INT91360

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Context Info
Confidence 0.54
First Reported 2000
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 17
Disease Relevance 10.46
Pain Relevance 12.89

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

transport (Slc12a2) plasma membrane (Slc12a2) transmembrane transport (Slc12a2)
Anatomy Link Frequency
spinal 3
visceral 1
Urine 1
Slc12a2 (Mus musculus)
Pain Link Frequency Relevance Heat
allodynia 560 99.56 Very High Very High Very High
Hyperalgesia 108 99.48 Very High Very High Very High
qutenza 227 99.46 Very High Very High Very High
Dopamine 242 99.00 Very High Very High Very High
Pain 108 98.40 Very High Very High Very High
intrathecal 210 98.08 Very High Very High Very High
Inflammation 91 97.92 Very High Very High Very High
agonist 102 96.84 Very High Very High Very High
Potency 3 94.36 High High
antagonist 38 93.60 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 52 99.96 Very High Very High Very High
Neuropathic Pain 570 99.56 Very High Very High Very High
Hyperalgesia 122 99.48 Very High Very High Very High
Nociception 21 98.62 Very High Very High Very High
Pain 70 98.40 Very High Very High Very High
Bartter Syndrome 3 98.32 Very High Very High Very High
INFLAMMATION 105 97.92 Very High Very High Very High
Acidosis 1 97.24 Very High Very High Very High
Diabetes Mellitus 1 96.76 Very High Very High Very High
Hypomagnesemia 1 95.44 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This finding likely reflects the long-lasting nociceptive stimulus evoked by intracolonic capsaicin [19] and illustrates that inhibition of NKCC1 is not sufficient to block the development of referred allodynia.
Negative_regulation (inhibition) of NKCC1 associated with nociception, allodynia and qutenza
1) Confidence 0.54 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 1.06 Pain Relevance 1.05
Urine responses were recorded in the absence and presence of a specific NKCC inhibitor, 10 µM bumetanide.
Negative_regulation (inhibitor) of NKCC in Urine
2) Confidence 0.48 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2806418 Disease Relevance 0 Pain Relevance 0.05
NKCC1 KO mice showed a reduction in stroking hyperalgesia (touch-evoked pain) compared to WT and HE mice but no differences were detected between the three groups in the expression of punctate hyperalgesia.
Negative_regulation (reduction) of NKCC1 associated with pain and hyperalgesia
3) Confidence 0.43 Published 2004 Journal Neurosci. Lett. Section Abstract Doc Link 15135928 Disease Relevance 0.79 Pain Relevance 1.04
We have recently disrupted Slc12a2, the gene encoding the secretory Na-K-2Cl cotransporter in mice (NKCC1) (Delpire et al., 1999).
Negative_regulation (disrupted) of Slc12a2
4) Confidence 0.42 Published 2000 Journal J. Neurosci. Section Abstract Doc Link 11027211 Disease Relevance 0.39 Pain Relevance 0.32
Spinal NKCC1 blockade inhibits intracolonic capsaicin-evoked referred, abdominal allodynia and hyperalgesia
Negative_regulation (blockade) of NKCC1 in Spinal associated with hyperalgesia, allodynia and qutenza
5) Confidence 0.40 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 1.24 Pain Relevance 1.67
We have demonstrated that spinal NKCC1 blockade and spinal TRPV1 antagonism attenuates referred allodynia in response to a painful visceral stimulus.
Negative_regulation (blockade) of NKCC1 in spinal associated with pain and allodynia
6) Confidence 0.40 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 0.78 Pain Relevance 1.24
Our findings demonstrate that spinally applied inhibitors of NKCC1 and TRPV1 attenuate referred allodynia evoked by a painful visceral stimulus and show that spinally applied TRPV1 agonists cause allodynia that is likewise inhibited by NKCC1 blockade.


Negative_regulation (inhibitors) of NKCC1 in visceral associated with pain, allodynia and agonist
7) Confidence 0.40 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 1.43 Pain Relevance 1.74
NADA-mediated stroking allodynia was inhibited by the NKCC1 inhibitor, BUM, suggesting a role for NKCC1 in this effect.
Negative_regulation (inhibitor) of NKCC1 associated with dopamine and allodynia
8) Confidence 0.39 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 1.52 Pain Relevance 1.90
On the other hand, BUM did effectively inhibit referred allodynia after its establishment both at 20 min and 4 hrs post intracolonic capsaicin injection suggesting that NKCC1 inhibitors might be clinically useful in cases of established inflammatory allodynia.
Negative_regulation (inhibitors) of NKCC1 associated with inflammation, qutenza and allodynia
9) Confidence 0.39 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 0.99 Pain Relevance 1.07
Therefore, it appears that 50 µM bumetanide only inhibited NKCC and not any KCC.
Negative_regulation (inhibited) of NKCC
10) Confidence 0.35 Published 2010 Journal The Journal of General Physiology Section Body Doc Link PMC2806418 Disease Relevance 0 Pain Relevance 0
These findings indicate that spinal NKCC1 blockade either before or after intracolonic capsaicin is capable of inhibiting referred allodynia.


Negative_regulation (blockade) of NKCC1 in spinal associated with allodynia and qutenza
11) Confidence 0.35 Published 2007 Journal Mol Pain Section Body Doc Link PMC1929059 Disease Relevance 1.15 Pain Relevance 1.88
In this sense NBC can be said to partly compensate for the loss of NKCC1.
Negative_regulation (loss) of NKCC1
12) Confidence 0.30 Published 2009 Journal PLoS Computational Biology Section Body Doc Link PMC2613522 Disease Relevance 0.14 Pain Relevance 0
In the mc4 case, the removal of NKCC1 causes a higher [K+]o in the excited state (Figure 4B and 4C, insets).
Negative_regulation (removal) of NKCC1
13) Confidence 0.22 Published 2009 Journal PLoS Computational Biology Section Body Doc Link PMC2613522 Disease Relevance 0.10 Pain Relevance 0
Then why is the predicted shrinkage reduction after NKCC1 knockout so slight?
Negative_regulation (reduction) of NKCC1 associated with targeted disruption
14) Confidence 0.19 Published 2009 Journal PLoS Computational Biology Section Body Doc Link PMC2613522 Disease Relevance 0.10 Pain Relevance 0
12) are initiated by the downregulation of NKCC1 and through a Calcium dependent transcriptional regulation the expression of a new transporter is enhanced: the K-Cl cotransporter KCC2.
Negative_regulation (downregulation) of NKCC1
15) Confidence 0.12 Published 2008 Journal Frontiers in Molecular Neuroscience Section Body Doc Link PMC2526003 Disease Relevance 0 Pain Relevance 0.34
Functional loss of NKCC, Kir1.1, ClC-Kb or Barttin is a cause of Bartter syndrome, in which nephrogenic diabetes insipides, hypokalemia, hypomagnesemia and hypocalcemia have been observed as variations in phenotype [82–84].
Negative_regulation (loss) of NKCC associated with hypomagnesemia, hypocalcemia, diabetes mellitus and bartter syndrome
16) Confidence 0.03 Published 2005 Journal Cell Mol Life Sci Section Body Doc Link PMC2792346 Disease Relevance 0.69 Pain Relevance 0
Unlike hSERT or mSERT, analogous substitutions in mouse dopamine transporter (V152M) or human norepinephrine transporter (V148M) result in transporters that bind substrate but are deficient in the subsequent translocation of the substrate.
Negative_regulation (deficient) of transporters associated with dopamine
17) Confidence 0.00 Published 2006 Journal J. Biol. Chem. Section Abstract Doc Link 16272152 Disease Relevance 0.07 Pain Relevance 0.57

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