INT18428

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Context Info
Confidence 0.92
First Reported 1984
Last Reported 2010
Negated 0
Speculated 1
Reported most in Abstract
Documents 9
Total Number 10
Disease Relevance 1.20
Pain Relevance 6.87

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 (Pdyn)
Anatomy Link Frequency
spinal 1
spinal cord 1
brain 1
central nervous system 1
Pdyn (Mus musculus)
Pain Link Frequency Relevance Heat
Dynorphin 78 100.00 Very High Very High Very High
Central nervous system 8 99.52 Very High Very High Very High
Spinal cord 11 99.36 Very High Very High Very High
antinociception 42 98.84 Very High Very High Very High
Catecholamine 3 97.26 Very High Very High Very High
tail-flick 10 97.08 Very High Very High Very High
electroacupuncture 9 94.08 High High
narcan 21 93.96 High High
Central grey 2 91.56 High High
Enkephalin 20 91.04 High High
Disease Link Frequency Relevance Heat
Spinal Cord Injury 2 99.50 Very High Very High Very High
Injury 3 98.68 Very High Very High Very High
Pheochromocytoma 2 93.84 High High
Nociception 7 91.80 High High
Urological Neuroanatomy 3 91.76 High High
Pox Virus Infection 2 90.60 High High
Toxicity 5 88.88 High High
Drug Induced Neurotoxicity 2 75.00 Quite High
Pain 14 5.00 Very Low Very Low Very Low
Syndrome 3 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
However, the catecholamine/Dyn ratio in the tissue extract (138 000) was much higher than that found in the cell extract (20 180), suggesting a possible selective degradation of Dyn in tissue extract as compared with cell extract or an induction of Dyn biosynthesis in cells which have been isolated from their natural microenvironment.
Spec (possible) Protein_catabolism (degradation) of Dyn associated with catecholamine
1) Confidence 0.92 Published 1984 Journal Can. J. Physiol. Pharmacol. Section Abstract Doc Link 6203634 Disease Relevance 0 Pain Relevance 0.61
The latter enzymes have been implicated in degradation of certain EOPs albeit not DYN.
Protein_catabolism (degradation) of DYN associated with dynorphin
2) Confidence 0.45 Published 2000 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 10672972 Disease Relevance 0 Pain Relevance 1.00
In other experiments, nitrous oxide antinociception was significantly enhanced by 30-min pretreatment with phosphoramidon, an inhibitor of endopeptidase 24.11, which has been implicated in DYN degradation, but not bestatin or captopril, which inhibit aminopeptidase and angiotensin-converting enzyme, respectively.
Protein_catabolism (degradation) of DYN associated with antinociception and dynorphin
3) Confidence 0.45 Published 2000 Journal Pharmacol. Biochem. Behav. Section Abstract Doc Link 10672972 Disease Relevance 0 Pain Relevance 1.02
The breakdown of DYN A at spinal level is very rapid.
Protein_catabolism (breakdown) of DYN in spinal
4) Confidence 0.33 Published 1985 Journal Neuropeptides Section Abstract Doc Link 2860601 Disease Relevance 0.17 Pain Relevance 0.28
Another experimental result implied that some special conditions might be necessary for Bestatin to inhibit Dyns’ degradation. [3H]Dyn A 1–8 and [3H]Dyn A 1–9 with suspensions of guinea pig brain membrane could be both degraded at 25 and at 0°C (Gillan et al., 1985).
Protein_catabolism (th degra) of Dyn in brain associated with dynorphin
5) Confidence 0.32 Published 2010 Journal Frontiers in Neuroscience Section Body Doc Link PMC2903224 Disease Relevance 0 Pain Relevance 0.76
The angiotensin converting enzyme inhibitor captopril reduced the degradation of Dyn A-(1-8) to a much lesser degree.
Protein_catabolism (degradation) of Dyn associated with dynorphin
6) Confidence 0.30 Published 1990 Journal J. Neurochem. Section Abstract Doc Link 1973455 Disease Relevance 0 Pain Relevance 0.83
Our findings suggest that dynorphin A and/or its metabolites may contribute significantly to neurodegeneration during spinal cord injury and that alterations in dynorphin A biosynthesis, metabolism, and/or degradation may be important in determining injury outcome.
Protein_catabolism (degradation) of dynorphin in spinal cord associated with dynorphin, injury and spinal cord
7) Confidence 0.20 Published 2001 Journal Exp. Neurol. Section Abstract Doc Link 11170722 Disease Relevance 0.50 Pain Relevance 1.10
These results suggest that: i) Met-enk hydrolyzing enzymes are involved in the degradation of not only Met-enk but also beta-end and Dyn in the rat central nervous system; ii) Met-enk and beta-end act on both supraspinal and spinal sites, while Dyn acts only on the spinal site; iii) EA antinociception is mediated by supraspinal Met-enk and/or beta-end; and iv) an anti-opiate peptide system may be activated by EA stimulation, being susceptible to Met-enk hydrolyzing enzymes.
Protein_catabolism (degradation) of Dyn in central nervous system associated with antinociception, opiate, central nervous system and electroacupuncture
8) Confidence 0.20 Published 1994 Journal Jpn. J. Pharmacol. Section Abstract Doc Link 7869621 Disease Relevance 0.18 Pain Relevance 1.28
The results demonstrate that PC1 cleaves proDyn at pairs of basic residues to yield 10 and 16 kDa high molecular weight (HMW) intermediates.
Protein_catabolism (cleaves) of proDyn
9) Confidence 0.03 Published 1994 Journal FEBS Lett. Section Abstract Doc Link 8276115 Disease Relevance 0.18 Pain Relevance 0
This demonstrates that PC1 cleaves proDyn at single and pairs of basic residues.
Protein_catabolism (cleaves) of proDyn
10) Confidence 0.03 Published 1994 Journal FEBS Lett. Section Abstract Doc Link 8276115 Disease Relevance 0.17 Pain Relevance 0

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