INT36030

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Context Info
Confidence 0.68
First Reported 1988
Last Reported 2010
Negated 4
Speculated 1
Reported most in Body
Documents 16
Total Number 17
Disease Relevance 11.42
Pain Relevance 4.87

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

signal transduction (Il1r1) intracellular (Il1r1) protein complex (Il1r1)
signal transducer activity (Il1r1)
Anatomy Link Frequency
Th17 cell 2
bone marrow 2
astrocytes 2
pyramidal cell 1
peritoneal cavity 1
Il1r1 (Mus musculus)
Pain Link Frequency Relevance Heat
antagonist 13 100.00 Very High Very High Very High
narcan 3 99.74 Very High Very High Very High
Hippocampus 54 99.44 Very High Very High Very High
cytokine 235 98.84 Very High Very High Very High
Eae 19 98.18 Very High Very High Very High
Inflammation 171 97.48 Very High Very High Very High
Pyramidal cell 2 95.36 Very High Very High Very High
Inflammatory response 33 94.84 High High
ischemia 23 94.64 High High
Glutamate 163 91.88 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 26 100.00 Very High Very High Very High
Injury 475 99.62 Very High Very High Very High
Stab Wounds 105 99.48 Very High Very High Very High
Penetrating Head Injuries 36 99.16 Very High Very High Very High
Hypertrophy 24 99.16 Very High Very High Very High
Sprains And Strains 9 98.66 Very High Very High Very High
Neuropathic Pain 7 98.04 Very High Very High Very High
Urological Neuroanatomy 1 97.60 Very High Very High Very High
INFLAMMATION 228 97.48 Very High Very High Very High
Multiple Sclerosis 14 97.00 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A database search using Allen Brain Atlas [23] revealed that, among the 20 most downregulated genes in the alpha-CaMKII +/- hippocampus, 5 genes (DSP, TDO2, NPNT, IL1R1, and PNCK) had highly selective expression in the DG (Figure 2E–2J, and Additional file 1, Figure S6).
Gene_expression (expression) of IL1R1 in Atlas associated with hippocampus
1) Confidence 0.68 Published 2008 Journal Mol Brain Section Body Doc Link PMC2562999 Disease Relevance 0.09 Pain Relevance 0.31
In summary, this study on the effect of a penetrating brain injury in mice lacking IL-1R1 demonstrates that IL-1R1 deletion results in: 1) attenuated hypertrophy of astrocytes; 2) delayed cellular GFAP induction; 3) diminished induction of PAR1; 4) intact induction of extracellular matrix proteins and 5) intact induction of glutamate transporters, glutamine synthetase and S-100B.
Gene_expression (deletion) of IL-1R1 in extracellular matrix associated with hypertrophy, glutamate and penetrating head injuries
2) Confidence 0.54 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.98 Pain Relevance 0.17
Similarly, administering IL-1 receptor antagonist or IL-1?
Gene_expression (antagonist) of IL-1 receptor associated with antagonist
3) Confidence 0.54 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 1.09 Pain Relevance 0.17
Induction of protease-activated receptor-1 (PAR-1) by stab wound injury is ablated by the deletion of IL-1R1 (Fig. 3 and 4)
Gene_expression (deletion) of IL-1R1 associated with injury and stab wounds
4) Confidence 0.54 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.82 Pain Relevance 0.09
Absence of IL-1R1 signaling leads to attenuated hypertrophy of astrocytes and delayed induction of GFAP (Fig. 1 and 2)
Gene_expression (signaling) of IL-1R1 in astrocytes associated with hypertrophy
5) Confidence 0.54 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.24 Pain Relevance 0.11
Absence of IL-1R1 signaling leads to attenuated hypertrophy of astrocytes and delayed induction of GFAP (Fig. 1 and 2)
Neg (Absence) Gene_expression (Absence) of IL-1R1 in astrocytes associated with hypertrophy
6) Confidence 0.54 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.24 Pain Relevance 0.11
By contrast, PAR-1 protein was not induced and remained undetectable in the IL-1R1-null mice.
Gene_expression (undetectable) of IL-1R1-null
7) Confidence 0.54 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.66 Pain Relevance 0.08
We also examined the expression of the protease-activated receptor 1 (PAR-1) in wild type (WT) and IL-1R1-null mice following a neocortical penetrating injury as this receptor has been implicated in astrocyte hyperplasia after brain injury [41].
Spec (examined) Gene_expression (expression) of IL-1R1-null in brain associated with injury, brain injury and hyperplasia
8) Confidence 0.48 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.82 Pain Relevance 0.15
The activity of rHu-IL-1 alpha and rHu-TNF, unlike mIFN alpha, was not naloxone-reversible. rHu-IL-1 alpha did not produce an increase in writhes counts even if injected directly into the peritoneal cavity.
Neg (not) Gene_expression (produce) of rHu-IL-1 alpha in peritoneal cavity associated with narcan
9) Confidence 0.25 Published 1988 Journal Eur. J. Pharmacol. Section Abstract Doc Link 3260869 Disease Relevance 0.37 Pain Relevance 0.40
In the present study, we tested the role of IL-1 in neuropathic pain models using two mouse strains impaired in IL-1 signaling: Deletion of the IL-1 receptor type I (IL-1rKO) and transgenic over-expression of the IL-1 receptor antagonist (IL-1raTG).
Gene_expression (over-expression) of IL-1rKO associated with targeted disruption, antagonist, eae and sprains and strains
10) Confidence 0.14 Published 2006 Journal Pain Section Abstract Doc Link 16426759 Disease Relevance 1.54 Pain Relevance 0.85
IL-1 receptor 1 (IL-1R1) expression in T cells, which was induced by IL-6, was necessary for the induction of experimental autoimmune encephalomyelitis and for early Th17 cell differentiation in vivo [11].
Gene_expression (expression) of IL-1R1 in Th17 cell associated with multiple sclerosis
11) Confidence 0.10 Published 2010 Journal Semin Immunopathol Section Body Doc Link PMC2836464 Disease Relevance 0.42 Pain Relevance 0.11
IL-1 receptor 1 (IL-1R1) expression in T cells, which was induced by IL-6, was necessary for the induction of experimental autoimmune encephalomyelitis and for early Th17 cell differentiation in vivo [11].
Gene_expression (expression) of IL-1 receptor 1 in Th17 cell associated with multiple sclerosis
12) Confidence 0.10 Published 2010 Journal Semin Immunopathol Section Body Doc Link PMC2836464 Disease Relevance 0.42 Pain Relevance 0.11
LPS-induced microglial activation is modified by IL-1Ra and absent in IL-1R-/-
Neg (absent) Gene_expression (absent) of IL-1R
13) Confidence 0.05 Published 2010 Journal Crit Care Section Body Doc Link PMC2911722 Disease Relevance 0.26 Pain Relevance 0.22
At 24 hours, after LPS in the IL-1R-/-, a time at which there was markedly increased cytokines and clear evidence of sickness behavior in untreated wild type mice, levels of IL-1?
Gene_expression (hours) of IL-1R associated with cytokine
14) Confidence 0.05 Published 2010 Journal Crit Care Section Body Doc Link PMC2911722 Disease Relevance 0.25 Pain Relevance 0.31
IL-1R1 is expressed throughout the rodent brain, with levels generally highest in neuronal rich areas including the dentate gyrus, the pyramidal cell layer of the hippocampus, and the hypothalamus [6,7].
Gene_expression (expressed) of IL-1R1 in pyramidal cell associated with pyramidal cell and hippocampus
15) Confidence 0.03 Published 2008 Journal J Neuroinflammation Section Body Doc Link PMC2335091 Disease Relevance 0.05 Pain Relevance 0.33
Finally, mice that lacked IL-1R expression on non-bone marrow-derived cells were also protected from the inflammatory effects of MSU [24], suggesting that the pro-inflammatory effects of IL-1 require mesenchymal cells such as the endothelium to respond to this cytokine.
Neg (lacked) Gene_expression (expression) of IL-1R in bone marrow associated with inflammation, crystal associated disease and cytokine
16) Confidence 0.01 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2592794 Disease Relevance 1.30 Pain Relevance 0.43
This was due not to TLR signaling, but required the IL-1R expressed on non-bone marrow-derived cells.
Gene_expression (expressed) of IL-1R in bone marrow
17) Confidence 0.01 Published 2010 Journal Gastroenterology Research and Practice Section Body Doc Link PMC2939438 Disease Relevance 1.85 Pain Relevance 0.92

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