INT182511

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.44
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 7
Total Number 7
Disease Relevance 8.25
Pain Relevance 1.40

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 (AGTR1) signal transducer activity (AGTR1)
Anatomy Link Frequency
sympathetic 1
immune system 1
AGTR1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 364 99.84 Very High Very High Very High
Inflammatory response 13 98.68 Very High Very High Very High
fibrosis 20 98.52 Very High Very High Very High
Inflammatory mediators 15 87.08 High High
antagonist 28 84.20 Quite High
agonist 6 83.56 Quite High
bradykinin 1 76.08 Quite High
Enkephalin 1 73.04 Quite High
chemokine 27 57.16 Quite High
cytokine 52 56.68 Quite High
Disease Link Frequency Relevance Heat
Cancer 456 99.92 Very High Very High Very High
INFLAMMATION 395 99.84 Very High Very High Very High
Disease 154 99.16 Very High Very High Very High
Increased Venous Pressure Under Development 93 98.92 Very High Very High Very High
Fibrosis 15 98.52 Very High Very High Very High
Stress 82 98.28 Very High Very High Very High
Infection 7 98.04 Very High Very High Very High
Hypoxia 70 97.84 Very High Very High Very High
Injury 47 97.32 Very High Very High Very High
Neurodegenerative Disease 10 97.16 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Taken together with the data presented in Fig. 1, A–D, these findings establish the formation of a previously unsuspected multiprotein complex involving TRPV4, AT1aR, and ?
Regulation (involving) of AT1aR
1) Confidence 0.44 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2943294 Disease Relevance 0 Pain Relevance 0
This key role of ox-LDL regarding AT1 is demonstrated by HMG Co-A reductase inhibitor causing the down-regulation of the AT1 receptor with consequential reduction in inflammatory response [37].
Regulation (regulation) of AT1 receptor associated with inflammatory response
2) Confidence 0.42 Published 2004 Journal J Inflamm (Lond) Section Body Doc Link PMC1074345 Disease Relevance 1.25 Pain Relevance 0.05
and lipopolysaccharides, through induction of NO and cGMP, all serve to down-regulate AT2 with no effect on AT1 leading to a quicker progression of fibrosis.
Neg (no) Regulation (effect) of AT1 associated with fibrosis
3) Confidence 0.25 Published 2004 Journal J Inflamm (Lond) Section Body Doc Link PMC1074345 Disease Relevance 0.90 Pain Relevance 0.31
Confirming the systemic role of the AT1 receptor in inflammation and disease
Regulation (role) of AT1 receptor associated with inflammation and disease
4) Confidence 0.25 Published 2004 Journal J Inflamm (Lond) Section Body Doc Link PMC1074345 Disease Relevance 1.56 Pain Relevance 0.28
This review proposes that cancer up-regulates the angiotensin II type 1 (AT1) receptor through systemic oxidative stress and hypoxia mechanisms, thereby triggering chronic inflammatory processes to remodel surrounding tissue and subdue the immune system.
Regulation (regulates) of angiotensin II type 1 in immune system associated with stress, inflammation, hypoxia and cancer
5) Confidence 0.25 Published 2004 Journal J Inflamm (Lond) Section Abstract Doc Link PMC1074345 Disease Relevance 1.80 Pain Relevance 0.24
The evidence suggests that regulation of the mutually antagonistic angiotensin II receptors (AT1 and AT2) is an essential process in the management of inflammation and wound recovery, and that it is an imbalance in the expression of these receptors that leads to disease.
Regulation (regulation) of AT1 associated with inflammation, injury and disease
6) Confidence 0.25 Published 2004 Journal J Inflamm (Lond) Section Abstract Doc Link PMC1074345 Disease Relevance 2.42 Pain Relevance 0.32
AII acts by stimulating specific receptors, in the human body we are able to distinguish two different types of receptors: AT1 and AT2. the AT1 receptors are responsible for known effects of AII; vasoconstriction, increase of aldosterone activity, myocardial hypertrophy, vessel wall smooth muscle proliferation, renal sodium reabsortion, increase in peripheral noradrenergic activity, vasopresin release, sympathetic stimulation, decrease in renal blood flow, etc.
Regulation (responsible) of AT1 in sympathetic associated with coronary heart disease and increased venous pressure under development
7) Confidence 0.16 Published 2006 Journal Cardiovasc Diabetol Section Body Doc Link PMC1434727 Disease Relevance 0.32 Pain Relevance 0.19

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox