INT102721

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Context Info
Confidence 0.53
First Reported 2002
Last Reported 2007
Negated 0
Speculated 3
Reported most in Body
Documents 2
Total Number 30
Disease Relevance 8.03
Pain Relevance 0.30

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

cytosol (MAP3K1) cytoskeleton (MAP3K1) cytoplasm (MAP3K1)
Anatomy Link Frequency
plasma 1
colon 1
MAP3K1 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 1 97.88 Very High Very High Very High
cytokine 29 83.92 Quite High
Inflammation 29 83.52 Quite High
Pain 29 52.04 Quite High
Immobilon 29 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 467 99.92 Very High Very High Very High
Stress 290 99.44 Very High Very High Very High
Colon Cancer 2 99.08 Very High Very High Very High
Cancer 204 98.24 Very High Very High Very High
INFLAMMATION 30 97.16 Very High Very High Very High
Shock 174 89.12 High High
Polyps 1 84.08 Quite High
Familial Adenomatous Polyposis 1 83.12 Quite High
Death 30 73.80 Quite High
Pain 29 52.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We observed inhibition of MEKK1 by other ITCs that have been implicated in cancer chemoprevention, including sulforaphane, at similar concentrations (not shown).


Negative_regulation (inhibition) of MEKK1 associated with cancer
1) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.25 Pain Relevance 0
As observed in experiments with intact cells, wild type MEKK1 was inhibited by PEITC treatment in a dose dependent manner, while the C1238V mutant was completely resistant to PEITC treatment (Figure 2B).
Negative_regulation (inhibited) of MEKK1
2) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.13 Pain Relevance 0
Thus, inhibition of MEKK1 by PEITC requires the cysteine residue at position 1238.
Negative_regulation (inhibition) of MEKK1
3) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.24 Pain Relevance 0
Inhibition of endogenous MEKK1 activity in intact LnCAP cells requires a relatively high concentration of PEITC compared to the dietary plasma levels in humans following a single oral dose of ITCs (measured at about 2 ?
Negative_regulation (Inhibition) of MEKK1 in plasma
4) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.45 Pain Relevance 0
Bio-ITC covalently labeled MEKK1, since dose dependent inhibition of MEKK1 (Figure 5B, top) resulted in wild type MEKK1 that was labeled with biotin, as demonstrated by detection with a streptavidin-enzyme conjugate (Figure 5B, middle).
Negative_regulation (inhibition) of MEKK1
5) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0 Pain Relevance 0
Inhibition of MEKK1 activity within 30 minutes of PEITC addition indicates that inhibition is a specific and acute effect that is not due to protein loss that might accompany measurements taken at later time points after apoptosis had commenced.
Negative_regulation (Inhibition) of MEKK1 associated with apoptosis
6) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.49 Pain Relevance 0
Thus PEITC inhibition of MEKK1 requires both access to the ATP-binding pocket of MEKK1 and the cysteine at position 1238.


Negative_regulation (inhibition) of MEKK1
7) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0 Pain Relevance 0
In contrast, ASK1 was not inhibited by PEITC treatment, even at the highest concentrations (Figure 1, right panel), demonstrating a specific mechanism of inhibition of MEKK1 by PEITC.
Negative_regulation (inhibition) of MEKK1
8) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.24 Pain Relevance 0
Inhibition of MEKK1 by PEITC is direct and requires cysteine 1238
Negative_regulation (Inhibition) of MEKK1
9) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.31 Pain Relevance 0
Specific inhibition of MEKK1, but not ASK1, by PEITC is compatible with the pro-apoptotic function of PEITC that might be enabled by this differential effect on protein kinase pathways.
Negative_regulation (inhibition) of MEKK1 associated with apoptosis
10) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.40 Pain Relevance 0
We describe here results that indicate that nutritional isothiocyanates are able to covalently and irreversibly inhibit MEKK1.
Negative_regulation (inhibit) of MEKK1
11) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.41 Pain Relevance 0
To determine whether inhibition of MEKK1 is due to direct modification of MEKK1 and not an effect on another member of the signaling pathway, we examined the sensitivity of purified MEKK1 to PEITC treatment in vitro.
Spec (whether) Negative_regulation (inhibition) of MEKK1
12) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.23 Pain Relevance 0
In vitro inhibition of MEKK1 by PEITC also supports a direct effect on catalytic activity, rather than a more complicated mechanism of regulation involving protein degradation or other regulators of MEKK1 function.
Negative_regulation (inhibition) of MEKK1
13) Confidence 0.53 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.37 Pain Relevance 0
Our data show that both endogenous and plasmid-expressed wild type MEKK1 are dose-dependently inhibited by ITCs, through stable, direct covalent modification in a manner requiring C1238.
Negative_regulation (inhibited) of MEKK1
14) Confidence 0.39 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.41 Pain Relevance 0
In an effort to identify cysteine reactive compounds that might likewise inhibit MEKK1 by targeting this residue, we considered physiologic agents that could result in protein modification on cysteine.
Spec (might) Negative_regulation (inhibit) of MEKK1
15) Confidence 0.39 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.60 Pain Relevance 0.06
In addition, ITCs inhibited the catalytic activity of endogenous MEKK1.
Negative_regulation (inhibited) of MEKK1
16) Confidence 0.39 Published 2007 Journal BMC Cancer Section Abstract Doc Link PMC2071920 Disease Relevance 0.06 Pain Relevance 0
Inhibition of MEKK1 catalytic activity was due to direct, covalent and irreversible modification of the MEKK1 protein itself.
Negative_regulation (Inhibition) of MEKK1
17) Confidence 0.39 Published 2007 Journal BMC Cancer Section Abstract Doc Link PMC2071920 Disease Relevance 0.06 Pain Relevance 0
However, we predict that all cellular targets of ITCs will parallel the mechanism of MEKK1 inactivation, i.e. through stable covalent modification resulting in altered protein function.


Negative_regulation (inactivation) of MEKK1
18) Confidence 0.39 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.20 Pain Relevance 0.05
It remains unproven whether modification and inhibition of MEKK1 plays a singular role in the effects of ITCs in apoptosis or cancer chemoprevention.
Spec (whether) Negative_regulation (inhibition) of MEKK1 associated with cancer and apoptosis
19) Confidence 0.39 Published 2007 Journal BMC Cancer Section Body Doc Link PMC2071920 Disease Relevance 0.32 Pain Relevance 0
This correlated with inhibition of the downstream target of MEKK1 activity, i.e. the SAPK/JNK kinase.
Negative_regulation (inhibition) of MEKK1
20) Confidence 0.39 Published 2007 Journal BMC Cancer Section Abstract Doc Link PMC2071920 Disease Relevance 0.05 Pain Relevance 0

General Comments

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