INT212762

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Context Info
Confidence 0.58
First Reported 2007
Last Reported 2009
Negated 2
Speculated 3
Reported most in Body
Documents 21
Total Number 24
Disease Relevance 2.95
Pain Relevance 0.26

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

cell differentiation (FLT1) endosome (FLT1) Golgi apparatus (FLT1)
cytoplasm (FLT1) extracellular space (FLT1) extracellular region (FLT1)
Anatomy Link Frequency
plasma 8
blood 1
muscle tissues 1
section 3 1
oviduct 1
FLT1 (Homo sapiens)
Pain Link Frequency Relevance Heat
tolerance 19 85.12 High High
Restless leg syndrome 19 69.60 Quite High
imagery 1 62.64 Quite High
antagonist 60 61.52 Quite High
Arthritis 1 58.56 Quite High
pain pelvic 2 49.72 Quite Low
addiction 57 12.52 Low Low
metalloproteinase 57 5.00 Very Low Very Low Very Low
ischemia 41 5.00 Very Low Very Low Very Low
Inflammation 24 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Ectopic Pregnancy 95 98.86 Very High Very High Very High
Pre-eclampsia 117 98.44 Very High Very High Very High
Lipoid Nephrosis 12 97.52 Very High Very High Very High
Disease 158 86.04 High High
Peripheral Arterial Disease 342 70.88 Quite High
Atherosclerosis 76 69.60 Quite High
Diabetes Mellitus 79 63.60 Quite High
Coronary Artery Disease 114 63.24 Quite High
Cancer 98 61.20 Quite High
Increased Venous Pressure Under Development 39 60.16 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Particularly relevant is the latter process of regulation through VEGFR1-VEGFR2 crosstalk, which possibly presents an opportunity for sVEGFR1, as a VEGFR1 competitor, to moderate VEGFR2 activation and internalization.
Spec (possibly) Regulation (regulation) of VEGFR1-VEGFR2
1) Confidence 0.58 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
The investigators hypothesized that misregulation of Flt-1 may provide a mechanism for the development of protenuria in MCN, thus, polymorphisms in this gene may predispose to MNC.
Regulation (misregulation) of Flt-1 associated with lipoid nephrosis
2) Confidence 0.44 Published 2008 Journal BMC Med Genet Section Body Doc Link PMC2496902 Disease Relevance 0.51 Pain Relevance 0
Alternatively, the penetrance of the Flt-1 gene may be modified by other factors, including distinct genetic loci that impart susceptibility.
Spec (may) Regulation (modified) of Flt-1 gene
3) Confidence 0.44 Published 2008 Journal BMC Med Genet Section Body Doc Link PMC2496902 Disease Relevance 0.49 Pain Relevance 0.03
The down-regulation of Flt-1 in the placental bed may result in a decreased maternal vascular adaptation to pregnancy [27].
Regulation (regulation) of Flt-1
4) Confidence 0.44 Published 2008 Journal BMC Med Genet Section Body Doc Link PMC2496902 Disease Relevance 0.17 Pain Relevance 0
As lymph flow directly transfers protein mass from the interstitial space into the blood, concentrations of VEGF and sVEGFR1 in muscle interstitia and in plasma could be sensitive to the muscle activity-dependent changes in lymph flow rates.
Regulation (sensitive) of sVEGFR1 in plasma
5) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.25 Pain Relevance 0.10
Free sVEGFR1 concentrations, however, changed in opposite directions: lowered with increasing VEGF-VEGFR1 affinity but rose with increasing VEGF-VEGFR2 affinity.
Regulation (changed) of sVEGFR1
6) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Simulation of VEGF-trapping did not recapitulate sVEGFR1's anti-angiogenic potential
Neg (not) Regulation (recapitulate) of sVEGFR1
7) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.16 Pain Relevance 0
1) for both VEGF and sVEGFR1 concentrations (Fig. 8A); increasing kL lessened VEGF gradients but steepened sVEGFR1 gradients (Fig. 9A); while decreasing kCL reduced VEGF gradients without much effect on sVEGFR1 gradients (Fig. 10).
Neg (without) Regulation (effect) of sVEGFR1
8) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
In summary, a 15-h period of daytime activity could elevate plasma concentrations to 42 pM and 1.1 pM above control for free sVEGFR1 and VEGF respectively.
Regulation (control) of sVEGFR1 in plasma
9) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
The effect of kP on free VEGF and sVEGFR1 concentrations (Fig. 8A) could be explained by their associated flow changes (Fig. 8B).
Regulation (effect) of sVEGFR1
10) Confidence 0.37 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Particularly relevant is the latter process of regulation through VEGFR1-VEGFR2 crosstalk, which possibly presents an opportunity for sVEGFR1, as a VEGFR1 competitor, to moderate VEGFR2 activation and internalization.
Spec (possibly) Regulation (regulation) of VEGFR1
11) Confidence 0.26 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
VEGF and sVEGFR1 distribution changes were also more drastic in blood than in interstitia.
Regulation (changes) of sVEGFR1 in blood
12) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Results section 1 covers the initial steps of finding the tissue secretion rates necessary to reproduce a healthy control subject's expected ranges of interstitial and plasma concentrations of VEGF and sVEGFR1 (Tables 9 and 10), with all other parameters (geometry, kinetics, transport and protein expression) set at values summarized for a supine healthy subject (Tables 3 to 8).
Regulation (concentrations) of sVEGFR1 in plasma
13) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0.40 Pain Relevance 0.04
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.
Regulation (concentrations) of sVEGFR1 in plasma
14) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Such characterization proved useful in explaining VEGF/sVEGFR1 system responses observed in subsequent parameter sensitivity analyses of: the secretion rates of VEGF and sVEGFR1 (Results section 2); surface receptor densities (section 3); VEGF-affinities of surface receptors (section 4); VEGF-affinities of interstitial matrix sites (section 5); and transport parameters (section 6).


Regulation (responses) of sVEGFR1 in section 3
15) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0.03
In our stepwise search for the set of secretion rates that could computationally replicate the interstitial and plasma concentrations of VEGF and sVEGFR1 expected from experimental data in our healthy control model, we first established the VEGF concentrations in absence of sVEGFR1, and then introduced sVEGFR1 at modified secretion rates.
Regulation (concentrations) of sVEGFR1 in plasma
16) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
On the other hand, sVEGFR1 concentrations were affected by VEGF-secretion rates in two asymmetrical ways.
Regulation (affected) of sVEGFR1
17) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Whereas these effects culminated into several-fold changes in total VEGF165 and sVEGFR1 in muscle tissues, the fractional occupancy of total matrix sites remained very low (at a consistent 0.19% irrespective of matrix site densities) and changing minutely with varying VEGF165-affinity (up to 0.55% at 10× control Kd(M,V165).

6.

Regulation (changes) of sVEGFR1 in muscle tissues
18) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
Fig. 3A illustrates the VEGF and sVEGFR1 responses to increasing sVEGFR1-secretion rates.
Regulation (responses) of sVEGFR1
19) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
We further showed that NRP1-dependent internalization of sVEGFR1 can be a major regulator of free sVEGFR1 levels in both interstitia and plasma, both directly (e.g., varying NRP1 densities) and indirectly (e.g., R2/R1 ratio and VEGF-VEGFR1 binding alter the availability of uncoupled NRP1s) (Fig. 5A, 6B).
Regulation (regulator) of sVEGFR1 in plasma
20) Confidence 0.22 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0

General Comments

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