INT81136

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Context Info
Confidence 0.48
First Reported 1999
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 6
Total Number 6
Disease Relevance 1.45
Pain Relevance 1.15

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

lyase activity (Npr1) plasma membrane (Npr1) intracellular (Npr1)
Anatomy Link Frequency
brain 1
body 1
Npr1 (Mus musculus)
Pain Link Frequency Relevance Heat
Dopamine 48 94.88 High High
nMDA receptor 28 92.00 High High
gABA 7 90.64 High High
Glutamate receptor 3 90.32 High High
Osteoarthritis 10 85.28 High High
Potency 3 82.12 Quite High
cINOD 52 81.04 Quite High
agonist 8 76.64 Quite High
Angina 1 76.16 Quite High
potassium channel 4 71.00 Quite High
Disease Link Frequency Relevance Heat
Natriuresis 8 100.00 Very High Very High Very High
Hypertension 45 86.24 High High
Osteoarthritis 10 85.28 High High
Glaucoma 1 76.68 Quite High
Cv General 3 Under Development 1 76.16 Quite High
Myocardial Infarction 2 64.68 Quite High
Coronary Heart Disease 3 63.96 Quite High
Acute Decompensated Heart Failure (ADHF) 1 61.52 Quite High
Pain 16 58.00 Quite High
Dislocations 1 56.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These hormones bind to the natriuretic peptide A receptor (NPRA) throughout the body, stimulating cGMP production and playing a key role in blood pressure control.
NPRA Binding (bind) of in body associated with natriuresis
1) Confidence 0.48 Published 2005 Journal Am. J. Physiol. Heart Circ. Physiol. Section Abstract Doc Link 15778276 Disease Relevance 0.55 Pain Relevance 0
Within the cell NO binds to a haeme-moiety of the enzyme guanylyl cyclase thus increasing concentrations of cyclic guanosine monophosphate (cGMP).
guanylyl cyclase Neg (NO) Binding (binds) of
2) Confidence 0.16 Published 1999 Journal Anasthesiol Intensivmed Notfallmed Schmerzther Section Abstract Doc Link 10189520 Disease Relevance 0 Pain Relevance 0.04
In addition to recent findings of S-nitrosylation of cysteine residues of specific proteins, NO has long been known to bind to soluble guanylyl cyclase, leading to cGMP production and cGK activation.
soluble guanylyl cyclase Binding (bind) of
3) Confidence 0.03 Published 2009 Journal Mol Pain Section Body Doc Link PMC2762960 Disease Relevance 0 Pain Relevance 0.34
Two different classes of compounds—stimulators and activators—interact with soluble guanylyl cyclase [20•, 21•].
soluble guanylyl cyclase Binding (interact) of
4) Confidence 0.03 Published 2010 Journal Curr Hypertens Rep Section Body Doc Link PMC2910890 Disease Relevance 0.59 Pain Relevance 0.14
In brain cells, NO switches on the associated guanylyl cyclase activity with no observable delay (with a 20-ms sampling time) and, on removal of NO, the activity decays with a half-time of 200 ms (Bellamy & Garthwaite, 2001b), kinetics not dissimilar to that of NMDA receptors or of metabotropic GABA or glutamate receptors (Dale & Roberts, 1985; Dutar & Nicoll, 1988; Batchelor & Garthwaite, 1997).
cyclase Binding (associated) of in brain associated with gaba, glutamate receptor and nmda receptor
5) Confidence 0.02 Published 2008 Journal The European Journal of Neuroscience Section Body Doc Link PMC2610389 Disease Relevance 0.06 Pain Relevance 0.18
Once NO is generated, it binds to the heme group of soluble guanylyl cyclase, which catalyzes the conversion of GTP to cGMP, leading to an intracellular increase in cGMP concentration [8]. cGMP then binds to and modifies the target domain of specific proteins, including protein kinases, ion channels, and phosphodiesterases, to elicit cellular responses.
guanylyl cyclase Binding (binds) of
6) Confidence 0.01 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2582807 Disease Relevance 0.20 Pain Relevance 0.46

General Comments

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