INT203314

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Context Info
Confidence 0.31
First Reported 2007
Last Reported 2007
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 6
Disease Relevance 4.74
Pain Relevance 4.03

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

transport (Slc12a5) plasma membrane (Slc12a5) intracellular (Slc12a5)
transmembrane transport (Slc12a5)
Anatomy Link Frequency
neurons 8
Slc12a5 (Mus musculus)
Pain Link Frequency Relevance Heat
allodynia 320 95.84 Very High Very High Very High
gABA 10 94.60 High High
Neuropathic pain 4 93.76 High High
Neurotransmitter 4 93.40 High High
intrathecal 120 86.96 High High
dorsal root ganglion 30 83.68 Quite High
Glutamate receptor 2 82.12 Quite High
hyperexcitability 2 80.08 Quite High
Inflammation 74 79.20 Quite High
potassium channel 2 78.88 Quite High
Disease Link Frequency Relevance Heat
Injury 6 96.88 Very High Very High Very High
Neuropathic Pain 324 95.84 Very High Very High Very High
Motor Neuron Diseases 214 94.00 High High
Death 38 93.12 High High
Dystonia 2 93.12 High High
Parkinson's Disease 12 92.40 High High
Hyperalgesia 68 88.04 High High
Ganglion Cysts 30 83.68 Quite High
Stress 44 81.72 Quite High
Hypersensitivity 4 80.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Indeed, down-regulation of SLC12A5 expression together with GABAA receptor-mediated excitation occurs after in-vivo axonal injury [31], and mouse SLC12A5 knockouts suffer severe motor deficits and immediate postnatal death by asphyxiation [32].
Negative_regulation (regulation) of Gene_expression (expression) of SLC12A5 associated with injury and death
1) Confidence 0.31 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 0.80 Pain Relevance 0.22
Increased excitability, and hence exacerbated excitotoxicity, may also derive from the reduced expression of ATP1A3, KCNC2, and SLC12A5.
Negative_regulation (reduced) of Gene_expression (expression) of SLC12A5
2) Confidence 0.30 Published 2007 Journal BMC Genomics Section Body Doc Link PMC1796866 Disease Relevance 0.36 Pain Relevance 0.04
Inhibition of KCC2 by BUM would be expected to have the opposite effect on touch-evoked responses because decreased KCC2 expression (analogous to pharmacological inhibition) or KCC2 blockade with DIOA reverses the polarity of GABAAR responses in a subset of lamina I and II neurons, leading to allodynia which has been proposed as a mechanism of neuropathic pain [28].
Negative_regulation (decreased) of Gene_expression (expression) of KCC2 in neurons associated with allodynia and neuropathic pain
3) Confidence 0.29 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 0.91 Pain Relevance 0.97
Inhibition of KCC2 by BUM would be expected to have the opposite effect on touch-evoked responses because decreased KCC2 expression (analogous to pharmacological inhibition) or KCC2 blockade with DIOA reverses the polarity of GABAAR responses in a subset of lamina I and II neurons, leading to allodynia which has been proposed as a mechanism of neuropathic pain [28].
Negative_regulation (blockade) of Gene_expression (expression) of KCC2 in neurons associated with allodynia and neuropathic pain
4) Confidence 0.21 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 0.86 Pain Relevance 0.92
Inhibition of KCC2 by BUM would be expected to have the opposite effect on touch-evoked responses because decreased KCC2 expression (analogous to pharmacological inhibition) or KCC2 blockade with DIOA reverses the polarity of GABAAR responses in a subset of lamina I and II neurons, leading to allodynia which has been proposed as a mechanism of neuropathic pain [28].
Negative_regulation (decreased) of Gene_expression (expression) of KCC2 in neurons associated with allodynia and neuropathic pain
5) Confidence 0.21 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 0.91 Pain Relevance 0.97
Inhibition of KCC2 by BUM would be expected to have the opposite effect on touch-evoked responses because decreased KCC2 expression (analogous to pharmacological inhibition) or KCC2 blockade with DIOA reverses the polarity of GABAAR responses in a subset of lamina I and II neurons, leading to allodynia which has been proposed as a mechanism of neuropathic pain [28].
Negative_regulation (decreased) of Gene_expression (expression) of KCC2 in neurons associated with allodynia and neuropathic pain
6) Confidence 0.21 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 0.90 Pain Relevance 0.91

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