INT63506

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Context Info
Confidence 0.77
First Reported 1996
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 21
Total Number 25
Disease Relevance 7.53
Pain Relevance 3.41

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 (F2) extracellular space (F2) extracellular region (F2)
Anatomy Link Frequency
platelets 3
synapse 2
bar 1
stroma 1
plasma 1
F2 (Mus musculus)
Pain Link Frequency Relevance Heat
Nerve growth factor 74 99.70 Very High Very High Very High
agonist 85 97.92 Very High Very High Very High
Inflammation 129 95.80 Very High Very High Very High
tetrodotoxin 17 95.32 Very High Very High Very High
Neuropeptide 61 95.08 Very High Very High Very High
Calcitonin gene-related peptide 102 94.20 High High
Central nervous system 2 93.44 High High
cytokine 18 90.44 High High
substance P 26 86.88 High High
Analgesic 10 86.60 High High
Disease Link Frequency Relevance Heat
Injury 77 99.98 Very High Very High Very High
Thrombosis 235 99.68 Very High Very High Very High
Coagulation Disorder 37 99.60 Very High Very High Very High
Rupture 13 99.56 Very High Very High Very High
Increased Venous Pressure Under Development 66 99.48 Very High Very High Very High
Nociception 108 99.44 Very High Very High Very High
Stress 25 99.36 Very High Very High Very High
Death 15 98.78 Very High Very High Very High
Stab Wounds 15 97.04 Very High Very High Very High
INFLAMMATION 131 95.80 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
The application of ACh to electrically blocked muscle cultures resulted in a 2.5-fold increase in thrombin activity released into the medium and a 2-fold increase in prothrombin gene expression.
Localization (released) of thrombin in muscle
1) Confidence 0.77 Published 1997 Journal Brain Res. Dev. Brain Res. Section Abstract Doc Link 9125468 Disease Relevance 0 Pain Relevance 0.38
Electrical blockade resulted in a decrease in thrombin release to about two-thirds of control values.
Localization (release) of thrombin
2) Confidence 0.77 Published 1997 Journal Brain Res. Dev. Brain Res. Section Abstract Doc Link 9125468 Disease Relevance 0 Pain Relevance 0.37
These results suggest that thrombin or a thrombin-like molecule released from muscle is required for activity-dependent synapse elimination and is regulated by neuromuscular activity.
Localization (released) of thrombin in synapse
3) Confidence 0.67 Published 1997 Journal Brain Res. Dev. Brain Res. Section Abstract Doc Link 9125468 Disease Relevance 0 Pain Relevance 0.33
These results suggest that thrombin or a thrombin-like molecule released from muscle is required for activity-dependent synapse elimination and is regulated by neuromuscular activity.
Localization (released) of thrombin in synapse
4) Confidence 0.67 Published 1997 Journal Brain Res. Dev. Brain Res. Section Abstract Doc Link 9125468 Disease Relevance 0 Pain Relevance 0.33
During injury thrombin is released and cleaves the protease-activated receptors (PARs), which subsequently induce plasma extravasation and inflammation.
Localization (released) of thrombin in plasma associated with inflammation and injury
5) Confidence 0.31 Published 2006 Journal J Neuroinflammation Section Body Doc Link PMC1533808 Disease Relevance 0.82 Pain Relevance 0.09
Interrogation of other factors along the coagulation cascade that are triggered by Factor VIII, such as Factor Xa and thrombin, suggests that thrombin, which is the terminal enzyme of the hemostatic system, is likely to be the actual mediator of this novel checkpoint of organ size control.
Localization (triggered) of thrombin
6) Confidence 0.29 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2791444 Disease Relevance 0.08 Pain Relevance 0
Furthermore, our ability to reverse the enhancement of implant size by treatment with the cleaved form of OPN that is released upon treatment with thrombin, strongly indicates that thrombin likely exerts its regulatory activity through interaction with OPN on stroma cells, as previously shown for maintenance of the blood tissue size under normal steady state hoemostasis[9], [10].


Localization (released) of thrombin in stroma
7) Confidence 0.29 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2791444 Disease Relevance 0.19 Pain Relevance 0
Thrombin is released by blood clotting following blood vessel damage or tissue injury, and can act on PAR1, 3 and 4 expressed in primary sensory nerve terminals present in the vicinity.
Localization (released) of Thrombin in blood vessel associated with coagulation disorder and injury
8) Confidence 0.25 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0.55 Pain Relevance 0.19
We next examined the histological characteristics of thrombin-responsive neurons, using translocation of PKC?
Localization (translocation) of thrombin in neurons
9) Confidence 0.23 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0.06 Pain Relevance 0.09
In the absence of neurotrophins few thrombin-responsive neurons bind IB4 (first bar in Fig. 8A).
Neg (absence) Localization (absence) of thrombin in bar
10) Confidence 0.23 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0 Pain Relevance 0.30
NGF increased the proportion of thrombin-responsive neurons but IB4 binding was not significantly increased.
Localization (proportion) of thrombin in IB4 associated with nerve growth factor
11) Confidence 0.23 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 0 Pain Relevance 0.29
The crystal structure of the active complex revealed binding of the D1 and D2 domains to prothrombin and insertion of the Ile1-Val2 N-terminus of Coa into the Ile16 pocket of prothrombin, inducing a functional active site in the zymogen through conformational change [20].
Localization (insertion) of prothrombin
12) Confidence 0.23 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2916881 Disease Relevance 0.36 Pain Relevance 0
Prevention of activity-dependent neuronal death: vasoactive intestinal polypeptide stimulates astrocytes to secrete the thrombin-inhibiting neurotrophic serpin, protease nexin I.
Localization (secrete) of thrombin in astrocytes associated with death
13) Confidence 0.23 Published 1996 Journal J. Neurobiol. Section Title Doc Link 8738754 Disease Relevance 0.95 Pain Relevance 0.11
Following injury and rupture of blood vessels the release of significant amounts of thrombin could act on nociceptive nerve terminals, sensitizing TRPV1 to heat stimuli and promoting the release of pro-inflammatory neuropeptides such as CGRP, as has been shown in this study.
Localization (release) of thrombin in nerve associated with nociception, inflammation, rupture, injury, neuropeptide and calcitonin gene-related peptide
14) Confidence 0.22 Published 2010 Journal Mol Pain Section Body Doc Link PMC2956715 Disease Relevance 1.06 Pain Relevance 0.76
We sought to determine where activated factor X (FXa), (pro)thrombin, and fibrin(ogen) are localized in thrombi formed under venous shear.


Localization (localized) of thrombin
15) Confidence 0.16 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2861630 Disease Relevance 0.06 Pain Relevance 0
Our in vitro work points to a role for fibrin(ogen) in supporting thrombin localization during thrombus formation.
Localization (localization) of thrombin associated with thrombosis
16) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.48 Pain Relevance 0
Collectively, these results reveal the distinct distribution of FXa, prothrombin, and thrombin on thrombi formed under shear, and confirm the important role of exposed PS for fibrin formation under flow.


Localization (distribution) of thrombin
17) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.25 Pain Relevance 0
Importantly, our in vivo data demonstrate that fibrin(ogen) and (pro)thrombin incorporated into large structures and were distributed throughout the thrombi.
Localization (incorporated) of thrombin
18) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.32 Pain Relevance 0
In isolated plasma under static conditions, phosphatidylserine (PS)-exposing platelets support coagulation factor activation and thrombin generation; however, their role in supporting coagulation factor binding under shear conditions remains unclear.
Localization (generation) of thrombin in platelets
19) Confidence 0.16 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2861630 Disease Relevance 0 Pain Relevance 0
Therefore, our findings of thrombin distribution on platelet-fibrin clots, suggest that fibrin may play an important role in localizing thrombin to clots.
Localization (localizing) of thrombin in platelet
20) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2861630 Disease Relevance 0.21 Pain Relevance 0

General Comments

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