INT265774

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Context Info
Confidence 0.12
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 5
Disease Relevance 0
Pain Relevance 0

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

Golgi apparatus (FLT1, GOPC) cytoplasm (FLT1, GOPC) plasma membrane (FLT1, GOPC)
cell differentiation (FLT1) endosome (FLT1) extracellular space (FLT1)
FLT1 (Homo sapiens)
GOPC (Homo sapiens)
Pain Link Frequency Relevance Heat
addiction 15 5.00 Very Low Very Low Very Low
metalloproteinase 15 5.00 Very Low Very Low Very Low
antagonist 15 5.00 Very Low Very Low Very Low
ischemia 10 5.00 Very Low Very Low Very Low
Restless leg syndrome 5 5.00 Very Low Very Low Very Low
Central nervous system 5 5.00 Very Low Very Low Very Low
cytokine 5 5.00 Very Low Very Low Very Low
Inflammation 5 5.00 Very Low Very Low Very Low
tolerance 5 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Peripheral Arterial Disease 90 5.00 Very Low Very Low Very Low
Disease 35 5.00 Very Low Very Low Very Low
Coronary Artery Disease 30 5.00 Very Low Very Low Very Low
Cancer 25 5.00 Very Low Very Low Very Low
Atherosclerosis 20 5.00 Very Low Very Low Very Low
Diabetes Mellitus 20 5.00 Very Low Very Low Very Low
Eclampsia 15 5.00 Very Low Very Low Very Low
Breast Cancer 10 5.00 Very Low Very Low Very Low
Leukemia 10 5.00 Very Low Very Low Very Low
Pressure And Volume Under Development 10 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The directional change in free sVEGFR1 thus followed that of VEGFR2-VEGF165-NRP1 complexes (Fig. 6A) – i.e., the more VEGFR2-VEGF165-NRP1 complexes formed, the less unbound NRP1 available for binding and internalization of free sVEGFR1 (Fig. 6C).

4.2.

VEGFR2-VEGF165-NRP1 Binding (binding) of Fig
1) Confidence 0.12 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
The directional change in free sVEGFR1 thus followed that of VEGFR2-VEGF165-NRP1 complexes (Fig. 6A) – i.e., the more VEGFR2-VEGF165-NRP1 complexes formed, the less unbound NRP1 available for binding and internalization of free sVEGFR1 (Fig. 6C).

4.2.

VEGFR2-VEGF165-NRP1 Binding (binding) of Fig
2) Confidence 0.12 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
At 105 NRP1/EC, almost all (97%) VEGFR1 became part of unligated VEGFR1-NRP1 complexes – a shift that dramatically reduced the availability of VEGFR1 for VEGF165-ligation (Fig. 5B).
VEGFR1 Binding (ligation) of Fig
3) Confidence 0.11 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
At 105 NRP1/EC, almost all (97%) VEGFR1 became part of unligated VEGFR1-NRP1 complexes – a shift that dramatically reduced the availability of VEGFR1 for VEGF165-ligation (Fig. 5B).
VEGFR1 Binding (ligation) of Fig
4) Confidence 0.10 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0
The directional change in free sVEGFR1 thus followed that of VEGFR2-VEGF165-NRP1 complexes (Fig. 6A) – i.e., the more VEGFR2-VEGF165-NRP1 complexes formed, the less unbound NRP1 available for binding and internalization of free sVEGFR1 (Fig. 6C).

4.2.

sVEGFR1 Binding (binding) of Fig
5) Confidence 0.10 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2663039 Disease Relevance 0 Pain Relevance 0

General Comments

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