INT16573

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Context Info
Confidence 0.07
First Reported 1991
Last Reported 2008
Negated 1
Speculated 2
Reported most in Body
Documents 18
Total Number 20
Disease Relevance 8.69
Pain Relevance 6.03

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
neurons 8
spinal 1
plasma cell 1
nociceptor 1
Cl (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammatory mediators 690 100.00 Very High Very High Very High
Inflammatory stimuli 30 99.92 Very High Very High Very High
Hyperalgesia 180 99.64 Very High Very High Very High
Dorsal horn 30 99.48 Very High Very High Very High
Inflammation 273 99.38 Very High Very High Very High
gABA 230 98.48 Very High Very High Very High
allodynia 60 97.92 Very High Very High Very High
nociceptor 180 97.84 Very High Very High Very High
Central nervous system 31 96.56 Very High Very High Very High
Pain 30 95.68 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 993 100.00 Very High Very High Very High
Hyperalgesia 180 99.64 Very High Very High Very High
Nociception 180 98.40 Very High Very High Very High
Neuropathic Pain 76 97.92 Very High Very High Very High
Pain 30 95.68 Very High Very High Very High
Apoptosis 171 93.36 High High
Nervous System Injury 15 90.56 High High
Epilepsy 16 89.72 High High
Injury 4 87.12 High High
Neurogenic Inflammation 30 76.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
At this point in time, the most conservative interpretation is that bestrophins may be one of many different kinds of channels that play a role in cell volume regulation (Nilius et al., 1996; Strange et al., 1996; Lang et al., 1998) or, possibly, that Cl?
Spec (possibly) Regulation (role) of Cl
1) Confidence 0.07 Published 2008 Journal The Journal of General Physiology Section Body Doc Link PMC2571971 Disease Relevance 0.06 Pain Relevance 0
exchange across the plasma cell membrane, regulating [Cl?]
Regulation (regulating) of Cl in plasma cell
2) Confidence 0.06 Published 2007 Journal PLoS ONE Section Body Doc Link PMC1950688 Disease Relevance 0 Pain Relevance 0.13
As a consequence of these findings, the regulation of Cl- transport proteins has become an important topic of nociceptor research [12].
Regulation (regulation) of Cl in nociceptor associated with nociceptor
3) Confidence 0.06 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.78 Pain Relevance 0.70
The rise of intracellular Cl- during treatment with inflammatory mediators points to a similiar shift in Cl- regulation as observed in various injured neurons [19].
Regulation (regulation) of Cl in neurons associated with inflammatory mediators
4) Confidence 0.05 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.58 Pain Relevance 0.29
These channels are involved in the regulation of Cl?
Regulation (regulation) of Cl
5) Confidence 0.05 Published 2008 Journal Current Neuropharmacology Section Body Doc Link PMC2647147 Disease Relevance 0.46 Pain Relevance 0.04
In addition, regulatory mechanisms that control the activity of Cl- transporters include phosphorylation [25-27] and dimerization [28].
Regulation (control) of Cl
6) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.39 Pain Relevance 0.39
KCC2 shows a very high turn-over rate at the plasma membrane (50% of labeled KCC2 is removed from the plasma membrane within 20 min in hippocampal neurons [48]) and, therefore, represents a suitable target for processes that regulate the rate of Cl- extrusion from the cell.
Regulation (regulate) of Cl in neurons
7) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.52 Pain Relevance 0.40
These results demonstrate that inflammatory mediators induce a change in the regime of Cl- handling in DRG neurons with a delay of 3 hr after the start of the inflammatory treatment.
Regulation (change) of Cl in neurons associated with inflammatory mediators and inflammation
8) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.26 Pain Relevance 0.13
Processes that control the dynamics of Cl- accumulation, consequently, play an important role in current concepts for the plasticity of the afferent pain pathway [3,5,8,12,30-35].
Regulation (control) of Cl associated with pain
9) Confidence 0.04 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.39 Pain Relevance 0.40
The increase in Isc was dependent on the presence of Cl- and HCO3- anions in the medium, but it was not affected by inhibitors of Cl-secretion such as furosemide or a Cl- channel blocker.
Neg (not) Regulation (affected) of Cl
10) Confidence 0.02 Published 1991 Journal Eicosanoids Section Abstract Doc Link 1838696 Disease Relevance 0 Pain Relevance 0.09
We studied the effects of inflammatory mediators on the intracellular Cl- concentration as well as on the expression of NKCC1 and KCC2.
Regulation (effects) of Cl associated with inflammatory mediators
11) Confidence 0.02 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.53 Pain Relevance 0.47
Over the 3-hr time course of the experiments, we did not detect any change in mRNA levels of either Cl- transporter (data not shown).
Regulation (change) of Cl
12) Confidence 0.02 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.41 Pain Relevance 0.21
The regulation of intracellular chloride, [Cl-]i, in DRG neurons has a distinct impact on the detection and transmission of the peripheral nociceptive signals.
Regulation (regulation) of Cl in neurons associated with nociception
13) Confidence 0.02 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.28 Pain Relevance 0.03
Based on the hypothesis that modulation of the peripheral Cl- homeostasis is involved in the generation of inflammatory hyperalgesia, we examined the effects of inflammatory mediators on intracellular Cl- concentrations and on the expression levels of Cl- transporters in rat DRG neurons.


Spec (examined) Regulation (effects) of Cl in neurons associated with inflammatory mediators, hyperalgesia and inflammation
14) Confidence 0.02 Published 2008 Journal Mol Pain Section Abstract Doc Link PMC2526990 Disease Relevance 0.69 Pain Relevance 0.39
These findings corroborate current concepts for the role of Cl- regulation in the generation of inflammatory hyperalgesia and allodynia.
Regulation (regulation) of Cl associated with hyperalgesia, allodynia and inflammation
15) Confidence 0.02 Published 2008 Journal Mol Pain Section Abstract Doc Link PMC2526990 Disease Relevance 0.79 Pain Relevance 0.51
Changes of gene transcription do not appear to contribute to the altered Cl- regulation within the time frame of our experiments.
Regulation (regulation) of Cl
16) Confidence 0.02 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.46 Pain Relevance 0.30
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].
Regulation (regulation) of Cl in spinal associated with hyperalgesia
17) Confidence 0.02 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.48 Pain Relevance 0.33
Based on the hypothesis that modulation of the peripheral Cl- homeostasis is involved in the generation of inflammatory hyperalgesia, we examined the effects of inflammatory mediators on intracellular Cl- concentrations and on the expression levels of Cl- transporters in rat DRG neurons.


Regulation (modulation) of Cl in neurons associated with inflammatory mediators, hyperalgesia and inflammation
18) Confidence 0.02 Published 2008 Journal Mol Pain Section Abstract Doc Link PMC2526990 Disease Relevance 0.68 Pain Relevance 0.37
Our data demonstrate an impact of inflammatory stimuli on Cl- regulation in DRG neurons and support concepts for the role of Cl- accumulation in the generation of hyperalgesia.


Regulation (regulation) of Cl in neurons associated with hyperalgesia and inflammatory stimuli
19) Confidence 0.02 Published 2008 Journal Mol Pain Section Body Doc Link PMC2526990 Disease Relevance 0.67 Pain Relevance 0.49
Thermodynamic regulation of NKCC1-mediated Cl- cotransport underlies plasticity of GABA(A) signaling in neonatal neurons.
Regulation (regulation) of Cl in neurons associated with gaba
20) Confidence 0.00 Published 2008 Journal J. Neurosci. Section Title Doc Link 18256250 Disease Relevance 0.27 Pain Relevance 0.37

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