INT36365

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Context Info
Confidence 0.41
First Reported 1987
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 15
Total Number 16
Disease Relevance 4.13
Pain Relevance 3.56

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
renal tubule 1
spike 1
microglia 1
hippocampus 1
blood 1
SK (Mus musculus)
Pain Link Frequency Relevance Heat
nMDA receptor 72 99.98 Very High Very High Very High
isoflurane 20 99.98 Very High Very High Very High
amygdala 40 99.14 Very High Very High Very High
Pyramidal cell 160 98.66 Very High Very High Very High
cytokine 2 98.48 Very High Very High Very High
noradrenaline 1 98.38 Very High Very High Very High
Inflammation 21 98.08 Very High Very High Very High
GABAergic 24 97.66 Very High Very High Very High
Hippocampus 34 96.58 Very High Very High Very High
midbrain 33 93.68 High High
Disease Link Frequency Relevance Heat
INFLAMMATION 23 98.08 Very High Very High Very High
Injury 9 93.76 High High
Cv Unclassified Under Development 4 92.80 High High
Increased Venous Pressure Under Development 19 91.12 High High
Necrosis 3 90.60 High High
Arthritis 8 89.92 High High
Myocardial Infarction 9 88.08 High High
Pain 1 86.64 High High
Disease 67 86.60 High High
Pressure Volume 2 Under Development 1 86.40 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These cascade of events include the activation of sphingosine kinase (SK), and subsequent production of the mitogenic and proinflammatory lipid sphingosine 1-phosphate (S1P).
Positive_regulation (activation) of SK
1) Confidence 0.41 Published 2010 Journal Carcinogenesis Section Abstract Doc Link 20688834 Disease Relevance 0.73 Pain Relevance 0.22
We sought to determine whether isoflurane stimulates sphingosine kinase (SK) activity and synthesis of sphingosine-1-phosphate (S1P) in renal proximal tubule cells to mediate renal protection via the S1P signaling pathway.
Spec (whether) Positive_regulation (stimulates) of SK in renal proximal tubule associated with isoflurane
2) Confidence 0.35 Published 2007 Journal Am. J. Physiol. Renal Physiol. Section Abstract Doc Link 17898040 Disease Relevance 0.65 Pain Relevance 0.53
Taken together, our findings indicate that isoflurane activates SK in renal tubule cells and initiates S1P-->S1P(1) receptor signaling to mediate the renal protective effects.
Positive_regulation (activates) of SK in renal tubule associated with isoflurane
3) Confidence 0.35 Published 2007 Journal Am. J. Physiol. Renal Physiol. Section Abstract Doc Link 17898040 Disease Relevance 0.60 Pain Relevance 0.59
Analysis of plasma creatine kinase curves (CK) from 7,632 patients demonstrates that the rate of input and disappearance of CK into the blood was significantly increased in SK patients.
Positive_regulation (increased) of SK in blood
4) Confidence 0.26 Published 1987 Journal Biomed. Pharmacother. Section Abstract Doc Link 3330456 Disease Relevance 0.54 Pain Relevance 0.09
The speed of coronary reperfusion was 40 +/- 26 min in patients with accelerated SK and this time was significantly shorter than the time of 60 +/- 24 min registered in the control group.
Positive_regulation (accelerated) of SK
5) Confidence 0.26 Published 1997 Journal Rom J Intern Med Section Abstract Doc Link 9562652 Disease Relevance 0.54 Pain Relevance 0.08
In Purkinje cells, the only output neurons in the cerebellar cortex, spike-triggered elevations in intracellular Ca2+ lead to the activation of SK channels mainly of the SK2 type [157].
Positive_regulation (activation) of SK in spike
6) Confidence 0.14 Published 2008 Journal Cell Mol Life Sci Section Body Doc Link PMC2798969 Disease Relevance 0.09 Pain Relevance 0.07
However, in juvenile SNR GABAergic neurons, Yanovsky and colleagues [146, 147] observed spontaneously occurring, transient outward currents due to the activation of SK channels by sparks of calcium released from ryanodine-sensitive intracellular stores (outward current pulses, OCPs), similar to those previously observed in midbrain dopaminergic neurons (spontaneous, miniature outward currents, SMOCs, [148, 149]).
Positive_regulation (activation) of SK in GABAergic neurons associated with gabaergic and midbrain
7) Confidence 0.14 Published 2008 Journal Cell Mol Life Sci Section Body Doc Link PMC2798969 Disease Relevance 0 Pain Relevance 0.29
Additionally, R-type Ca2+ channels are found selectively on dendritic spines of hippocampal pyramidal neurons and also Ca2+ influx through R-type Ca2+ channels leads also to the activation of SK channels in dendritic spines, resulting in a local dampening of synaptically driven Ca2+ transients and somatic potentials [105].
Positive_regulation (activation) of SK in pyramidal neurons associated with pyramidal cell
8) Confidence 0.11 Published 2008 Journal Cell Mol Life Sci Section Body Doc Link PMC2798969 Disease Relevance 0 Pain Relevance 0.32
Although the relative contribution of each of these mechanisms and their possible interplay are still somewhat controversial and might depend on the type of blood vessel and stimulation, a considerable consensus has been reached that the initial step of EDHF-dependent relaxation is the activation of SK (in particular SK3) and IK channels in the endothelium (reviewed in [177–179]), as supported also by findings in genetically modified mice overexpressing or lacking SK3 [181] or lacking IK channels [182].
Positive_regulation (activation) of SK in blood vessel
9) Confidence 0.11 Published 2008 Journal Cell Mol Life Sci Section Body Doc Link PMC2798969 Disease Relevance 0.10 Pain Relevance 0
Instead, a coupling similar to that described in the hippocampus between SK channels and NMDA receptors has been observed at glutamatergic synapses in pyramidal neurons of the lateral amygdala, where Ca2+ influx through NMDA receptors activates SK channels and shunts the ensuing synaptic potentials [103].
Positive_regulation (activates) of SK in hippocampus associated with pyramidal cell, nmda receptor, hippocampus and amygdala
10) Confidence 0.11 Published 2008 Journal Cell Mol Life Sci Section Body Doc Link PMC2798969 Disease Relevance 0.08 Pain Relevance 0.50
The proposed mechanism in the absence of apamin is that SK channels are activated by Ca2+ entering the spine through NMDA receptors.
Positive_regulation (activated) of SK in spine associated with nmda receptor
11) Confidence 0.10 Published 2008 Journal Cell Mol Life Sci Section Body Doc Link PMC2798969 Disease Relevance 0 Pain Relevance 0.39
The activation of SK channels in Purkinje cells is selectively linked to Ca2+ influx through P/Q-type Ca2+ channels [158, 160], so that small alterations in P/Q-type Ca2+ currents can have a strong impact on the firing properties of the Purkinje cells through their modulation of SK channel activity [161].
Positive_regulation (activation) of SK in Purkinje cells
12) Confidence 0.10 Published 2008 Journal Cell Mol Life Sci Section Body Doc Link PMC2798969 Disease Relevance 0.06 Pain Relevance 0.04
In Purkinje cells, the only output neurons in the cerebellar cortex, spike-triggered elevations in intracellular Ca2+ lead to the activation of SK channels mainly of the SK2 type [157].
Positive_regulation (activation) of SK in cerebellar cortex
13) Confidence 0.05 Published 2008 Journal Cell Mol Life Sci Section Body Doc Link PMC2798969 Disease Relevance 0.09 Pain Relevance 0.07
To monitor iNOS and nitric oxide, microglia were plated at 50,000 cells/well in a 96-well plate, cultured overnight (37°C; 5% CO2), and then stimulated for 24 h with LPS in the presence or absence of an SK blocker. iNOS induction was monitored with a mouse monoclonal antibody (1:200; Cell Signaling) and a Cy3-conjugated secondary antibody (1:500; Jackson Labs).
Positive_regulation (induction) of SK in microglia
14) Confidence 0.03 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0 Pain Relevance 0
In contrast to the abnormal responsiveness of CPRs, the intra-arterial injection of noradrenaline caused the expected decrease in SkBF in all animals tested, and in no instances increases in SkBF were observed.
Positive_regulation (increases) of SkBF in SkBF associated with noradrenaline
15) Confidence 0.01 Published 1996 Journal J. Auton. Nerv. Syst. Section Abstract Doc Link 8832516 Disease Relevance 0.67 Pain Relevance 0.28
The primary finding of these studies is that there are at least two independent mechanisms contributing to the rise in SkBF during nonpainful local heating: a fast-responding vasodilator system mediated by the axon reflexes and a more slowly responding vasodilator system that relies on local production of NO.
Positive_regulation (rise) of SkBF
16) Confidence 0.00 Published 2001 Journal J. Appl. Physiol. Section Abstract Doc Link 11568143 Disease Relevance 0 Pain Relevance 0.09

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