INT106760

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Context Info
Confidence 0.59
First Reported 2002
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 16
Total Number 18
Disease Relevance 8.50
Pain Relevance 3.35

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

nucleoplasm (Dusp1) nucleus (Dusp1) cell cycle (Dusp1)
Anatomy Link Frequency
brain 2
trigeminal ganglia 1
myocardium 1
urinary bladder 1
osteoblast 1
Dusp1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Inflammatory response 27 98.84 Very High Very High Very High
central sensitization 42 94.56 High High
cytokine 110 93.64 High High
Inflammation 311 90.88 High High
adenocard 6 88.56 High High
Snapping jaw 48 86.20 High High
potassium channel 6 82.96 Quite High
isoflurane 19 80.40 Quite High
fifth nerve 3 79.12 Quite High
Lasting pain 12 76.16 Quite High
Disease Link Frequency Relevance Heat
Hypoxia 290 99.98 Very High Very High Very High
Hyperplasia 9 99.76 Very High Very High Very High
Renal Disease 6 99.72 Very High Very High Very High
Osteoporosis 27 99.44 Very High Very High Very High
Infection 54 99.20 Very High Very High Very High
INFLAMMATION 363 98.84 Very High Very High Very High
Stress 29 97.16 Very High Very High Very High
Sepsis 6 96.96 Very High Very High Very High
Apoptosis 136 96.92 Very High Very High Very High
Urological Neuroanatomy 24 95.80 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Intriguingly, the expression level of MKP1 was significantly increased in both S and P groups, while it was higher in S group than that in P group.
Positive_regulation (increased) of MKP1
1) Confidence 0.59 Published 2010 Journal Cardiovasc Ther Section Abstract Doc Link 20074256 Disease Relevance 0.13 Pain Relevance 0.07
The activation of DUSP1 seems to counterbalance the inflammatory response to PAR (protease-activated receptors) activation by avoiding prolonged activation of p38 MAPK and increased cytokine production in the rat urinary bladder, which was revealed using IPA [35].
Positive_regulation (activation) of DUSP1 in urinary bladder associated with inflammatory response and cytokine
2) Confidence 0.53 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2688838 Disease Relevance 0.61 Pain Relevance 0.27
Importantly, DUSP1 increases migration of smooth muscle cells to soluble collagen protein(s) through chemotaxis [37], and hence is also involved in the remodeling process.
Positive_regulation (increases) of DUSP1 in smooth muscle cells
3) Confidence 0.38 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2688838 Disease Relevance 0.74 Pain Relevance 0.22
DUSP1 (dual specificity phosphatase 1, synonym: MKP-1) is highly up-regulated at day 3 and day 25 (Table 1).
Positive_regulation (up-regulated) of DUSP1
4) Confidence 0.36 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2688838 Disease Relevance 0.64 Pain Relevance 0.27
Similarly, Bernaudin et al. [43] found increased expression of 18 genes in the neonatal rat brain following hypoxia (8% O2 for 3 h) including several known hypoxia inducible genes such as MAP kinase phosphatase-1 (MKP-1), several HIF-1 target genes including VEGF and GLUT-1, genes implicated in apoptosis, signal transduction molecules, and transcription factors.
Positive_regulation (inducible) of MKP-1 in brain associated with hypoxia and apoptosis
5) Confidence 0.31 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2635851 Disease Relevance 0.98 Pain Relevance 0.22
Similarly, Bernaudin et al. [43] found increased expression of 18 genes in the neonatal rat brain following hypoxia (8% O2 for 3 h) including several known hypoxia inducible genes such as MAP kinase phosphatase-1 (MKP-1), several HIF-1 target genes including VEGF and GLUT-1, genes implicated in apoptosis, signal transduction molecules, and transcription factors.
Positive_regulation (inducible) of MAP kinase phosphatase-1 in brain associated with hypoxia and apoptosis
6) Confidence 0.31 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2635851 Disease Relevance 0.98 Pain Relevance 0.22
Animals treated with GSE had a significant increase in the staining intensity for MKP-1 (1.65 ± 0.12, P < 0.01) when compared to control animals (1.00 ± 0.09) (Figure 1C).
Positive_regulation (increase) of MKP-1
7) Confidence 0.25 Published 2010 Journal Mol Pain Section Body Doc Link PMC3009976 Disease Relevance 0.07 Pain Relevance 0.03
We further confirmed mitogen-activated protein kinase phosphatase-1 (MKP-1) was activated but phospho-p38 was inhibited by curcumin by western blot assay.
Positive_regulation (activated) of MKP-1
8) Confidence 0.25 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2945766 Disease Relevance 0.76 Pain Relevance 0.10
We further confirmed mitogen-activated protein kinase phosphatase-1 (MKP-1) was activated but phospho-p38 was inhibited by curcumin by western blot assay.
Positive_regulation (activated) of mitogen-activated protein kinase phosphatase-1
9) Confidence 0.25 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2945766 Disease Relevance 0.78 Pain Relevance 0.10
Thus we proved that curcumin might inhibit the phosphorylation of p38 by activating MKP-1, and eventually reduced the inflammatory response.
Positive_regulation (activating) of MKP-1 associated with inflammatory response
10) Confidence 0.25 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2945766 Disease Relevance 0.33 Pain Relevance 0.32
Interestingly, MKP-1 was induced concurrently with the inactivation of JNK and p38, whereas blocking MKP-1 induction by triptolide prevented this inactivation.
Positive_regulation (induction) of MKP-1
11) Confidence 0.21 Published 2002 Journal J. Immunol. Section Abstract Doc Link 12444149 Disease Relevance 0.13 Pain Relevance 0.15
Interestingly, MKP-1 was induced concurrently with the inactivation of JNK and p38, whereas blocking MKP-1 induction by triptolide prevented this inactivation.
Positive_regulation (induced) of MKP-1
12) Confidence 0.21 Published 2002 Journal J. Immunol. Section Abstract Doc Link 12444149 Disease Relevance 0.12 Pain Relevance 0.12
We propose that the basal increase in MKP-1 mediated by dietary GSE is responsible, at least in part, for the repressed expression of P-p38 in trigeminal ganglia and TNC neurons and glia in response to CFA since MKP-1 is a primary regulator of p38 activity [33].
Positive_regulation (increase) of MKP-1 in trigeminal ganglia
13) Confidence 0.17 Published 2010 Journal Mol Pain Section Body Doc Link PMC3009976 Disease Relevance 0.57 Pain Relevance 0.47
To our knowledge, this is the first study to provide evidence that GSE can lead to sustained, elevated levels of MKP-1, an enzyme that plays a fundamental role in regulating the activity of MAP kinases and thus, controlling development of peripheral and central sensitization.
Positive_regulation (elevated) of MKP-1 associated with central sensitization
14) Confidence 0.17 Published 2010 Journal Mol Pain Section Body Doc Link PMC3009976 Disease Relevance 0.27 Pain Relevance 0.28
Induction of MKP-1 by LPS was found to be extracellular signal-regulated kinase dependent and involved enhanced gene expression and increased protein stability.
Positive_regulation (Induction) of MKP-1
15) Confidence 0.15 Published 2002 Journal J. Immunol. Section Abstract Doc Link 12444149 Disease Relevance 0.16 Pain Relevance 0.21
ERK, a target protein of MKP-1, was not activated by ischemic postconditioning in the aged myocardium, but was restored in aged hearts treated by a MKP-1 inhibitor [38].
Positive_regulation (activated) of MKP-1 in hearts
16) Confidence 0.11 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2872846 Disease Relevance 0.07 Pain Relevance 0.12
Furthermore, levels of the phosphatase MKP-1 were increased in the aged myocardium, and inhibition of MKP-1 resulted in the restoration of cardioprotection by ischemic postconditioning [23].
Positive_regulation (increased) of MKP-1 in myocardium
17) Confidence 0.11 Published 2010 Journal Korean Journal of Anesthesiology Section Body Doc Link PMC2872846 Disease Relevance 0.08 Pain Relevance 0.18
We find that GCs mediate their inhibitory effects on osteoblast proliferation in vitro via up-regulation of the vanadate-sensitive dual-specificity phosphatase, MKP-1, which profoundly represses the ERK mitogenic signalling pathway (Engelbrecht et al. 2003).
Positive_regulation (up-regulation) of MKP-1 in osteoblast associated with osteoporosis
18) Confidence 0.08 Published 2007 Journal The Journal of Endocrinology Section Body Doc Link PMC2173947 Disease Relevance 1.08 Pain Relevance 0

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