INT12463

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Context Info
Confidence 0.48
First Reported 1985
Last Reported 2010
Negated 1
Speculated 1
Reported most in Abstract
Documents 21
Total Number 23
Disease Relevance 3.16
Pain Relevance 7.98

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

endosome (FPR1) signal transduction (FPR1) plasma membrane (FPR1)
signal transducer activity (FPR1)
Anatomy Link Frequency
neutrophils 10
fourth ventricle 1
FPR1 (Homo sapiens)
Pain Link Frequency Relevance Heat
antagonist 36 100.00 Very High Very High Very High
cINOD 59 99.78 Very High Very High Very High
Paracetamol 6 99.76 Very High Very High Very High
IPN 38 99.56 Very High Very High Very High
agonist 39 99.36 Very High Very High Very High
diclofenac 28 98.72 Very High Very High Very High
Potency 4 98.52 Very High Very High Very High
Opioid 134 98.04 Very High Very High Very High
Enkephalin 88 97.04 Very High Very High Very High
anesthesia 3 95.76 Very High Very High Very High
Disease Link Frequency Relevance Heat
Inflammatory Pain 38 99.56 Very High Very High Very High
INFLAMMATION 176 97.12 Very High Very High Very High
Hemorrhage 3 91.52 High High
Disease 17 79.52 Quite High
Crystal Associated Disease 2 78.16 Quite High
Heart Rate Under Development 1 77.20 Quite High
Pressure And Volume Under Development 1 76.56 Quite High
Gastritis 2 75.00 Quite High
Alzheimer's Dementia 2 71.64 Quite High
Adult Respiratory Distress Syndrome 2 71.56 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
All three NSAID inhibited FMLP binding in a dose dependent manner with the potency order being meclofenamate greater than ibuprofen greater than tolmetin.
FMLP Binding (binding) of associated with cinod and potency
1) Confidence 0.48 Published 1989 Journal Gen. Pharmacol. Section Abstract Doc Link 2545509 Disease Relevance 0.07 Pain Relevance 0.22
In general, drugs that inhibited O2-. production inhibited fMLP-receptor interactions in a consistent dose dependent fashion, showing noncompetitive kinetics.
fMLP-receptor Binding (interactions) of
2) Confidence 0.48 Published 1985 Journal J. Rheumatol. Section Abstract Doc Link 2997448 Disease Relevance 0.39 Pain Relevance 0.26
Three levels of effects were studied: (1) overall inhibition of O2-. production, (2) the inhibition of interaction between fMLP and specific receptors at the cell surface, and (3) intermediate proenzyme and enzyme effects.
fMLP Binding (interaction) of
3) Confidence 0.48 Published 1985 Journal J. Rheumatol. Section Abstract Doc Link 2997448 Disease Relevance 0.35 Pain Relevance 0.20
Gpp(NH)p, a GTPase insensitive analog of GTP, also inhibited the binding of FMLP but, paradoxically, enhanced superoxide anion generation and lysozyme release.
FMLP Binding (binding) of
4) Confidence 0.48 Published 1990 Journal Inflammation Section Abstract Doc Link 2138998 Disease Relevance 0.15 Pain Relevance 0.80
Chemotactic factors such as fMLP interact with their specific cell surface receptors, which results in multiple biological responses through a G protein-coupled signal pathway.
fMLP Binding (interact) of
5) Confidence 0.45 Published 2008 Journal Pharmazie Section Abstract Doc Link 19069235 Disease Relevance 0 Pain Relevance 0
NSAIDs, but not acetaminophen, inhibited binding of radiolabeled FMLP to purified neutrophil membranes.
FMLP Binding (binding) of in neutrophil associated with paracetamol and cinod
6) Confidence 0.42 Published 1990 Journal Inflammation Section Abstract Doc Link 2138998 Disease Relevance 0.16 Pain Relevance 0.71
To explore the structure-activity relationship of this family of drugs for f-Met-Leu-Phe receptor binding, 36 drugs with the 3,5-P structure, a structure related to antipyrine, or an unrelated structure were tested as competitors for the binding of f-Met-Leu-Phe-Lys-fluorescein isothiocyanate on human neutrophils by flow cytometric analysis.
f-Met-Leu-Phe receptor Binding (binding) of in neutrophils
7) Confidence 0.42 Published 1991 Journal Can. J. Physiol. Pharmacol. Section Abstract Doc Link 1647850 Disease Relevance 0 Pain Relevance 0.12
A FPR was suggested to be mediated by axons passing between the nucleus fastigii and the fourth ventricle.
FPR Binding (mediated) of in fourth ventricle
8) Confidence 0.33 Published 1993 Journal Neurosurgery Section Abstract Doc Link 8474661 Disease Relevance 0.41 Pain Relevance 0.14
To explore the structure-activity relationship of this family of drugs for f-Met-Leu-Phe receptor binding, 36 drugs with the 3,5-P structure, a structure related to antipyrine, or an unrelated structure were tested as competitors for the binding of f-Met-Leu-Phe-Lys-fluorescein isothiocyanate on human neutrophils by flow cytometric analysis.
f-Met-Leu-Phe-Lys-fluorescein Binding (binding) of in neutrophils
9) Confidence 0.31 Published 1991 Journal Can. J. Physiol. Pharmacol. Section Abstract Doc Link 1647850 Disease Relevance 0 Pain Relevance 0.16
Effects of tenoxicam on superoxide anion formation, beta-glucuronidase release and fMLP binding in human neutrophils: comparison with other NSAIDs.
fMLP Binding (binding) of in neutrophils associated with cinod
10) Confidence 0.31 Published 1991 Journal Pharmacol. Res. Section Title Doc Link 1652137 Disease Relevance 0.18 Pain Relevance 0.44
At drug concentrations causing a significant suppression of O2- generation, diclofenac showed a slight and tolfenamic acid a marked inhibition of [3H]FMLP binding to its cellular receptor; indomethacin has earlier been shown to inhibit FMLP-binding slightly.
FMLP Binding (binding) of associated with diclofenac
11) Confidence 0.28 Published 1986 Journal Scand. J. Rheumatol. Section Abstract Doc Link 3008321 Disease Relevance 0.07 Pain Relevance 0.27
It is concluded that the inhibition of O2- production is due to a combined effect on FMLP binding and on cellular O2- metabolism.
FMLP Binding (binding) of
12) Confidence 0.28 Published 1986 Journal Scand. J. Rheumatol. Section Abstract Doc Link 3008321 Disease Relevance 0.06 Pain Relevance 0.25
In this study, the effects of tenoxicam, an oxicam derivative with a thienothiazine structure, on neutrophil activation were evaluated by the assessment of the following parameters: (1) superoxide anion generation by neutrophils and whole blood stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP), the calcium ionophore A23187 and serum treated zymosan (STZ); (2) beta-glucuronidase release from neutrophils stimulated with fMLP, A23187 and STZ; (3) binding of [3H]fMLP to intact neutrophils.
fMLP Binding (binding) of in neutrophil
13) Confidence 0.27 Published 1991 Journal Pharmacol. Res. Section Abstract Doc Link 1652137 Disease Relevance 0.15 Pain Relevance 0.43
Specific binding of [3H]fMLP to neutrophils was inhibited by the three NSAIDs tested in a dose-dependent fashion and tenoxicam was the most potent.
fMLP Binding (binding) of in neutrophils associated with cinod
14) Confidence 0.27 Published 1991 Journal Pharmacol. Res. Section Abstract Doc Link 1652137 Disease Relevance 0 Pain Relevance 0.41
In this study, the effects of tenoxicam, an oxicam derivative with a thienothiazine structure, on neutrophil activation were evaluated by the assessment of the following parameters: (1) superoxide anion generation by neutrophils and whole blood stimulated with N-formyl-methionyl-leucyl-phenylalanine (fMLP), the calcium ionophore A23187 and serum treated zymosan (STZ); (2) beta-glucuronidase release from neutrophils stimulated with fMLP, A23187 and STZ; (3) binding of [3H]fMLP to intact neutrophils.
fMLP Binding (binding) of in neutrophil
15) Confidence 0.27 Published 1991 Journal Pharmacol. Res. Section Abstract Doc Link 1652137 Disease Relevance 0.15 Pain Relevance 0.43
The mechanism of inhibition of [3H]fMLP binding by tenoxicam was non-competitive.
fMLP Binding (binding) of
16) Confidence 0.27 Published 1991 Journal Pharmacol. Res. Section Abstract Doc Link 1652137 Disease Relevance 0 Pain Relevance 0.40
On the other, we have previously reported a distinct functional behavour of peptide Ac2-26 compared to AnxA1 in human neutrophils [16]; this was explained with the ability of this peptide to bind many receptors of the FPR family [14].
FPR Binding (bind) of in neutrophils
17) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2941452 Disease Relevance 0.09 Pain Relevance 0.04
To test these FPR antagonists in vivo we intraplantarly injected rats with complete Freund's adjuvant and either antagonist together with fMLP.
fMLP Binding (injected) of associated with antagonist
18) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2657213 Disease Relevance 0.06 Pain Relevance 0.73
Blockade of FPR in vivo increased inflammatory pain by inhibiting tonic opioid peptide release
FPR Binding (in vivo) of associated with ipn and opioid
19) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2657213 Disease Relevance 0.10 Pain Relevance 1.02
We have recently transfected human FPR and ALX (the only two receptors of the group expressed by human PMN) in HEK293 cells finding that while AnxA1 displays selectivity for binding to ALX, the shorter and more flexible peptide Ac2-26, binds to both FPR and ALX with approximately equal affinity [16].
FPR Binding (binds) of
20) Confidence 0.21 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2941452 Disease Relevance 0.26 Pain Relevance 0.09

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