INT86729

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Context Info
Confidence 0.07
First Reported 2000
Last Reported 2010
Negated 1
Speculated 2
Reported most in Body
Documents 37
Total Number 39
Disease Relevance 18.74
Pain Relevance 10.76

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

extracellular region (CDCP1) plasma membrane (CDCP1)
Anatomy Link Frequency
plasma 2
chondrocytes 1
tail 1
MTP 1
platelets 1
CDCP1 (Homo sapiens)
Pain Link Frequency Relevance Heat
Inflammation 112 100.00 Very High Very High Very High
Kinase C 84 100.00 Very High Very High Very High
cINOD 87 99.98 Very High Very High Very High
rheumatoid arthritis 11 99.80 Very High Very High Very High
Dorsal horn neuron 1 99.04 Very High Very High Very High
Osteoarthritis 75 98.80 Very High Very High Very High
antagonist 22 98.66 Very High Very High Very High
opioid receptor 8 98.12 Very High Very High Very High
tetrodotoxin 7 97.84 Very High Very High Very High
Pain 27 97.36 Very High Very High Very High
Disease Link Frequency Relevance Heat
INFLAMMATION 135 100.00 Very High Very High Very High
Neurodegenerative Disease 10 100.00 Very High Very High Very High
Rheumatoid Arthritis 149 99.80 Very High Very High Very High
Colon Cancer 33 99.72 Very High Very High Very High
Stress 42 99.66 Very High Very High Very High
Apoptosis 409 99.34 Very High Very High Very High
Osteoarthritis 80 98.80 Very High Very High Very High
Cancer 282 98.28 Very High Very High Very High
Injury 23 98.28 Very High Very High Very High
Nociception 2 98.12 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
A 25 microM H(2)O(2), unable to stimulate by itself the MAP kinases, promote an almost complete activation of MAP kinases in the presence of NSAIDs.
Positive_regulation (activation) of kinases associated with cinod
1) Confidence 0.07 Published 2002 Journal Biochem. Pharmacol. Section Abstract Doc Link 11841790 Disease Relevance 0.46 Pain Relevance 0.93
We report that in human colorectal carcinoma cells NSAIDs stimulated the three families of MAPK, extracellular regulated kinases, c-Jun N-terminal kinases, p38 MAPK and that this stimulation is prevented by N-acetyl cysteine.
Positive_regulation (stimulated) of kinases associated with colon cancer and cinod
2) Confidence 0.07 Published 2002 Journal Biochem. Pharmacol. Section Abstract Doc Link 11841790 Disease Relevance 0.37 Pain Relevance 0.66
The mobility on SDS-PAGE of the apoptosis signal-regulating kinase, which activates C-Jun N-terminal kinases and p38 MAPK cascades, was reduced by H(2)O(2) and NSAIDs, suggesting, that H(2)O(2) and NSAIDs activated apoptosis signal-regulating kinase by increasing its state of phosphorylation.
Positive_regulation (activates) of kinases associated with cinod and apoptosis
3) Confidence 0.07 Published 2002 Journal Biochem. Pharmacol. Section Abstract Doc Link 11841790 Disease Relevance 0.46 Pain Relevance 1.02
A 25 microM H(2)O(2), unable to stimulate by itself the MAP kinases, promote an almost complete activation of MAP kinases in the presence of NSAIDs.
Neg (unable) Positive_regulation (stimulate) of kinases associated with cinod
4) Confidence 0.07 Published 2002 Journal Biochem. Pharmacol. Section Abstract Doc Link 11841790 Disease Relevance 0.46 Pain Relevance 0.87
In cultured astrocytes, a biological system less sensitive to oxidative stress, we show that a short treatment by NSAIDs strongly activated the three MAP kinases in the presence of H(2)O(2).
Positive_regulation (activated) of kinases in astrocytes associated with stress and cinod
5) Confidence 0.07 Published 2002 Journal Biochem. Pharmacol. Section Abstract Doc Link 11841790 Disease Relevance 0.46 Pain Relevance 0.84
In conclusion, we demonstrate that various NSAIDs can activate the three families of MAP kinases and that this activation depends on the presence of reactive oxygenated species.
Positive_regulation (activate) of kinases associated with cinod
6) Confidence 0.07 Published 2002 Journal Biochem. Pharmacol. Section Abstract Doc Link 11841790 Disease Relevance 0.36 Pain Relevance 0.87
Recently, opioid receptors have been shown to interact with the pertussis toxin (PTX)-insensitive Gz (a member of the Gi subfamily), which inhibits adenylyl cyclase and stimulates mitogen-activated protein kinases (MAPKs).
Positive_regulation (stimulates) of kinases associated with bordatella infection and opioid receptor
7) Confidence 0.02 Published 2000 Journal J. Neurochem. Section Abstract Doc Link 10737627 Disease Relevance 0.19 Pain Relevance 0.56
Although salicylates inhibited the in vivo activation of Janus kinases, their kinase activity was not affected in vitro by salicylates, suggesting that other kinases were involved in IL-4-induced STAT6 activation.
Positive_regulation (activation) of kinases
8) Confidence 0.02 Published 2002 Journal J. Immunol. Section Abstract Doc Link 11801685 Disease Relevance 0.70 Pain Relevance 0.25
Recent studies have shown that pharmacological activation of these kinases is associated with recruitment of anti-apoptotic signaling components such as the phosphorylation and inhibition of the proapoptotic proteins Bax and Bad, the inhibition of caspase 3 activation, the phosphorylation and activation of p70S6K (which acts to inhibit Bad) and the phosphorylation and activation of the antiapoptotic protein Bcl-2 (Harada et al 2001; Hausenloy and Yellon 2007).
Positive_regulation (activation) of kinases associated with apoptosis
9) Confidence 0.02 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.48 Pain Relevance 0.10
Although it has been shown that ischemic preconditioning prevents the increased permeability of the transition pore by the activation of kinases, Akt, PI3 kinase, and ERK1/2, the mechanism through which the RISK pathway inhibits the opening of the MTP is unclear.
Positive_regulation (activation) of kinases in MTP
10) Confidence 0.02 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.57 Pain Relevance 0
As mentioned above, activation of kinases of the RISC pathway has been implicated in mediating the cardioprotection associated with ischemic preconditioning (Housenloy et al 2005; Hausenloy and Yellon 2007).
Positive_regulation (activation) of kinases
11) Confidence 0.02 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.50 Pain Relevance 0.12
In particular, mitogen-activated protein kinases (MAPKs), consisting of extracellular signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), are downstream to many kinases and are activated in primary sensory and dorsal horn neurons by nociceptive activity, growth factors and inflammatory mediators, contributing to the induction and maintenance of pain sensitization via posttranslational, translational, and transcriptional regulation.
Positive_regulation (activated) of kinases in dorsal horn associated with nociception, pain, inflammatory mediators and dorsal horn neuron
12) Confidence 0.01 Published 2007 Journal Handb Exp Pharmacol Section Abstract Doc Link 17087130 Disease Relevance 1.56 Pain Relevance 1.26
These genes, which facilitate some of the neurodegenerative pathways, such as ubiquitin, proteasome, inflammation and kinases, were identified to be up- or down-regulated for the TTX treatment.
Positive_regulation (facilitate) of kinases associated with tetrodotoxin, inflammation and neurodegenerative disease
13) Confidence 0.01 Published 2004 Journal Toxicon Section Abstract Doc Link 15501285 Disease Relevance 0.82 Pain Relevance 0.71
Members of this superfamily appear to regulate a diverse array of cellular events, including the control of cell growth, cytoskeletal reorganization, and the activation of protein kinases.
Positive_regulation (activation) of kinases
14) Confidence 0.01 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2855702 Disease Relevance 0.46 Pain Relevance 0.13
promotes activation of ERK1/2, p38, and JNK (Janus kinases) in rheumatoid arthritis and osteoarthritis inducing joint inflammation, although a clear-cut mechanism remains to be elucidated (14, 15).
Positive_regulation (activation) of kinases in joint associated with inflammation, rheumatoid arthritis, osteoarthritis and arthritis
15) Confidence 0.01 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2963399 Disease Relevance 1.14 Pain Relevance 0.44
that the activation of c-Jun N-terminal kinases (JNKs) induces phosphorylation
Positive_regulation (activation) of kinases
16) Confidence 0.01 Published 2008 Journal PPAR Research Section Body Doc Link PMC2408709 Disease Relevance 0.20 Pain Relevance 0
A downstream target of all of the upregulated MAP kinases (ERK5 (MAPK7), p38?
Positive_regulation (upregulated) of kinases
17) Confidence 0.01 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2901320 Disease Relevance 0.76 Pain Relevance 0
complex to activate G-coupled receptors kinases (GRKs) and to desensitize the receptor, leading to a priming mechanism for example by inducing a sustained activation of downstream protein kinases involved in the degranulatory event, such as p38-MAPK [44]; b) the long-lasting activation of G??
Positive_regulation (activation) of kinases
18) Confidence 0.01 Published 2010 Journal Clin Mol Allergy Section Body Doc Link PMC2949734 Disease Relevance 0 Pain Relevance 0.17
complex to activate G-coupled receptors kinases (GRKs) and to desensitize the receptor, leading to a priming mechanism for example by inducing a sustained activation of downstream protein kinases involved in the degranulatory event, such as p38-MAPK [44]; b) the long-lasting activation of G??
Positive_regulation (activate) of kinases
19) Confidence 0.01 Published 2010 Journal Clin Mol Allergy Section Body Doc Link PMC2949734 Disease Relevance 0 Pain Relevance 0.11
In fact, recently published in vitro experiments show that Src family kinases are highly activated in cetuximab-resistant cells and that they enhance EGF-R activation despite the cetuximab-bound receptor.
Positive_regulation (activated) of kinases
20) Confidence 0.01 Published 2010 Journal Head Neck Oncol Section Body Doc Link PMC2868849 Disease Relevance 0.63 Pain Relevance 0

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