INT14853

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Context Info
Confidence 0.59
First Reported 1981
Last Reported 2010
Negated 1
Speculated 4
Reported most in Abstract
Documents 80
Total Number 84
Disease Relevance 30.87
Pain Relevance 45.06

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

extracellular space (Tac1) extracellular region (Tac1) plasma membrane (Tac1)
Anatomy Link Frequency
spinal cord 6
nerves 4
brain 2
tail skin 2
lung 2
Tac1 (Mus musculus)
Pain Link Frequency Relevance Heat
substance P 422 100.00 Very High Very High Very High
qutenza 229 100.00 Very High Very High Very High
antagonist 149 100.00 Very High Very High Very High
Pain 97 100.00 Very High Very High Very High
Neuropeptide 56 100.00 Very High Very High Very High
Spinal cord 48 100.00 Very High Very High Very High
Dorsal horn 27 100.00 Very High Very High Very High
nociceptor 25 100.00 Very High Very High Very High
intrathecal 25 99.98 Very High Very High Very High
fluoxetine 5 99.98 Very High Very High Very High
Disease Link Frequency Relevance Heat
Pain 90 100.00 Very High Very High Very High
Nervous System Injury 15 100.00 Very High Very High Very High
Hepatotoxicity 4 99.96 Very High Very High Very High
Generalized Anxiety Disorder 7 99.90 Very High Very High Very High
Targeted Disruption 87 99.84 Very High Very High Very High
Pressure And Volume Under Development 5 99.82 Very High Very High Very High
Nociception 77 99.76 Very High Very High Very High
Pulmonary Disease 53 99.68 Very High Very High Very High
Hyperalgesia 52 99.68 Very High Very High Very High
Pneumonia 19 99.62 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Deficits in visceral pain and hyperalgesia of mice with a disruption of the tachykinin NK1 receptor gene.
Negative_regulation (disruption) of NK1 in visceral associated with hyperalgesia, visceral pain and qutenza
1) Confidence 0.59 Published 2000 Journal Neuroscience Section Title Doc Link 10854767 Disease Relevance 1.01 Pain Relevance 1.55
We have now disrupted the mouse preprotachykinin A gene (PPT-A), which encodes substance P and a related tachykinin, neurokinin A.
Negative_regulation (disrupted) of PPT-A associated with substance p
2) Confidence 0.57 Published 1998 Journal Nature Section Abstract Doc Link 9537322 Disease Relevance 0.43 Pain Relevance 1.16
Disruption of the substance P receptor (neurokinin-1) gene does not prevent upregulation of preprotachykinin-A mRNA in the spinal cord of mice following peripheral inflammation.
Negative_regulation (Disruption) of neurokinin-1 in spinal cord associated with inflammation, spinal cord and substance p
3) Confidence 0.57 Published 1999 Journal Eur. J. Neurosci. Section Title Doc Link 10564361 Disease Relevance 0.57 Pain Relevance 0.99
Collectively, these results extend previous data from our group indicating that glutamatergic-mediated pain responses, specifically those mediated by metabotropic receptor subtype, together with inhibition of neurokinin NK(1)-mediated response, account for the antinociceptive action of dipyrone in mice.
Negative_regulation (inhibition) of neurokinin NK associated with pain and antinociceptive
4) Confidence 0.56 Published 2004 Journal Brain Res. Section Abstract Doc Link 15019564 Disease Relevance 0.44 Pain Relevance 0.65
Here we have further examined this role by comparing the behavioural responses to intradermal capsaicin of mutant mice with a disruption of the NK1 receptor (NK1 KO) and wild-type (WT) mice.
Negative_regulation (disruption) of NK1 associated with qutenza
5) Confidence 0.55 Published 2001 Journal Pain Section Abstract Doc Link 11166975 Disease Relevance 0.34 Pain Relevance 0.87
Further, the lack of secondary hyperalgesia in NK1 KO mice is largely due to the loss of central rather than peripheral NK1 receptors.
Negative_regulation (loss) of NK1 associated with hyperalgesia
6) Confidence 0.55 Published 2001 Journal Pain Section Abstract Doc Link 11166975 Disease Relevance 0.58 Pain Relevance 1.26
Likewise, aerosols of FK 224 (10(-5) M; 1 min), another inhibitor of NK1 and NK2 receptors, or lidocaine (4%, 1 min) significantly inhibited phosphoramidon (3 x 10(-3) mol/kg)-induced cough (p < 0.01).
Negative_regulation (inhibitor) of NK1 associated with cough, lidocaine and substance p
7) Confidence 0.50 Published 1993 Journal Am. Rev. Respir. Dis. Section Abstract Doc Link 7504893 Disease Relevance 0.74 Pain Relevance 0.47
Here, we analysed components of the HPA axis in mice lacking a functional neurokinin-1 receptor (NK1-/-) on two backgrounds: backcrossed C57BL/6 (B6) and mixed C57BL/6 x 129/sv (129B6).
Spec (analysed) Negative_regulation (lacking) of neurokinin-1 receptor
8) Confidence 0.43 Published 2008 Journal Eur. J. Neurosci. Section Abstract Doc Link 18279320 Disease Relevance 0.45 Pain Relevance 0.03
Here, we analysed components of the HPA axis in mice lacking a functional neurokinin-1 receptor (NK1-/-) on two backgrounds: backcrossed C57BL/6 (B6) and mixed C57BL/6 x 129/sv (129B6).
Spec (analysed) Negative_regulation (lacking) of NK1
9) Confidence 0.43 Published 2008 Journal Eur. J. Neurosci. Section Abstract Doc Link 18279320 Disease Relevance 0.45 Pain Relevance 0.03
Blocking the NK1 receptor pharmacologically reproduced, in an enantiomere-selective manner, the data from NK1-/- mice, with no evidence for recruitment of descending inhibition at the lumbar cord level after forepaw stimulation.
Negative_regulation (Blocking) of NK1
10) Confidence 0.43 Published 2001 Journal J. Neurosci. Section Abstract Doc Link 11157089 Disease Relevance 0.17 Pain Relevance 0.35
This study examined the role of neurokinin peptides in 3- and 21-day-old rat pups using the preprotachykinin-A (PPTA) knockout mouse, lacking neurokinin A and substance P.
Negative_regulation (lacking) of neurokinin associated with targeted disruption and substance p
11) Confidence 0.43 Published 2003 Journal Neuroreport Section Abstract Doc Link 14502084 Disease Relevance 0.35 Pain Relevance 0.18
In contrast, withdrawal latencies to radiant heat decreased up to 2 weeks after nerve injury in both the NK-1 and the wild-type mice.
Negative_regulation (decreased) of NK-1 in nerve associated with nervous system injury and withdrawal
12) Confidence 0.42 Published 2000 Journal Exp. Neurol. Section Abstract Doc Link 10739640 Disease Relevance 1.41 Pain Relevance 1.02
Sendide is a selective and extremely potent antagonist of neurokinin-1 (NK1) receptors in the mouse spinal cord.
Negative_regulation (antagonist) of neurokinin-1 in spinal cord associated with antagonist and spinal cord
13) Confidence 0.42 Published 1995 Journal Pain Section Abstract Doc Link 7540280 Disease Relevance 0.05 Pain Relevance 0.46
We previously reported that mice with a deletion of the preprotachykinin-A (pptA) gene, from which substance P (SP) and neurokinin A (NKA) are derived, exhibit reduced behavioral responses to intense stimuli, but that behavioral hypersensitivity after injury is unaltered.
Negative_regulation (deletion) of preprotachykinin-A associated with injury, hypersensitivity and substance p
14) Confidence 0.42 Published 2004 Journal J. Neurophysiol. Section Abstract Doc Link 14711972 Disease Relevance 0.27 Pain Relevance 0.36
We previously reported that mice with a deletion of the preprotachykinin-A (pptA) gene, from which substance P (SP) and neurokinin A (NKA) are derived, exhibit reduced behavioral responses to intense stimuli, but that behavioral hypersensitivity after injury is unaltered.
Negative_regulation (deletion) of pptA associated with injury, hypersensitivity and substance p
15) Confidence 0.42 Published 2004 Journal J. Neurophysiol. Section Abstract Doc Link 14711972 Disease Relevance 0.27 Pain Relevance 0.36
Treatment with PPT for 24 h caused a 5-fold decrease in Tac1 mRNA while DNP and estren had no significant effects (Fig 1A).
Negative_regulation (decrease) of Tac1
16) Confidence 0.41 Published 2009 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2724541 Disease Relevance 0 Pain Relevance 0
Using a knockout strategy, we have also raised mice with a deletion of the preprotachykinin-A (PPT-A) gene, which encodes for SP and neurokinin A (NKA), and have identified a specific behavioral phenotype in which the animals do not detect a window of "pain" intensities; this window cuts across stimulus modalities.
Negative_regulation (deletion) of preprotachykinin-A associated with targeted disruption, pain and substance p
17) Confidence 0.41 Published 1999 Journal Reg Anesth Pain Med Section Abstract Doc Link 9952097 Disease Relevance 1.09 Pain Relevance 1.04
We have now disrupted the mouse preprotachykinin A gene (PPT-A), which encodes substance P and a related tachykinin, neurokinin A.
Negative_regulation (disrupted) of preprotachykinin A associated with substance p
18) Confidence 0.41 Published 1998 Journal Nature Section Abstract Doc Link 9537322 Disease Relevance 0.43 Pain Relevance 1.16
Kyo-responses were also abolished by the local pretreatment with capsaicin to deplete substance P from nociceptor endings, and in tachykinin 1 gene K/O mice.
Negative_regulation (abolished) of tachykinin 1 in nociceptor associated with qutenza, nociceptor and substance p
19) Confidence 0.41 Published 1999 Journal Brain Res. Mol. Brain Res. Section Abstract Doc Link 10366753 Disease Relevance 0.16 Pain Relevance 0.65
In a previous report, we compared the properties of lamina V neurons of the spinal cord dorsal horn in wild-type mice and in mice with a deletion of the preprotachykinin-A (PPT-A) gene, which encodes substance P (SP) and neurokinin A (NKA).
Negative_regulation (deletion) of preprotachykinin-A in lamina associated with dorsal horn, substance p and spinal cord
20) Confidence 0.41 Published 2007 Journal J. Neurosci. Section Abstract Doc Link 17251415 Disease Relevance 0.07 Pain Relevance 0.24

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