INT193847

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Context Info
Confidence 0.65
First Reported 2006
Last Reported 2010
Negated 4
Speculated 0
Reported most in Body
Documents 22
Total Number 22
Disease Relevance 6.60
Pain Relevance 0.24

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 4
brain 1
M cell 1
epithelial cells 1
Met (Mus musculus)
Pain Link Frequency Relevance Heat
cytokine 48 66.20 Quite High
anesthesia 49 61.48 Quite High
isoflurane 41 60.60 Quite High
Potency 1 57.76 Quite High
agonist 2 52.88 Quite High
imagery 34 50.00 Quite Low
ketamine 8 5.00 Very Low Very Low Very Low
Thoracotomy 3 5.00 Very Low Very Low Very Low
halothane 3 5.00 Very Low Very Low Very Low
cINOD 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Cancer 313 99.80 Very High Very High Very High
Stress 16 99.78 Very High Very High Very High
Glioblastoma 198 98.52 Very High Very High Very High
Targeted Disruption 180 98.32 Very High Very High Very High
Pancreatic Cancer 20 94.80 High High
Hyperplasia 26 93.56 High High
Thrombosis 4 90.80 High High
Immunotherapy Of Cancer 1 87.12 High High
Necrosis 36 86.48 High High
Urological Neuroanatomy 1 84.56 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
-secretase, BACE1; PAMP and PARL, two novel putative metalloproteases; Omi/HtrA2, a serine protease involved in the mammalian cellular stress response; Met1, a novel putative methyltransferase; mitochondrial immunophilin FKBP38; a splice variant of glial fibrillary acidic protein, etc.
Gene_expression (methyltransferase) of Met1 associated with stress
1) Confidence 0.65 Published 2006 Journal Mol Neurodegener Section Body Doc Link PMC1513131 Disease Relevance 0.48 Pain Relevance 0
The critical role of c-Met in activation of the downstream mediator Erk1/2 during liver regeneration has been established using a liver-specific c-Met conditional knockout mouse model [7].
Gene_expression (established) of c-Met in liver associated with targeted disruption
2) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.19 Pain Relevance 0
Deletion of c-Met in hepatocytes did not affect the early phosphorylation of Erk1/2 at 6–12 hr following PH but it completely abolished the second peak between 36–48 hr coincidently with a defective progression through G2 phase of cell cycle (Figure 4A).
Gene_expression (Deletion) of c-Met in hepatocytes
3) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.18 Pain Relevance 0
Only genes with more than 1.5-fold expression differences between control and c-Met mutant mice in at least 80% of samples were included in the list of significant genes.
Gene_expression (expression) of c-Met mutant
4) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0 Pain Relevance 0
Accordingly, microarray profiling of c-Met deficient regenerating livers revealed downregulation of genes known to control chromosome congression, alignment and segregation (Esco2, CENPs, SMC2, Nuf1, etc.) along with others implicated in spindle organization and biogenesis (Ect2, ASPM, Nusap1, and Stmn1, 3 and 4).
Gene_expression (deficient) of c-Met in livers
5) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0 Pain Relevance 0
This was consistent with the observation that the number of S phase cells was reduced in c-Met mutant livers after 36 hr of liver regeneration as cells failed to transit into next S phase providing further support that c-Met deletion has a broad impact on cell cycle progression (Figure 1).
Gene_expression (deletion) of c-Met in livers
6) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0 Pain Relevance 0
We report that absence of c-Met signaling in hepatocytes results in G2/M cell cycle arrest along with the lack of Erk1/2 activation and downregulation of broad G2/M regulatory networks.
Neg (absence) Gene_expression (absence) of c-Met in M cell
7) Confidence 0.63 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.06 Pain Relevance 0
As expected, c-Met protein was not detectable in whole cell lysates prepared from the mutant livers at any time point during liver regeneration (Figure 4A).
Neg (not) Gene_expression (detectable) of c-Met in liver
8) Confidence 0.57 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.19 Pain Relevance 0
Expression of c-Met was not detectable in Metfl/fl;Alb-Cre+/?
Neg (not) Gene_expression (detectable) of c-Met
9) Confidence 0.57 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.15 Pain Relevance 0
The lack of c-Met expression in hepatocytes was confirmed by PCR analysis and immunohistochemistry (Figure S1A and B).
Gene_expression (expression) of c-Met in hepatocytes
10) Confidence 0.57 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.24 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.
Gene_expression (express) of c-Met in hepatocytes
11) Confidence 0.57 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.16 Pain Relevance 0
Expression of c-Met was not detectable in Metfl/fl;Alb-Cre+/?
Gene_expression (Expression) of c-Met
12) Confidence 0.57 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.15 Pain Relevance 0
By employing a model deficient for c-met exclusively in hepatocytes, we found that c-met ablation affected neither early hepatic Erk1/2 activation nor induction of the initial round of DNA replication.
Gene_expression (ablation) of c-met in hepatocytes
13) Confidence 0.55 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0 Pain Relevance 0
To evaluate the effect of c-met deletion on cell cycle progression, we used 5-bromo-2?
Gene_expression (deletion) of c-met
14) Confidence 0.55 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2940888 Disease Relevance 0.38 Pain Relevance 0.15
Although c-Met is not exposed on the apical surface of epithelia, we hypothesized that InlB could activate c-Met because of the local loss of cell polarity that occurs at MCJs.
Neg (not) Gene_expression (exposed) of c-Met
15) Confidence 0.18 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0 Pain Relevance 0
To test the role of c-Met on apical invasion of polarized epithelial cells, we pretreated the confluent polarized monolayers with SU11274 to inhibit c-Met signaling or DMSO as a control, then infected them with WT or ?
Gene_expression (signaling) of c-Met in epithelial cells
16) Confidence 0.18 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2869327 Disease Relevance 0.24 Pain Relevance 0.03
As an explanation for their highly invasive nature, we show that DBM2 tumors not only express both c-Met and uPAR, the receptor of urokinase signaling pathway, but also strongly respond to HGF (data not shown) indicating that the c-Met signaling pathway may play an important role in the invasion of DBM2 orthotopic tumors into the brain parenchyma [24,27,40,44].
Gene_expression (express) of c-Met in HGF associated with cancer
17) Confidence 0.14 Published 2008 Journal J Transl Med Section Body Doc Link PMC2645376 Disease Relevance 1.83 Pain Relevance 0
Aberrant expression of receptor tyrosine kinases such as EGFR and c-Met, and loss of the ERK phosphatase DUSP6 occur during cancer progression and activate the ERK pathway [3].
Gene_expression (expression) of c-Met associated with cancer
18) Confidence 0.11 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2955043 Disease Relevance 0.54 Pain Relevance 0.03
Analysis of tissue sections from DBM2 tumors for human c-MET and uPAR expression pinpointed the location of invasive glioblastoma cells in the brain parenchyma and at the same time examined an important mechanism for cellular invasion (Figure 3B). c-MET oncoprotein signaling promotes the activation of urokinase and its receptor (uPAR) [27] and both are associated with GBM invasion in patient tumors [24,27-29].
Gene_expression (expression) of c-MET in brain associated with glioblastoma and cancer
19) Confidence 0.09 Published 2008 Journal J Transl Med Section Body Doc Link PMC2645376 Disease Relevance 1.64 Pain Relevance 0.03
After the third cellular division, expression of c-met, Scn-1b, ?
Gene_expression (expression) of c-met
20) Confidence 0.08 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2262151 Disease Relevance 0.06 Pain Relevance 0

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