2004 Journal Anesthesiology Section Body Doc Link 15277926 Disease Relevance 0 Pain Relevance 0
The inhibition of KCNQ2/Q3 channels by bupivacaine resulted in a significant and reversible depolarization of the membrane potential.
Negative_regulation (inhibition) of KCNQ2
3) Confidence 0.41 Published 2004 Journal Anesthesiology Section Body Doc Link 15277926 Disease Relevance 0 Pain Relevance 0
The abnormal ocular movement in this patient, which has nerve been reported in the literature, was considered to be due to a disinhibition of excitatory burst neuron (EBN) caused by the dysfunction of omnipause neuron, and possibly due to a delay of feed-back information of saccade to the EBN.
Spec (possibly) Negative_regulation (disinhibition) of EBN in nerve
4) Confidence 0.36 Published 1992 Journal Rinsho Shinkeigaku Section Abstract Doc Link 1424343 Disease Relevance 0.43 Pain Relevance 0.06

General Comments

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