INT46201

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Context Info
Confidence 0.53
First Reported 1983
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 21
Total Number 21
Disease Relevance 3.01
Pain Relevance 2.87

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 (KLKB1) extracellular space (KLKB1) extracellular region (KLKB1)
plasma membrane (KLKB1)
Anatomy Link Frequency
plasma 16
CSF 2
blood 1
lymph 1
endothelium 1
KLKB1 (Homo sapiens)
Pain Link Frequency Relevance Heat
algil 9 99.00 Very High Very High Very High
metalloproteinase 45 97.36 Very High Very High Very High
Restless leg syndrome 15 97.22 Very High Very High Very High
Gabapentin 16 96.92 Very High Very High Very High
gABA 2 84.04 Quite High
bradykinin 29 83.88 Quite High
Pain 6 79.80 Quite High
Inflammation 16 67.96 Quite High
b2 receptor 8 53.08 Quite High
antagonist 49 40.00 Quite Low
Disease Link Frequency Relevance Heat
Pressure And Volume Under Development 31 99.64 Very High Very High Very High
Peripheral Arterial Disease 270 99.52 Very High Very High Very High
Sprains And Strains 20 99.04 Very High Very High Very High
Increased Venous Pressure Under Development 30 98.62 Very High Very High Very High
Atherosclerosis 60 97.22 Very High Very High Very High
Facioscapulohumeral Muscular Dystrophy 75 96.56 Very High Very High Very High
Hereditary Angioedema 92 93.00 High High
Anaphylaxis 4 91.76 High High
Shock 1 83.60 Quite High
Pain 5 79.80 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
No DH sites were observed at two other proximal 4q35.2 genes, KLKB1 and F11, which encode proteins involved in blood coagulation.
Gene_expression (sites) of KLKB1 in blood
1) Confidence 0.53 Published 2009 Journal Nucleic Acids Research Section Body Doc Link PMC2794184 Disease Relevance 0.27 Pain Relevance 0
Human plasma kallikrein-kinin system: physiological and biochemical parameters.
Gene_expression (system) of plasma kallikrein-kinin in plasma
2) Confidence 0.19 Published 2009 Journal Cardiovascular & hematological agents in medicinal chemistry Section Title Doc Link 19689262 Disease Relevance 0.46 Pain Relevance 0.46
No linear relationship was observed between plasma and CSF levels in these patients.
Gene_expression (levels) of plasma in plasma
3) Confidence 0.11 Published 1995 Journal Epilepsy Res. Section Abstract Doc Link 8536677 Disease Relevance 0.30 Pain Relevance 0.69
Ecallantide (Kalbitor, Dyax Inc.) is a novel, potent and specific plasma kallikrein inhibitor produced in the Pichia pastoris strain of yeast that was identified using phage display technology for a library of rationally designed variants of the first Kunitz domain of human lipoprotein-associated coagulation inhibitor (LACI) [62,63].
Gene_expression (produced) of plasma kallikrein in plasma associated with sprains and strains
4) Confidence 0.07 Published 2010 Journal Allergy Asthma Clin Immunol Section Body Doc Link PMC2921104 Disease Relevance 0.83 Pain Relevance 0.12
The much lower complexed fractions from experimental data may indicate that in vivo, other soluble receptors (e.g., sVEGFR2, sNRP1, plasma fibronectin) can strongly compete with sVEGFR1 as plasma reservoirs for VEGF, or significant quantities of other ligands (e.g., PlGF, VEGF-B) are present to compete with VEGF for sVEGFR1 binding.
Gene_expression (reservoirs) of plasma in plasma
5) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
The implications of such an association would be significant: (i) impaired ambulation (due to the PAD symptoms of intermittent claudication) and the associated reductions in leg muscle contractions and lymph flow rate may partially account for the tissue edema [62] and lowered plasma sVEGFR1 levels observed in PAD [44], [45]; conversely, (ii) the success of exercise rehabilitation for PAD patients can potentially be explained by the restoration of lymph flow rate with increased leg muscle contractions [61], [63], [64].


Gene_expression (levels) of plasma in lymph associated with pressure and volume under development, restless leg syndrome and peripheral arterial disease
6) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.49 Pain Relevance 0.10
The significance here is that the physiological variation in transport rates offers a case example where the common circulating angiogenic markers become unreliable, i.e., apparent changes in free VEGF or sVEGFR1 levels in the plasma do not correlate with changes in the actual angiogenic signaling potential in the tissues.
Gene_expression (changes) of plasma in plasma
7) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
However, 9 h of sleep was adequate for plasma free sVEGFR1 to fall back to below control levels regardless of whether the subject was active or inactive during waking hours (?
Gene_expression (free) of plasma in plasma
8) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Transport parameters affected concentrations of plasma VEGF, plasma sVEGFR1 and interstitial sVEGFR1, but not surface-bound VEGFR occupancy
Gene_expression (concentrations) of plasma in plasma
9) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Secondly, the transendothelial gradient of sVEGFR1 at control favored net extravasation, hence increasing kP resulted in: lower plasma concentrations of free sVEGFR1; as well as increased free sVEGFR1 in the interstitium facing the endothelium where kP was upregulated, at the expense of a decrease in interstitial free sVEGFR1 in the other tissue compartment (e.g., “Control” vs.
Gene_expression (concentrations) of plasma in endothelium
10) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
The clinical implication is that pathological levels of plasma sVEGFR1 may not necessarily indicate altered sVEGFR1 production or altered availability of free VEGF, because they may partially reflect altered receptor expression in tissues.
Gene_expression (levels) of plasma in plasma
11) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
A dynamic simulation of the diurnal changes of kL over a combination of “bed-rest days” and “active days”, as illustrated in Fig. 9C, suggested that physiological variation of kL over the course of a day can still account for significant variation in plasma concentrations of VEGF and sVEGFR1.
Gene_expression (concentrations) of plasma in plasma
12) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
At the control secretion rates of VEGF and sVEGFR1 needed to reproduce these selected plasma concentrations, our predicted interstitial concentrations ([V]IS?
Gene_expression (concentrations) of plasma in plasma
13) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Abnormal plasma levels of MMPs in PAD [148], [149] may suggest a role for proteolytic degradation or release of VEGF165 in causing pathological bioavailabilities of VEGF.
Gene_expression (levels) of plasma in plasma associated with peripheral arterial disease
14) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.27 Pain Relevance 0.13
Since lymph flow represented a unidirectional flushing of VEGF and sVEGFR1 from the interstitium into blood, increasing kL resulted in higher plasma and lower interstitial concentrations of free VEGF and sVEGFR1.
Gene_expression (resulted) of plasma in plasma associated with increased venous pressure under development
15) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.10 Pain Relevance 0
Steady-state analyses showed that fluctuations in the VEGF-binding affinity and densities of interstitial matrix sites had no detectable effects on the concentrations of all soluble species (in both plasma and interstitial fluid), nor on surface receptor occupancies (Fig. 7).
Gene_expression (occupancies) of plasma in plasma
16) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
However, 9 h of sleep was adequate for plasma free sVEGFR1 to fall back to below control levels regardless of whether the subject was active or inactive during waking hours (?
Gene_expression (fall) of plasma in plasma
17) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
From the waking hour (e.g., 48th h in Fig. 9C), plasma concentration of free sVEGFR1 followed a steady rise over the next 15 h before the onset of sleep.
Gene_expression (concentration) of plasma in plasma
18) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
This predicted complexed fraction of VEGF was much higher than that experimentally measured by Belgore et al. in healthy human plasma (?
Gene_expression (healthy) of plasma in plasma
19) Confidence 0.05 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Thus, transfer from plasma to CSF occurs relatively rapidly.
Gene_expression (transfer) of plasma in CSF
20) Confidence 0.05 Published 1983 Journal Acta Anaesthesiol Scand Section Abstract Doc Link 6880582 Disease Relevance 0 Pain Relevance 0.68

General Comments

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