INT49259

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Context Info
Confidence 0.61
First Reported 1995
Last Reported 2009
Negated 0
Speculated 4
Reported most in Abstract
Documents 8
Total Number 12
Disease Relevance 6.29
Pain Relevance 1.92

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 (EDN1) extracellular region (EDN1) cell-cell signaling (EDN1)
cytoplasm (EDN1)
Anatomy Link Frequency
endothelial cells 10
vascular endothelium 4
EDN1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Neuropeptide 3 99.80 Very High Very High Very High
Somatostatin 2 99.00 Very High Very High Very High
Inflammation 22 98.96 Very High Very High Very High
Pain 15 98.96 Very High Very High Very High
substance P 1 98.44 Very High Very High Very High
antagonist 70 96.04 Very High Very High Very High
Kinase C 3 94.08 High High
Cancer pain 6 93.16 High High
bradykinin 2 91.52 High High
central sensitization 2 90.64 High High
Disease Link Frequency Relevance Heat
Sprains And Strains 2 100.00 Very High Very High Very High
Cancer 10 99.68 Very High Very High Very High
INFLAMMATION 26 98.96 Very High Very High Very High
Pain 9 98.96 Very High Very High Very High
Glaucoma 202 98.28 Very High Very High Very High
Natriuresis 5 96.72 Very High Very High Very High
Stress 12 94.16 High High
Increased Venous Pressure Under Development 207 93.24 High High
Cancer Pain 6 93.16 High High
Disease 85 92.76 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Spec (examined) Regulation (effects) of Localization (release) of ET-1 in endothelial cells
1) Confidence 0.61 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Spec (examined) Regulation (effects) of Localization (release) of endothelin-1 in endothelial cells
2) Confidence 0.45 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
The former effect appears to be based on the inhibition of ET-1 degradation by neutral endopeptidase 24.11 (NEP), since kelatorphan, a specific NEP inhibitor, produced a similar increasing effect on ET-1 release.
Regulation (effect) of Localization (release) of ET-1
3) Confidence 0.45 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Spec (examined) Regulation (effects) of Localization (release) of endothelin-1 in endothelial cells
4) Confidence 0.45 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
Using cultured human aortic endothelial cells, we examined the effects of phosphoramidon, an endothelin converting enzyme (ECE) inhibitor, on the release of endogenous endothelin-1 (ET-1) and big endothelin-1 (big ET-1), and on the generation of ET-1 from exogenously applied big ET-1.
Spec (examined) Regulation (effects) of Localization (release) of ET-1 in endothelial cells
5) Confidence 0.45 Published 1995 Journal Biol. Pharm. Bull. Section Abstract Doc Link 7550091 Disease Relevance 0 Pain Relevance 0
The vascular endothelium regulates the microcirculation through release of vasoactive factors, the most potent of which are the vasodilator nitric oxide (NO) and the vasoconstrictor endothelin-1 (ET-1) (Adams 2006).
Regulation (regulates) of Localization (release) of ET-1 in vascular endothelium
6) Confidence 0.43 Published 2008 Journal Clinical Ophthalmology (Auckland, N.Z.) Section Body Doc Link PMC2699797 Disease Relevance 1.65 Pain Relevance 0.08
The vascular endothelium regulates the microcirculation through release of vasoactive factors, the most potent of which are the vasodilator nitric oxide (NO) and the vasoconstrictor endothelin-1 (ET-1) (Adams 2006).
Regulation (regulates) of Localization (release) of vasoconstrictor endothelin-1 in vascular endothelium
7) Confidence 0.43 Published 2008 Journal Clinical Ophthalmology (Auckland, N.Z.) Section Body Doc Link PMC2699797 Disease Relevance 1.65 Pain Relevance 0.08
The effect of this intervention on the release of ET-1 and NOx is still unclear.
Regulation (effect) of Localization (release) of ET-1
8) Confidence 0.39 Published 2006 Journal BMC Musculoskelet Disord Section Body Doc Link PMC1693561 Disease Relevance 0.80 Pain Relevance 0.55
ET-1 release via a constitutive pathway is regulated principally at the level of gene transcription.
Regulation (regulated) of Localization (release) of ET-1
9) Confidence 0.32 Published 2008 Journal Drug design, development and therapy Section Body Doc Link PMC2761178 Disease Relevance 0.42 Pain Relevance 0.13
The aims of this study were to test the hypothesis that propofol may alter strain-induced endothelin-1 (ET-1) secretion and nitric oxide production, and to identify the putative underlying signaling pathways in human umbilical vein endothelial cells.
Regulation (alter) of Localization (secretion) of ET-1 in endothelial cells associated with sprains and strains
10) Confidence 0.26 Published 2009 Journal Anesthesiology Section Abstract Doc Link 19104173 Disease Relevance 0.27 Pain Relevance 0.09
As tumor expression and release of ET-1 has been shown to be regulated by the local environment, location specific expression and release of ET-1 by tumor cells may provide insight into the mechanisms that underlie the heterogeneity of bone cancer pain that is frequently observed in humans with multiple skeletal metastases.
Regulation (regulated) of Localization (release) of ET-1 associated with cancer pain, cancer and metastasis
11) Confidence 0.26 Published 2004 Journal Neuroscience Section Abstract Doc Link 15207337 Disease Relevance 1.22 Pain Relevance 0.73
A number of other neurotrasmitters and neuropeptides can also modulate prolactin secretion, among which galanin, endothelin, TGFbeta1, angiotensin, somatostatin, substance P, neurotensin, calcitonin, EGF, natriuretic atrial peptide, bombesin, colecistokinine, acetylcholine, vasopressin (Figure 1).
Regulation (modulate) of Localization (secretion) of endothelin associated with natriuresis, somatostatin, neuropeptide and substance p
12) Confidence 0.03 Published 2007 Journal Therapeutics and Clinical Risk Management Section Body Doc Link PMC2376090 Disease Relevance 0.28 Pain Relevance 0.27

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