INT4824

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Context Info
Confidence 0.70
First Reported 1982
Last Reported 2011
Negated 4
Speculated 13
Reported most in Abstract
Documents 169
Total Number 182
Disease Relevance 66.10
Pain Relevance 123.46

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 (Tacr1) response to stress (Tacr1) cytoplasm (Tacr1)
signal transducer activity (Tacr1)
Anatomy Link Frequency
neurons 23
dorsal horn 15
spinal cord 10
spinal 9
joints 6
Tacr1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
substance P 2275 100.00 Very High Very High Very High
Inflammation 812 100.00 Very High Very High Very High
bradykinin 654 100.00 Very High Very High Very High
Pain 455 100.00 Very High Very High Very High
Spinal cord 444 100.00 Very High Very High Very High
Dorsal horn 328 100.00 Very High Very High Very High
antagonist 290 100.00 Very High Very High Very High
agonist 191 100.00 Very High Very High Very High
Cholecystokinin 175 100.00 Very High Very High Very High
Calcitonin gene-related peptide 105 100.00 Very High Very High Very High
Disease Link Frequency Relevance Heat
Ganglion Cysts 2093 100.00 Very High Very High Very High
INFLAMMATION 794 100.00 Very High Very High Very High
Pain 456 100.00 Very High Very High Very High
Urological Neuroanatomy 35 100.00 Very High Very High Very High
Pressure And Volume Under Development 24 100.00 Very High Very High Very High
Adhesions 7 100.00 Very High Very High Very High
Nociception 423 99.98 Very High Very High Very High
Increased Venous Pressure Under Development 17 99.90 Very High Very High Very High
Salivary Gland Disease 4 99.88 Very High Very High Very High
Arthritis 489 99.76 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In the ipsilateral lumbar dorsal hom, NK-1R mRNA levels were significantly increased at 2 and 6 hr after formalin injection.
Positive_regulation (increased) of NK-1R mRNA in dorsal
1) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.29 Pain Relevance 0.21
Pretreatment of rats with the selective NK-1R antagonist LY306,740 was used to determine the role of NK-1R activation in the regulation of nociception-induced NK-1R mRNA levels.
Spec (determine) Positive_regulation (activation) of NK-1R associated with nociception and antagonist
2) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.32 Pain Relevance 0.23
Levels of the NK-1R pre-mRNA containing both introns A and B were significantly increased 1 hr after formalin treatment, and levels of NK-1R pre-mRNAs containing intron A were significantly elevated at 2 hr after formalin treatment.
Positive_regulation (increased) of NK-1R
3) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.30 Pain Relevance 0.24
The stimulation of NK-1R gene expression by activation of the NK-1R provides a homologous mechanism for altering the sensitivity of dorsal horn cells to substance P, potentially via the actions of second messengers, which presumably results in the maintenance of proper sensory information processing during long term nociception.
Positive_regulation (activation) of NK-1R in dorsal horn associated with nociception, dorsal horn and substance p
4) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.39 Pain Relevance 0.30
Increased NK-1R mRNA levels could result from increased mRNA stability or an increased rate of NK-1R mRNA transcription.
Positive_regulation (Increased) of NK-1R mRNA
5) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.17 Pain Relevance 0.20
Thus, activation of the NK-1R during nociception increases dorsal horn NK-1R mRNA levels through activation of transcriptional or splicing mechanisms.
Positive_regulation (activation) of NK-1R in dorsal horn associated with nociception and dorsal horn
6) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.32 Pain Relevance 0.32
Increased NK-1R mRNA levels could result from increased mRNA stability or an increased rate of NK-1R mRNA transcription.
Positive_regulation (result) of NK-1R mRNA
7) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.17 Pain Relevance 0.20
Pretreatment of rats with the selective NK-1R antagonist LY306,740 was used to determine the role of NK-1R activation in the regulation of nociception-induced NK-1R mRNA levels.
Positive_regulation (induced) of NK-1R mRNA associated with nociception and antagonist
8) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.32 Pain Relevance 0.26
Pretreatment with LY306,740 (but not LY307,679) completely blocked the formalin-induced increase in dorsal horn NK-1R mRNA levels and significantly reduced formalin-induced behavioral activity.
Positive_regulation (increase) of NK-1R mRNA in dorsal horn associated with dorsal horn
9) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.32 Pain Relevance 0.31
Levels of the NK-1R pre-mRNA containing both introns A and B were significantly increased 1 hr after formalin treatment, and levels of NK-1R pre-mRNAs containing intron A were significantly elevated at 2 hr after formalin treatment.
Positive_regulation (increased) of NK-1R
10) Confidence 0.70 Published 1996 Journal Mol. Pharmacol. Section Abstract Doc Link 8913350 Disease Relevance 0.24 Pain Relevance 0.24
This study examined endogenous substance P (SP) activation of the substance P receptor (SPR) on enteric neurons in the rat ileum after exposure to intraluminal Clostridium difficile toxin A.
Spec (examined) Positive_regulation (activation) of substance P in neurons associated with clostridium difficile infection and substance p
11) Confidence 0.70 Published 1996 Journal Gastroenterology Section Abstract Doc Link 8898641 Disease Relevance 0.27 Pain Relevance 0.14
These results show that acute noxious visceral stimuli induce activation of spinal lamina I neurons expressing the SPR and, that after visceral inflammation, there is a marked increase in both the number and rostrocaudal extent of lamina I SPR neurons activated in response to both normally non-noxious and noxious distention of the colon.
Positive_regulation (activated) of SPR in visceral associated with inflammation
12) Confidence 0.70 Published 2002 Journal J Pain Section Abstract Doc Link 14622848 Disease Relevance 0.56 Pain Relevance 0.45
These results show that acute noxious visceral stimuli induce activation of spinal lamina I neurons expressing the SPR and, that after visceral inflammation, there is a marked increase in both the number and rostrocaudal extent of lamina I SPR neurons activated in response to both normally non-noxious and noxious distention of the colon.
Positive_regulation (increase) of SPR in visceral associated with inflammation
13) Confidence 0.70 Published 2002 Journal J Pain Section Abstract Doc Link 14622848 Disease Relevance 0.57 Pain Relevance 0.47
In long-term inflammatory pain models (CFA and polyarthritis) the same pattern of SP release and SPR activation occurs as is observed in short-term inflammation with the addition that there is a significant upregulation of the SPR in lamina I neurons.
Positive_regulation (activation) of SPR in neurons associated with inflammation, ipn, arthritis and substance p
14) Confidence 0.69 Published 1999 Journal J. Neurosci. Section Abstract Doc Link 10460273 Disease Relevance 0.95 Pain Relevance 1.10
The effects of substance P are mediated by activation of the neurokinin 1 receptor.
Positive_regulation (activation) of neurokinin 1 receptor associated with substance p
15) Confidence 0.69 Published 1999 Journal Neuroscience Section Abstract Doc Link 10077333 Disease Relevance 0.26 Pain Relevance 0.65
These results provide direct evidence suggesting that the spinal substance P-induced thermal hyperalgesia is mediated by an increase in spinal prostaglandin E2 via activation of the neurokinin 1 receptor.
Positive_regulation (activation) of neurokinin 1 receptor in spinal associated with thermal hyperalgesia and substance p
16) Confidence 0.69 Published 1999 Journal Neuroscience Section Abstract Doc Link 10077333 Disease Relevance 0.48 Pain Relevance 1.21
Neurokinin-1 receptor messenger RNA levels were, however, significantly increased in hindpaw tissues inflamed by formalin for 6 h.
Positive_regulation (increased) of Neurokinin-1 receptor messenger RNA
17) Confidence 0.69 Published 1999 Journal Neuroscience Section Abstract Doc Link 10430499 Disease Relevance 0.21 Pain Relevance 0.55
Activation of the neurokinin-1 receptor by substance P during chronic nociception increases neurokinin-1 receptor gene expression in the spinal cord.
Positive_regulation (Activation) of neurokinin-1 receptor in spinal cord associated with nociception, spinal cord and substance p
18) Confidence 0.69 Published 1999 Journal Neuroscience Section Abstract Doc Link 10430499 Disease Relevance 0.42 Pain Relevance 0.44
Thus the continuous infusion of SP stimulates plasma extravasation in the rat pancreas via activation of the NK1-R, and these effects are terminated by both desensitization of the NK1-R and the cell-surface protease NEP.
Positive_regulation (activation) of NK1-R in pancreas associated with substance p
19) Confidence 0.69 Published 2000 Journal Am. J. Physiol. Gastrointest. Liver Physiol. Section Abstract Doc Link 11005759 Disease Relevance 0 Pain Relevance 0.40
By contrast, NK-1R mRNA levels were increased in thymocytes from CPS-treated rats.
Positive_regulation (increased) of NK-1R mRNA in thymocytes associated with qutenza
20) Confidence 0.69 Published 2004 Journal Neuroimmunomodulation Section Abstract Doc Link 15067207 Disease Relevance 0.34 Pain Relevance 1.44

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