INT244393

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Context Info
Confidence 0.65
First Reported 2008
Last Reported 2008
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 5
Disease Relevance 1.92
Pain Relevance 1.12

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 (Slc12a2)
Anatomy Link Frequency
spinal 2
neurons 2
Slc12a2 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammatory mediators 230 99.98 Very High Very High Very High
Hyperalgesia 60 99.36 Very High Very High Very High
imagery 25 94.04 High High
Dorsal horn 10 94.04 High High
Inflammation 90 91.96 High High
bradykinin 20 91.12 High High
Dorsal horn neuron 5 88.96 High High
Root ganglion neuron 5 47.84 Quite Low
Central nervous system 5 38.56 Quite Low
substance P 50 30.40 Quite Low
Disease Link Frequency Relevance Heat
INFLAMMATION 330 99.78 Very High Very High Very High
Hyperalgesia 60 99.36 Very High Very High Very High
Nociception 60 92.96 High High
Ganglion Cysts 10 75.00 Quite High
Neuropathic Pain 25 25.00 Low Low
Targeted Disruption 5 14.48 Low Low
Neurological Disease 5 6.72 Low Low
Peripheral Arterial Disease 20 5.00 Very Low Very Low Very Low
Pain 10 5.00 Very Low Very Low Very Low
Neurogenic Inflammation 10 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Changes of Cl- regulation that led to disinhibition of these spinal neurons and to referred mechanical hyperalgesia involved a rapid and transient increase of NKCC1 phosphorylation followed by increased recruitment of NKCC1 protein to the plasma membrane within 3 hours [33].
Positive_regulation (increase) of Phosphorylation (phosphorylation) of NKCC1 in spinal associated with hyperalgesia
1) Confidence 0.65 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.42 Pain Relevance 0.31
To test whether NKCC1 phosphorylation may contribute to the early rise of Cl- levels (< 3 hr), we stained 9 DRG sections from 3 animals with an antibody raised specifically against the phosphorylated form of NKCC1 (p-NKCC1).
Spec (may) Positive_regulation (contribute) of Phosphorylation (phosphorylation) of NKCC1
2) Confidence 0.47 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.17 Pain Relevance 0.08
The early rise of intracellular Cl- levels coincides with phosphorylation of NKCC1
Positive_regulation (coincides) of Phosphorylation (phosphorylation) of NKCC1
3) Confidence 0.47 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.23 Pain Relevance 0.12
This effect coincided with enhanced phosphorylation of the Na+-K+-2Cl- cotransporter NKCC1, suggesting that an increased activity of that transporter caused the early rise of intracellular Cl- levels.
Positive_regulation (enhanced) of Phosphorylation (phosphorylation) of NKCC1
4) Confidence 0.44 Published 2008 Journal Mol Pain Section Abstract Doc Link PMC2526990 Disease Relevance 0.70 Pain Relevance 0.39
These data demonstrate that the inflammatory mediators induce the phosphorylation of NKCC1 in DRG neurons and suggest that this phosphorylation causes the early (< 3 hr) phase of enhanced Cl- accumulation observed by 2P-FLIM in response to the stimulus.


Positive_regulation (induce) of Phosphorylation (phosphorylation) of NKCC1 in neurons associated with inflammatory mediators
5) Confidence 0.44 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.40 Pain Relevance 0.23

General Comments

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