INT90774

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Context Info
Confidence 0.45
First Reported 2000
Last Reported 2010
Negated 1
Speculated 1
Reported most in Body
Documents 2
Total Number 13
Disease Relevance 2.57
Pain Relevance 0.42

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 (Kcnn3) cytoplasm (Kcnn3)
Anatomy Link Frequency
neurons 3
microglia 3
striatum 1
Kcnn3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Spinal cord 12 94.44 High High
Action potential 25 89.60 High High
Inflammation 108 86.00 High High
potassium channel 1 85.36 High High
Hippocampus 24 75.00 Quite High
Dismenorea 1 71.04 Quite High
Migraine 12 63.68 Quite High
midbrain 12 48.64 Quite Low
cva 132 39.32 Quite Low
Neuronal excitability 12 37.60 Quite Low
Disease Link Frequency Relevance Heat
Infection 12 98.00 Very High Very High Very High
Apoptosis 72 97.04 Very High Very High Very High
Drug Induced Neurotoxicity 60 95.44 Very High Very High Very High
Stroke 252 95.28 Very High Very High Very High
Hypoxia 1 90.56 High High
INFLAMMATION 120 86.00 High High
Death 24 85.40 High High
Sprains And Strains 12 84.08 Quite High
Ganglion Cysts 12 73.52 Quite High
Schizophrenia 36 68.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
If apamin affected the function of interest, then 5 nM tamapin (Alomone) was used, which fully blocks SK2 (Kd = 24 pM) and significantly blocks SK3 (Kd = 1.7 nM) [41].
Negative_regulation (blocks) of SK3
1) Confidence 0.45 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0.13 Pain Relevance 0
An absence of SK3 did not present overt phenotypic consequences.
Negative_regulation (absence) of SK3
2) Confidence 0.43 Published 2000 Journal Science Section Abstract Doc Link 10988076 Disease Relevance 0.09 Pain Relevance 0.16
KCNN3 mRNA was prevalent in cultured microglia and increased after lipopolysaccharide-induced activation; SK3 channel blockade inhibited microglial activation and reduced their ability to kill neurons.
Negative_regulation (blockade) of SK3 in neurons
3) Confidence 0.33 Published 2010 Journal J Neuroinflammation Section Abstract Doc Link PMC2819255 Disease Relevance 0.40 Pain Relevance 0.03
Thus, contributions of SK3 to microglia functions are likely to extend to other CNS areas, including regions where SK3 is lacking in neurons.
Negative_regulation (lacking) of SK3 in microglia
4) Confidence 0.33 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0.69 Pain Relevance 0.15
In the relatively undamaged surrounding striatum at the lower left, the distribution of SK3 is the same as in the undamaged striatum (compare with Figure 6B), including diffuse SK3 staining between white matter tracts.
Negative_regulation (distribution) of SK3 in striatum
5) Confidence 0.33 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0.31 Pain Relevance 0.04
Each experiment followed the same format: if 100 nM apamin (blocks SK1, SK2, SK3) had an effect, then 5 nM tamapin (blocks SK2, SK3) was tested; if effective, then 250 pM tamapin (blocks only SK2) was tested.
Negative_regulation (blocks) of SK3
6) Confidence 0.33 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0 Pain Relevance 0
Because no specific SK3 inhibitors are available, we designed a subtractive protocol to unequivocally discriminate roles of SK3 channels, based on affinities of apamin and tamapin for cloned SK channels [26].
Neg (no) Negative_regulation (inhibitors) of SK3
7) Confidence 0.33 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0.18 Pain Relevance 0
Together, these results show that blocking SK3 channels in activated microglia reduces their ability to kill neurons by apoptosis.


Negative_regulation (blocking) of SK3 in neurons associated with apoptosis
8) Confidence 0.33 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0.27 Pain Relevance 0
A specific role for SK3 was deduced if a function was inhibited by apamin and 5 nM tamapin only.
Negative_regulation (deduced) of SK3
9) Confidence 0.33 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0 Pain Relevance 0
These results provide the first evidence that blocking SK3 channels in microglia can reduce their cytotoxicity, but does not globally inhibit their functions.
Negative_regulation (blocking) of SK3 in microglia
10) Confidence 0.29 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0.30 Pain Relevance 0.04
Because one potential outcome of peroxynitrite formation is nitration of cell proteins, we asked whether blocking the SK3 channel in microglia reduces tyrosine nitration in the target neuron cultures.
Spec (whether) Negative_regulation (blocking) of SK3 in neuron
11) Confidence 0.29 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0.21 Pain Relevance 0
Effects of apamin on microglia are most likely due to SK3 channel block because KCNN2 was nearly undetectable in LPS-activated microglia, and rodent KCNN1 apparently does not form functional channels [44,45].
Negative_regulation (block) of SK3 in microglia
12) Confidence 0.29 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0 Pain Relevance 0
Each experiment followed the same format: if 100 nM apamin (blocks SK1, SK2, SK3) had an effect, then 5 nM tamapin (blocks SK2, SK3) was tested; if effective, then 250 pM tamapin (blocks only SK2) was tested.
Negative_regulation (blocks) of SK3
13) Confidence 0.14 Published 2010 Journal J Neuroinflammation Section Body Doc Link PMC2819255 Disease Relevance 0 Pain Relevance 0

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