INT3332

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Context Info
Confidence 0.87
First Reported 1978
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 23
Total Number 24
Disease Relevance 3.17
Pain Relevance 4.39

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 (AGT) small molecule metabolic process (AGT) aging (AGT)
extracellular region (AGT) extracellular matrix organization (AGT) cell-cell signaling (AGT)
Anatomy Link Frequency
cleavage 4
myocardium 1
cerebrospinal fluid 1
vesicles 1
platelets 1
AGT (Homo sapiens)
Pain Link Frequency Relevance Heat
Enkephalin 32 100.00 Very High Very High Very High
bradykinin 28 100.00 Very High Very High Very High
substance P 47 99.48 Very High Very High Very High
Somatostatin 1 95.52 Very High Very High Very High
antagonist 116 94.44 High High
Neuropeptide 12 93.16 High High
Opioid 6 93.04 High High
Central nervous system 7 84.64 Quite High
Potency 8 78.08 Quite High
opioid receptor 2 77.04 Quite High
Disease Link Frequency Relevance Heat
Cardiovascular Disease 17 98.32 Very High Very High Very High
Sperm Disorder 30 91.52 High High
Lung Cancer 16 87.04 High High
Increased Venous Pressure Under Development 22 81.12 Quite High
Pressure And Volume Under Development 57 75.52 Quite High
Nicotine Addiction 5 75.00 Quite High
Angina 1 75.00 Quite High
Heart Rate Under Development 52 74.64 Quite High
Pulmonary Hypertension 31 73.92 Quite High
Cough 7 73.60 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Using thin layer chromatography, degradation of 125I-angiotensin II by platelets could be demonstrated in the presence of various enzyme inhibitors.
Protein_catabolism (degradation) of angiotensin II in platelets
1) Confidence 0.87 Published 1985 Journal J. Hypertens. Section Abstract Doc Link 2991370 Disease Relevance 0 Pain Relevance 0
Renin is the rate-limiting step of the RAAS and has unique specificity for its substrate, angiotensinogen.
Protein_catabolism (substrate) of angiotensin
2) Confidence 0.86 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350136 Disease Relevance 0.15 Pain Relevance 0.16
Renin is the rate-limiting step of the RAAS and has unique specificity for its substrate, angiotensinogen.
Protein_catabolism (substrate) of angiotensinogen
3) Confidence 0.86 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2350136 Disease Relevance 0.15 Pain Relevance 0.16
However, these cells could not be used for studies of specific binding, since enzymatic degradation of 125I-angiotensin II could not be prevented despite addition of various enzyme inhibitors.
Protein_catabolism (degradation) of angiotensin II
4) Confidence 0.77 Published 1985 Journal J. Hypertens. Section Abstract Doc Link 2991370 Disease Relevance 0 Pain Relevance 0.14
Over the last two decades, a growing number of experimental and clinical studies provided evidence of an important role played by angiotensin II along the different steps of the cardiovascular disease continuum.5 It is well known that angiotensin II is produced through the aminoacid cleavage of angiotensin I operated by the angiotensin-converting enzyme (ACE) in some tissues including the lung, as well as in the myocardium, through the effects of specific proteases on angiotensin I.
Protein_catabolism (cleavage) of angiotensin I in myocardium associated with cardiovascular disease
5) Confidence 0.60 Published 2009 Journal Vascular Health and Risk Management Section Body Doc Link PMC2788599 Disease Relevance 1.13 Pain Relevance 0
Although the neutral endopeptidase did not convert angiotensin I to II, it did hydrolyze angiotensin I at Pro7-Phe8 and inactivate angiotensin II by cleavage at the Tyr4-Ile5 bond.
Protein_catabolism (cleavage) of angiotensin II in cleavage
6) Confidence 0.57 Published 1983 Journal Biochemistry Section Abstract Doc Link 6349683 Disease Relevance 0 Pain Relevance 0.27
The hydrolysis of angiotensin I is inhibited by the specific ACE inhibitors captopril and lisonopril (Ic50 = 50 nM).
Protein_catabolism (hydrolysis) of angiotensin I
7) Confidence 0.53 Published 1997 Journal Regul. Pept. Section Abstract Doc Link 9178346 Disease Relevance 0 Pain Relevance 0.14
Proportional to its cellular distribution, AmM hydrolyzed the N-terminus of kallidin to produce bradykinin, and degraded des(Asp1)angiotensin I, angiotensin III, hepta(5-11)substance P and Met5-enkephalin.
Protein_catabolism (degraded) of angiotensin III associated with enkephalin, bradykinin and substance p
8) Confidence 0.46 Published 1989 Journal Biochem. Pharmacol. Section Abstract Doc Link 2462880 Disease Relevance 0 Pain Relevance 0.44
Proportional to its cellular distribution, AmM hydrolyzed the N-terminus of kallidin to produce bradykinin, and degraded des(Asp1)angiotensin I, angiotensin III, hepta(5-11)substance P and Met5-enkephalin.
Protein_catabolism (degraded) of angiotensin I associated with enkephalin, bradykinin and substance p
9) Confidence 0.46 Published 1989 Journal Biochem. Pharmacol. Section Abstract Doc Link 2462880 Disease Relevance 0 Pain Relevance 0.43
Angiotensin I, dynorphins 1-8 and 1-9 and substance P also behaved as good substrates while neuromedin N, angiotensin II, leucine and methionine enkephalin and neurokinin A resisted degradation by human endopeptidase 3.4.24.16.
Protein_catabolism (degradation) of angiotensin II associated with enkephalin and substance p
10) Confidence 0.44 Published 1996 Journal Brain Res. Section Abstract Doc Link 8869556 Disease Relevance 0 Pain Relevance 0.24
In excess, the magnitude of which varies among individuals, trypsin at first produces activation and later a decline in PRA, probably due to degradation of the reactants (prorenin, renin, angiotensinogen) and of the initial product (angiotensin I).
Protein_catabolism (degradation) of angiotensin I
11) Confidence 0.37 Published 1978 Journal Can. J. Physiol. Pharmacol. Section Abstract Doc Link 709420 Disease Relevance 0 Pain Relevance 0
NEP and NEP2 participate in degradation of other peptides, such as angiotensin-1, bradykinin and enkephalins which are also implicated in sperm cell function [27,28] and might thus be relevant to explain the tachykinin antagonist-resistant component of the response to phosphoramidon.
Protein_catabolism (degradation) of angiotensin-1 in sperm cell associated with antagonist, enkephalin and bradykinin
12) Confidence 0.34 Published 2010 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2936315 Disease Relevance 0.05 Pain Relevance 0.49
Human NEP2 has much higher substrate specificity and only degrades tachykinins and angiotensin I with efficiency similar to NEP [28].
Protein_catabolism (degrades) of angiotensin I
13) Confidence 0.25 Published 2010 Journal Reprod Biol Endocrinol Section Body Doc Link PMC2936315 Disease Relevance 0.09 Pain Relevance 0.32
Reproducible product patterns consistent with cleavage of the peptide bond at proline for angiotensin I, Lys-bradykinin, and myoglobin are demonstrated using capillary electrophoresis.
Protein_catabolism (cleavage) of angiotensin I in cleavage associated with bradykinin
14) Confidence 0.20 Published 2007 Journal Anal. Chem. Section Abstract Doc Link 17297930 Disease Relevance 0 Pain Relevance 0.13
AngII is an octapeptide produced by cleavage of the inactive decapeptide Angiotensin I (AngI) by Angiotensin I-converting enzyme (ACE), a zinc metalloprotease found in the circulation or bound to the cell membrane.
Protein_catabolism (cleavage) of Angiotensin I in cleavage
15) Confidence 0.16 Published 2008 Journal Mol Cancer Section Body Doc Link PMC2615789 Disease Relevance 0.47 Pain Relevance 0.04
AngI itself is produced by enzymatic cleavage of the angiotensinogen precursor by renin.
Protein_catabolism (cleavage) of angiotensinogen precursor in cleavage
16) Confidence 0.16 Published 2008 Journal Mol Cancer Section Body Doc Link PMC2615789 Disease Relevance 0.36 Pain Relevance 0.04
The K(m), V(max), K(cat) and K(cat)/K(m) values of gACE at optimal pH (pH 7.2) were 680 microM, 1.0 micromol/mg/min, 33.1 s(-1) and 4.87 x 10(4) s(-1) M(-1) for Z-Val-Lys-Met-MCA, respectively. gACE was potently inhibited by EDTA, 1,10-phenanthroline, captopril and lisinopril, and it promptly released the dipeptides His-Leu and Phe-Arg from angiotensin I and bradykinin.
Protein_catabolism (bradykinin) of angiotensin I associated with bradykinin
17) Confidence 0.14 Published 2007 Journal Comp. Biochem. Physiol. B, Biochem. Mol. Biol. Section Abstract Doc Link 17145192 Disease Relevance 0 Pain Relevance 0.15
The hydrolysis of angiotensin I is inhibitable at 80% by captopril (IC50 = 175 nM) and lisinopril (IC50 = 35 nM).
Protein_catabolism (hydrolysis) of angiotensin I
18) Confidence 0.10 Published 1996 Journal Peptides Section Abstract Doc Link 8844761 Disease Relevance 0 Pain Relevance 0.14
BACKGROUND: Angiotensin converting enzyme (ACE) perhaps plays roles in regulating coronary vasomotor tone by producing angiotensin II and degrading bradykinin.
Protein_catabolism (degrading) of angiotensin II associated with bradykinin
19) Confidence 0.10 Published 1999 Journal Coron. Artery Dis. Section Abstract Doc Link 10376201 Disease Relevance 0.15 Pain Relevance 0.12
For example, angiotensin I is processed extracellularly in the lung by angiotensin-converting enzyme (ACE; E.C. 3.4.15.1), a peptidyl dipeptidase, to form the potent vasoconstrictor hormone angiotensin II.
Protein_catabolism (processed) of angiotensin I in lung
20) Confidence 0.09 Published 1993 Journal Crit Rev Neurobiol Section Abstract Doc Link 8221910 Disease Relevance 0 Pain Relevance 0.04

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