INT314205

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Context Info
Confidence 0.43
First Reported 2010
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 2
Disease Relevance 1.24
Pain Relevance 2.30

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

mitochondrion (Mapk14) cell morphogenesis (Mapk14) response to stress (Mapk14)
cytoplasm (Mapk14) cytosol (Mapk14) extracellular space (Ngf)
Ngf (Mus musculus)
Mapk14 (Mus musculus)
Pain Link Frequency Relevance Heat
Nerve growth factor 90 100.00 Very High Very High Very High
Trk A 22 100.00 Very High Very High Very High
substance P 18 97.76 Very High Very High Very High
Lasting pain 2 89.72 High High
Dorsal horn 2 88.64 High High
Spinal cord 12 88.16 High High
Inflammation 30 84.00 Quite High
intrathecal 20 83.36 Quite High
Pain 34 81.32 Quite High
Inflammatory mediators 16 71.36 Quite High
Disease Link Frequency Relevance Heat
Pain 30 89.72 High High
INFLAMMATION 46 84.00 Quite High
Diabetes Mellitus 88 80.48 Quite High
Neuropathic Pain 96 70.84 Quite High
Diabetic Neuropathy 72 46.72 Quite Low
Hyperalgesia 14 5.00 Very Low Very Low Very Low
Nociception 12 5.00 Very Low Very Low Very Low
Nervous System Injury 6 5.00 Very Low Very Low Very Low
Hyperglycemia 6 5.00 Very Low Very Low Very Low
Diabetes Complications 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
There are two potential signaling mechanisms that may underlie this effect: 1) NGF may directly induce Trk A-dependent p38 phosphorylation, or 2) NGF could indirectly activate interleukin 1-beta-dependent p38 activation to promote SP expression [36].
NGF Positive_regulation (activate) of Phosphorylation (phosphorylation) of p38 associated with nerve growth factor, trk a and substance p
1) Confidence 0.43 Published 2010 Journal Mol Pain Section Body Doc Link PMC2881061 Disease Relevance 0.65 Pain Relevance 1.16
There are two potential signaling mechanisms that may underlie this effect: 1) NGF may directly induce Trk A-dependent p38 phosphorylation, or 2) NGF could indirectly activate interleukin 1-beta-dependent p38 activation to promote SP expression [36].
NGF Spec (may) Positive_regulation (induce) of Phosphorylation (phosphorylation) of p38 associated with nerve growth factor, trk a and substance p
2) Confidence 0.40 Published 2010 Journal Mol Pain Section Body Doc Link PMC2881061 Disease Relevance 0.59 Pain Relevance 1.14

General Comments

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