INT50105

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Context Info
Confidence 0.78
First Reported 1994
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 29
Total Number 29
Disease Relevance 10.98
Pain Relevance 5.21

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

peptidase activity (CTSB) mitochondrion (CTSB) extracellular space (CTSB)
extracellular region (CTSB) intracellular (CTSB) lysosome (CTSB)
Anatomy Link Frequency
neuronal 3
cleavage 2
brain 2
vesicle 2
macrophage 1
CTSB (Homo sapiens)
Pain Link Frequency Relevance Heat
Abeta 9 100.00 Very High Very High Very High
cINOD 21 99.52 Very High Very High Very High
sSRI 96 99.50 Very High Very High Very High
Neurotransmitter 14 99.36 Very High Very High Very High
bradykinin 5 99.24 Very High Very High Very High
Central nervous system 24 99.12 Very High Very High Very High
tetrodotoxin 13 98.96 Very High Very High Very High
Neuropeptide 8 96.64 Very High Very High Very High
Chronic pancreatitis 3 96.44 Very High Very High Very High
Inflammation 52 96.20 Very High Very High Very High
Disease Link Frequency Relevance Heat
Alzheimer's Dementia 86 100.00 Very High Very High Very High
Rupture 3 99.68 Very High Very High Very High
Disease 216 98.68 Very High Very High Very High
Death 5 98.50 Very High Very High Very High
Pruritus 46 98.44 Very High Very High Very High
Skin Allergy 3 98.28 Very High Very High Very High
Necrosis 5 97.98 Very High Very High Very High
Cancer 5 97.80 Very High Very High Very High
Pancreatitis 23 96.44 Very High Very High Very High
Neurodegenerative Disease 25 96.36 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We show that the combination of tumor necrosis factor alpha and interferon gamma triggers the production of beta-amyloid peptides and inhibits the secretion of soluble APPs by human neuronal and extraneuronal cells.
Localization (secretion) of APPs in neuronal associated with necrosis, cancer and alzheimer's dementia
1) Confidence 0.78 Published 1999 Journal FASEB J. Section Abstract Doc Link 9872930 Disease Relevance 1.14 Pain Relevance 0.31
A recent study showed that cathepsin B is abundantly present in the secretory compartment of the healthy human pancreas and is secreted together with trypsinogen and active trypsin into the pancreatic juice of patients with chronic pancreatitis [8].
Localization (secreted) of cathepsin B in pancreas associated with chronic pancreatitis
2) Confidence 0.53 Published 2002 Journal BMC Gastroenterol Section Body Doc Link PMC117221 Disease Relevance 0.53 Pain Relevance 0.15
Recent studies have identified secretory vesicle cathepsin B as a novel beta-secretase for production of the neurotoxic beta-amyloid (Abeta) peptide of Alzheimer disease.
Localization (secretory) of cathepsin B in vesicle associated with alzheimer's dementia and abeta
3) Confidence 0.29 Published 2006 Journal BioDrugs Section Abstract Doc Link 16626168 Disease Relevance 0.77 Pain Relevance 0.30
Gamma-secretase is a multi-component enzyme complex that performs an intramembranous cleavage, releasing amyloid-beta (Abeta) peptides from processing intermediates of the beta-amyloid precursor protein.
Localization (releasing) of Gamma-secretase in cleavage associated with alzheimer's dementia and abeta
4) Confidence 0.23 Published 2004 Journal J. Biol. Chem. Section Abstract Doc Link 15304503 Disease Relevance 0.51 Pain Relevance 0.27
Secretion of APPs, a secreted proteolytic derivative that is cleaved within the beta A4 domain of APP, is increased many-fold by the activation of cell-surface receptors, like the muscarinic m1 and m3 receptor subtypes, which are coupled to protein kinase C.
Localization (secreted) of APPs associated with kinase c
5) Confidence 0.23 Published 1994 Journal J. Neural Transm. Suppl. Section Abstract Doc Link 7897393 Disease Relevance 0.43 Pain Relevance 0.07
Other receptors that stimulate APPs secretion include those for bradykinin, vasopressin, and interleukin-1 receptors.
Localization (secretion) of APPs associated with bradykinin
6) Confidence 0.23 Published 1994 Journal J. Neural Transm. Suppl. Section Abstract Doc Link 7897393 Disease Relevance 0.36 Pain Relevance 0.25
A similar control mechanism is present in rat brain tissue slices, in which the release of both APPs and endogenous neurotransmitters is increased by electrical depolarization.
Localization (release) of APPs in brain associated with neurotransmitter
7) Confidence 0.23 Published 1994 Journal J. Neural Transm. Suppl. Section Abstract Doc Link 7897393 Disease Relevance 0.34 Pain Relevance 0.27
Secretion of APPs, a secreted proteolytic derivative that is cleaved within the beta A4 domain of APP, is increased many-fold by the activation of cell-surface receptors, like the muscarinic m1 and m3 receptor subtypes, which are coupled to protein kinase C.
Localization (Secretion) of APPs associated with kinase c
8) Confidence 0.23 Published 1994 Journal J. Neural Transm. Suppl. Section Abstract Doc Link 7897393 Disease Relevance 0.44 Pain Relevance 0.07
This increase is tetrodotoxin-sensitive and frequency-dependent, suggesting that APPs release may normally depend on neuronal activity.
Localization (release) of APPs in neuronal associated with tetrodotoxin
9) Confidence 0.23 Published 1994 Journal J. Neural Transm. Suppl. Section Abstract Doc Link 7897393 Disease Relevance 0.32 Pain Relevance 0.27
RESULT: The relative risks for affirming the sue MD statement relative to the healthy community sample for various groups were as follows in order of ascending risk: APPs in rehabilitation; nonhealthy community members; rehabilitation patients in general; rehabilitation patients without pain; CPPs in rehabilitation; and with the highest risk being rehabilitation patients with worker's compensation litigation.
Localization (rehabilitation) of APPs
10) Confidence 0.20 Published 2008 Journal Pain Med Section Body Doc Link 18657217 Disease Relevance 0 Pain Relevance 0
All three ChEI elevated APPs release significantly above control levels.
Localization (release) of APPs
11) Confidence 0.18 Published 1995 Journal Neuroreport Section Abstract Doc Link 7605915 Disease Relevance 0.15 Pain Relevance 0.08
All three ChEI elevated APPs release significantly above control levels.
Localization (release) of APPs
12) Confidence 0.16 Published 1996 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 8624119 Disease Relevance 0.15 Pain Relevance 0.08
The effect of cholinesterase inhibitors on the secretion of APPS from rat brain cortex.
Localization (secretion) of APPS in cortex
13) Confidence 0.16 Published 1996 Journal Ann. N. Y. Acad. Sci. Section Title Doc Link 8624119 Disease Relevance 0.15 Pain Relevance 0.06
Cholinesterase inhibitors increase secretion of APPs in rat brain cortex.
Localization (secretion) of APPs in brain
14) Confidence 0.15 Published 1995 Journal Neuroreport Section Title Doc Link 7605915 Disease Relevance 0.16 Pain Relevance 0.07
Three ChEI, both reversible and irreversible, were tested for their ability to enhance the release of nonamyloidogenic soluble derivatives (APPs).
Localization (release) of APPs
15) Confidence 0.15 Published 1995 Journal Neuroreport Section Abstract Doc Link 7605915 Disease Relevance 0.15 Pain Relevance 0.06
Electrical field stimulation significantly increased the release of APPs within 50 min.
Localization (release) of APPs
16) Confidence 0.15 Published 1995 Journal Neuroreport Section Abstract Doc Link 7605915 Disease Relevance 0.16 Pain Relevance 0.09
Three ChEI, both reversible and irreversible were tested for their ability to enhance the release of non-amyloidogenic soluble derivatives (APPs).
Localization (release) of APPs
17) Confidence 0.14 Published 1996 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 8624119 Disease Relevance 0.14 Pain Relevance 0.06
Electrical field stimulation significantly increased the release of APPs within 50 min.
Localization (release) of APPs
18) Confidence 0.14 Published 1996 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 8624119 Disease Relevance 0.15 Pain Relevance 0.09
We previously showed that elevations in cAMP, perhaps generated in response to prostaglandins, can suppress APPs secretion.
Localization (secretion) of APPs
19) Confidence 0.14 Published 2000 Journal Ann. N. Y. Acad. Sci. Section Abstract Doc Link 11193162 Disease Relevance 0.20 Pain Relevance 0.42
Calpain has also been implicated in neuronal death following ischaemic insult by initiating lysosomal rupture and subsequent cathepsin B release [59,60].
Localization (release) of cathepsin B in neuronal associated with rupture and death
20) Confidence 0.08 Published 2009 Journal Microb Cell Fact Section Body Doc Link PMC2674406 Disease Relevance 0.62 Pain Relevance 0

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