INT310012

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Context Info
Confidence 0.65
First Reported 2010
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 9
Total Number 17
Disease Relevance 3.57
Pain Relevance 0.19

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 (Met) plasma membrane (Met) kinase activity (Met)
cytoplasm (Met)
Anatomy Link Frequency
liver 4
hepatocytes 1
HGF 1
Met (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 10 90.00 High High
cytokine 14 83.76 Quite High
imagery 20 25.00 Low Low
anesthesia 31 17.84 Low Low
isoflurane 21 16.96 Low Low
ketamine 10 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Infection 470 96.72 Very High Very High Very High
Targeted Disruption 104 93.44 High High
Acquired Immune Deficiency Syndrome Or Hiv Infection 10 86.48 High High
Sarcoma 10 85.36 High High
Disease 40 83.16 Quite High
Adhesions 50 81.68 Quite High
Apoptosis 17 78.40 Quite High
Bacterial Respiratory Disease 10 75.60 Quite High
Sprains And Strains 237 61.04 Quite High
Enteritis 10 55.96 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Nonetheless, a subset of immediate-early genes implicated in the control of cell cycle progression, such as c-Fos and Egr1, exhibited an impaired activation in c-Met mutant livers, particularly at the later time points of liver regeneration (Figure S3).
Positive_regulation (activation) of c-Met mutant in livers
1) Confidence 0.65 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0 Pain Relevance 0.04
In addition, we observed only minimal if any changes in phosphorylation of Akt, another important downstream mediator of c-Met pathway.
Positive_regulation (mediator) of c-Met
2) Confidence 0.47 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.12 Pain Relevance 0
Recent work by Borowiak and colleagues has shown that conditional inactivation of c-met using a ubiquitously expressed alpha/beta interferon-inducible promoter resulted in suppressed Erk1/2 activation and defective exit from quiescence in regenerating mouse liver [7].
Positive_regulation (inactivation) of c-met in liver
3) Confidence 0.47 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.28 Pain Relevance 0
hepatocytes express a kinase-inactive c-Met receptor which is irresponsive to HGF stimulation [8], these data indicate that c-Met signaling in hepatocytes is dispensable for initiation but required for sustaining a long-term Erk1/2 phosphorylation during liver regeneration.
Positive_regulation (required) of c-Met in hepatocytes
4) Confidence 0.47 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.15 Pain Relevance 0
To determine more precisely when c-Met activity is required for transition into mitosis, we examined histone H3 phosphorylation as a differential marker for G2 and M phase cells.
Positive_regulation (required) of c-Met
5) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.05 Pain Relevance 0
However, a complete absence of EGFR in the liver was insufficient to suppress c-Met and Erk1/2 activation [23] consistent with c-Met being a major determinant of mitogen-activated protein kinase cascades in regenerating liver [7].
Positive_regulation (activation) of c-Met in liver
6) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.15 Pain Relevance 0
However, a complete absence of EGFR in the liver was insufficient to suppress c-Met and Erk1/2 activation [23] consistent with c-Met being a major determinant of mitogen-activated protein kinase cascades in regenerating liver [7].
Positive_regulation (activation) of c-Met in liver
7) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.16 Pain Relevance 0
Since c-Met is not readily available in the apical surface, we wondered whether InlB acts as a soluble factor or whether c-Met is activated locally at the MCJs after bacterial attachment.
Spec (whether) Positive_regulation (activated) of c-Met
8) Confidence 0.19 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.05 Pain Relevance 0.04
We show that while InlB is dispensable for attachment, it synergistically promotes invasion of MCJs through activation of c-Met kinase signaling.
Positive_regulation (activation) of c-Met
9) Confidence 0.19 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.25 Pain Relevance 0
Finally, we considered that InlB might promote Lm invasion by increasing endocytosis of junctional E-cadherin through c-Met activation as shown for HGF action on nonpolarized cells [46], [47].
Positive_regulation (activation) of c-Met in HGF
10) Confidence 0.19 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.44 Pain Relevance 0
Thus, c-Met activation is required for InlB activity during apical invasion of the MCJs.
Positive_regulation (activation) of c-Met
11) Confidence 0.19 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.11 Pain Relevance 0.04
Since activation of c-Met results in the co-endocytosis of both receptors, InlB has evolved to provide a local increase in junctional remodeling that allows for enhanced dynamin-dependent Lm internalization (Figure 6B).


Positive_regulation (activation) of c-Met
12) Confidence 0.19 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.17 Pain Relevance 0
Since InlB increases the rate of Lm internalization through activation of c-Met at MCJs, we also wondered whether MCJs are intrinsically different in their endocytic activity as compared to the rest of the apical surface.
Positive_regulation (activation) of c-Met
13) Confidence 0.14 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.51 Pain Relevance 0
To further address whether c-Met activation is restricted to the immediate surrounding of individual bacteria, we tested whether the c-Met kinase inhibitor used in a mixed infection would reduce both WT and ?
Spec (whether) Positive_regulation (activation) of c-Met associated with infection
14) Confidence 0.14 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.60 Pain Relevance 0.03
On the other hand, Lm invade cells through tight membrane invaginations without apparent changes of cell surfaces where bacteria are absent, suggesting that InlB associated with the bacterial surface mediates c-Met activation within close proximity to each individual bacterium [14], [63], [69].
Positive_regulation (activation) of c-Met
15) Confidence 0.14 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.27 Pain Relevance 0.04
Furthermore, c-Met activation at cell extrusion sites induces uptake of E-cadherin, accelerating invasion of Lm.
Positive_regulation (activation) of c-Met
16) Confidence 0.13 Published 2010 Journal PLoS Pathogens Section Abstract Doc Link PMC2869327 Disease Relevance 0.13 Pain Relevance 0
Here, we find that basolateral c-Met, a receptor tyrosine kinase used by Lm for invasion of cells in tissue culture, is also activated as a consequence of its exposure on the apical side at cell extrusion sites.
Positive_regulation (activated) of c-Met
17) Confidence 0.13 Published 2010 Journal PLoS Pathogens Section Abstract Doc Link PMC2869327 Disease Relevance 0.15 Pain Relevance 0

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