INT84921

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Revision as of 21:56, 22 August 2012

Context Info
Confidence 3.5816533200
First Reported 1999
Last Reported 2009
Negated 0
Speculated 0
Reported most in NULL
Documents 13
Total Number 13

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

endosome (NGF, NTRK1) cell differentiation (NTRK1) signal transduction (NGF)
extracellular space (NGF) extracellular region (NGF) plasma membrane (NTRK1)
Anatomy Mention Frequency
nerve 9
joints 1
NGF (Homo sapiens)
NTRK1 (Homo sapiens)

Sentences Mentioned In

Key: Protein Event Anatomy Negation Speculation Pain term
Congenital insensitivity to pain with anhidrosis (CIPA) is identified as a genetic disorder of mutations in the human TrkA known as high affinity receptor of <span style="background-color:#FFFF00">nerve growth factor</span> (NGF).
nerve growth factor Binding (receptor) of TrkA in nerve
1) Confidence 0.500419017877067 Published 2004 Journal N/A Section N/A Doc Link 15114061
Congenital insensitivity to pain with anhidrosis (CIPA) is identified as a genetic disorder of mutations in the human TrkA known as high affinity receptor of nerve growth factor (NGF).
NGF Binding (receptor) of TrkA in nerve
2) Confidence 0.500419017877067 Published 2004 Journal N/A Section N/A Doc Link 15114061
<span style="background-color:#FFFF00">Nerve growth factor</span> (NGF) and its high-affinity receptor TrkA are involved in stimulating epithelial cancer cell growth and perineural invasion, as well as in pain generation in chronic benign disorders.
Nerve growth factor Binding (affinity) of TrkA in Nerve
3) Confidence 0.357942189063972 Published 1999 Journal N/A Section N/A Doc Link 10561305
Nerve growth factor (NGF) and its high-affinity receptor TrkA are involved in stimulating epithelial cancer cell growth and perineural invasion, as well as in pain generation in chronic benign disorders.
NGF Binding (affinity) of TrkA in Nerve
4) Confidence 0.357942189063972 Published 1999 Journal N/A Section N/A Doc Link 10561305
Interactions of nerve growth factor (NGF) and its receptor tropomyosin-related kinase (trkA) appear to be critical for maintaining HSV latency.
NGF Binding (Interactions) of trkA in nerve
5) Confidence 0.299022112721328 Published 2008 Journal N/A Section N/A Doc Link 19016376
The purpose of this study was to prove the presence of NGF (<span style="background-color:#FFFF00">nerve growth factor</span>) and its receptor TrkA (tyrosine kinase receptor) with immunofluorescence.
nerve growth factor Binding (presence) of TrkA in nerve
6) Confidence 0.265922640619896 Published 2009 Journal N/A Section N/A Doc Link 19399531
The analysis of these specimens revealed the presence of the neurotrophin (NGF) and its own receptor (TrkA) in all cases: the immunohistochemical reaction between the specimens and the specific antibodies marked with FITC was seen under fluoromicroscopy, but in none of the control cases treated with FITC only.
NGF Binding (presence) of TrkA
7) Confidence 0.265922640619896 Published 2009 Journal N/A Section N/A Doc Link 19399531
The purpose of this study was to prove the presence of NGF (<span style="background-color:#FFFF00">nerve growth factor</span>) and its receptor TrkA (tyrosine kinase receptor) with immunofluorescence.
nerve growth factor Binding (presence) of TrkA in nerve
8) Confidence 0.265922640619896 Published 2009 Journal N/A Section N/A Doc Link 19399531
The purpose of this study was to prove the presence of NGF (nerve growth factor) and its receptor TrkA (tyrosine kinase receptor) with immunofluorescence.
NGF Binding (presence) of TrkA in nerve
9) Confidence 0.265922640619896 Published 2009 Journal N/A Section N/A Doc Link 19399531
This study demonstrated the presence of NGF and TrkA in specimens collected from degenerative facet joints, suggesting that specific molecules could be used in order to modulate chronic pain in patients with degenerative lumbar spine.
NGF Binding (presence) of TrkA in joints
10) Confidence 0.265922640619896 Published 2009 Journal N/A Section N/A Doc Link 19399531

General Comments

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