INT10041

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Context Info
Confidence 0.96
First Reported 1983
Last Reported 2009
Negated 0
Speculated 0
Reported most in Abstract
Documents 18
Total Number 18
Disease Relevance 2.71
Pain Relevance 9.81

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 (Cck) extracellular region (Cck)
Anatomy Link Frequency
pancreas 2
brain 2
nucleus accumbens 1
liver 1
4th ventricle 1
Cck (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Cholecystokinin 82 100.00 Very High Very High Very High
Enkephalin 51 100.00 Very High Very High Very High
antagonist 5 100.00 Very High Very High Very High
Endogenous opioid 1 100.00 Very High Very High Very High
substance P 16 99.96 Very High Very High Very High
Opioid 7 98.96 Very High Very High Very High
Nucleus accumbens 18 98.68 Very High Very High Very High
Neuropeptide 14 98.16 Very High Very High Very High
Neurotransmitter 1 96.24 Very High Very High Very High
spastic colon 6 95.68 Very High Very High Very High
Disease Link Frequency Relevance Heat
Urological Neuroanatomy 22 97.76 Very High Very High Very High
Irritable Bowel Syndrome /

Irritable Bowel Syndrome Super

4 95.68 Very High Very High Very High
Pain 3 94.72 High High
Constipation 1 88.56 High High
Diarrhoea 1 87.92 High High
Functional Bowel Disorder 2 82.84 Quite High
Opiate Addiction 2 75.00 Quite High
Body Weight 8 63.88 Quite High
Pancreatitis 32 50.00 Quite Low
Nicotine Addiction 14 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A cholecystokinin octapeptide (CCK-8)-degrading peptidase was purified from rat liver cytosol by heat precipitation of other proteins followed by gel filtration, ion exchange chromatography and preparative gel electrophoresis, using a silicate binding assay to quantitate the degradation of radiolabeled CCK-8.
Protein_catabolism (degradation) of CCK in liver associated with cholecystokinin
1) Confidence 0.96 Published 1994 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 8297367 Disease Relevance 0 Pain Relevance 0.26
Unlabeled Leu-enkephalin, beta-casomorphin and neurotensin competitively inhibited the degradation of 125I-CCK-8, suggesting that these opioids are also substrates for the enzyme.
Protein_catabolism (degradation) of CCK associated with enkephalin and opioid
2) Confidence 0.96 Published 1994 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 8297367 Disease Relevance 0 Pain Relevance 0.37
CCK-8 peptidase rapidly degraded radiolabeled Met-enkephalin as well as 125I-CCK-8, but not a series of other unrelated peptides.
Protein_catabolism (degraded) of CCK associated with enkephalin
3) Confidence 0.86 Published 1994 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 8297367 Disease Relevance 0 Pain Relevance 0.36
Neuropeptide metabolism on intact, regional brain slices: effect of dopaminergic agents on substance P, cholecystokinin and Met-enkephalin degradation.
Protein_catabolism (degradation) of cholecystokinin in brain associated with neuropeptide, enkephalin, cholecystokinin and substance p
4) Confidence 0.83 Published 1995 Journal J. Pharmacol. Exp. Ther. Section Title Doc Link 7543572 Disease Relevance 0.06 Pain Relevance 0.97
Inhibitors of either aminopeptidases or serine proteases produced small reductions (13-30%) in CCK degradation in each region.
Protein_catabolism (degradation) of CCK associated with cholecystokinin
5) Confidence 0.63 Published 1995 Journal J. Neurochem. Section Abstract Doc Link 7595577 Disease Relevance 0.36 Pain Relevance 0.63
Recently the existence of regulatory mechanisms between both systems have been proposed, and the physiological antagonism between CCK and endogenous opioid systems has been definitely demonstrated by coadministration of CCK-B selective antagonists with RB 101, a systemically active inhibitor, which fully protects enkephalins from their degradation.
Protein_catabolism (degradation) of CCK associated with antagonist, endogenous opioid, enkephalin and cholecystokinin
6) Confidence 0.60 Published 1996 Journal Neurochem. Res. Section Abstract Doc Link 8947930 Disease Relevance 0.24 Pain Relevance 1.68
CCK 8-(sulfated) degradation on slices from caudate-putamen, nucleus accumbens, and frontal cortex was not altered by inhibitors of neutral endopeptidase 24.11, metalloendopeptidase 24.15, angiotensin converting enzyme, or thiol proteases.
Protein_catabolism (degradation) of CCK in nucleus accumbens associated with nucleus accumbens, urological neuroanatomy and cholecystokinin
7) Confidence 0.55 Published 1995 Journal J. Neurochem. Section Abstract Doc Link 7595577 Disease Relevance 0.42 Pain Relevance 0.84
In the present study, the effect of neuroleptics and other dopaminergic compounds on substance P (SP), cholecystokinin and met-enkephalin degradation was determined on intact, regional, rat brain slices.
Protein_catabolism (degradation) of cholecystokinin in brain associated with enkephalin, cholecystokinin and substance p
8) Confidence 0.55 Published 1995 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 7543572 Disease Relevance 0.06 Pain Relevance 0.90
Integrity of the pancreas (pancreatic function) was assessed by determining the ability of acinar cells to release amylase in response to graded doses of cholecystokinin.


Protein_catabolism (graded) of cholecystokinin in pancreas associated with cholecystokinin
9) Confidence 0.47 Published 2003 Journal Tob Induc Dis Section Body Doc Link PMC2669561 Disease Relevance 0.06 Pain Relevance 0.27
Integrity of the pancreas (pancreatic function) was assessed by determining the ability of acinar cells to release amylase in response to graded doses of cholecystokinin.


Protein_catabolism (graded) of cholecystokinin in pancreas associated with cholecystokinin
10) Confidence 0.47 Published 2003 Journal Tob Induc Dis Section Body Doc Link PMC2671550 Disease Relevance 0.06 Pain Relevance 0.27
Using Western blot analysis, we show that the robust increase in tyrosine hydroxylase phosphorylation obtained with intraperitoneal CCK is significantly attenuated in rats pretreated with the ERK-pathway blocker U0126 injected into the 4th ventricle.
Protein_catabolism (with) of CCK in 4th ventricle
11) Confidence 0.47 Published 2009 Journal Am. J. Physiol. Regul. Integr. Comp. Physiol. Section Abstract Doc Link 19176891 Disease Relevance 0 Pain Relevance 0.18
The proposed technique is based on our novel observation that intact CCK-8, but not its degradation product(s), binds to Lloyd reagent, a form of aluminum silicate.
Protein_catabolism (degradation) of CCK-8
12) Confidence 0.42 Published 1992 Journal Anal. Biochem. Section Abstract Doc Link 1456442 Disease Relevance 0 Pain Relevance 0.08
Our aim here was to develop a rapid and sensitive assay for the measurement of degradation of cholecystokinin octapeptide (CCK-8) as well as other short, hydrophobic peptides.
Protein_catabolism (degradation) of CCK-8 associated with cholecystokinin
13) Confidence 0.37 Published 1992 Journal Anal. Biochem. Section Abstract Doc Link 1456442 Disease Relevance 0 Pain Relevance 0.09
The decrease in binding closely paralleled the extent of CCK-8 degradation over time as assessed by high-performance liquid chromatography and immunoprecipitation with specific polyclonal antibodies to CCK-8.
Protein_catabolism (degradation) of CCK-8
14) Confidence 0.24 Published 1992 Journal Anal. Biochem. Section Abstract Doc Link 1456442 Disease Relevance 0 Pain Relevance 0.20
The levels of CCK-8 reached in the peripheral circulation and degradation of the peptide in vitro and in vivo were used to evaluate metabolism of cholecystokinin.
Protein_catabolism (metabolism) of cholecystokinin associated with cholecystokinin
15) Confidence 0.22 Published 1991 Journal Am. J. Physiol. Section Abstract Doc Link 2058671 Disease Relevance 0.33 Pain Relevance 0.60
CCK 8-(sulfated) degradation on slices from caudate-putamen, nucleus accumbens, and frontal cortex was not altered by inhibitors of neutral endopeptidase 24.11, metalloendopeptidase 24.15, angiotensin converting enzyme, or thiol proteases.
Protein_catabolism (degradation) of CCK in frontal cortex associated with nucleus accumbens, urological neuroanatomy and cholecystokinin
16) Confidence 0.19 Published 1995 Journal J. Neurochem. Section Abstract Doc Link 7595577 Disease Relevance 0.42 Pain Relevance 0.84
CCK 8-(sulfated) degradation on slices from caudate-putamen, nucleus accumbens, and frontal cortex was not altered by inhibitors of neutral endopeptidase 24.11, metalloendopeptidase 24.15, angiotensin converting enzyme, or thiol proteases.
Protein_catabolism (degradation) of CCK in caudate-putamen associated with nucleus accumbens, urological neuroanatomy and cholecystokinin
17) Confidence 0.19 Published 1995 Journal J. Neurochem. Section Abstract Doc Link 7595577 Disease Relevance 0.42 Pain Relevance 0.84
In vitro degradation of the C-terminal octapeptide of cholecystokinin by 'enkephalinase A'.
Protein_catabolism (degradation) of cholecystokinin associated with cholecystokinin
18) Confidence 0.08 Published 1983 Journal FEBS Lett. Section Title Doc Link 6132834 Disease Relevance 0 Pain Relevance 0.43

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