INT204449

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Context Info
Confidence 0.32
First Reported 2007
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 17
Total Number 18
Disease Relevance 9.77
Pain Relevance 4.77

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

nucleus (T) DNA binding (T) cytoplasm (T)
Anatomy Link Frequency
neurons 3
dorsal horn 2
brain 1
astrocytes 1
synapses 1
T (Mus musculus)
Pain Link Frequency Relevance Heat
qutenza 140 100.00 Very High Very High Very High
agonist 37 100.00 Very High Very High Very High
Dorsal horn 56 99.38 Very High Very High Very High
nociceptor 14 99.04 Very High Very High Very High
Pain 126 98.72 Very High Very High Very High
spinal dorsal horn 70 97.76 Very High Very High Very High
Inflammatory response 22 96.84 Very High Very High Very High
Inflammation 250 94.32 High High
tolerance 1 92.20 High High
induced neuropathy 14 91.28 High High
Disease Link Frequency Relevance Heat
Targeted Disruption 145 99.80 Very High Very High Very High
Pain 154 98.72 Very High Very High Very High
Down Syndrome 14 98.68 Very High Very High Very High
Hypersensitivity 205 98.28 Very High Very High Very High
Death 15 97.32 Very High Very High Very High
INFLAMMATION 273 96.48 Very High Very High Very High
Disease 31 94.40 High High
Nervous System Injury 28 92.40 High High
Neuropathic Pain 98 90.64 High High
Myocardial Infarction 26 87.68 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Thus, our results demonstrating attenuation in thermal and mechanical sensitivity in the absence of trkB.T1 could be because increased trkB.T1 expression induces increased intracellular calcium signaling which promotes hypersensitivity.
Gene_expression (expression) of T1 associated with hypersensitivity
1) Confidence 0.32 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.73 Pain Relevance 0.43
The prevailing view has been that trkB.T1 expression leads to dominant negative inhibition of full-length trkB signaling and a reduction in the activation of downstream signaling molecules [17-23,33].
Gene_expression (expression) of T1
2) Confidence 0.32 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.68 Pain Relevance 0.34
We have shown that neurons from a mouse model of neurodegeneration over-express trkB.T1, resulting in a significant increase in resting intracellular calcium; reducing trkB.T1 expression in those neurons reduced intracellular calcium to wildtype levels [23].
Gene_expression (express) of T1 in neurons
3) Confidence 0.32 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.45 Pain Relevance 0.41
The expression of trkB.FL and trkB.T1 is conserved across species and throughout evolution, and trkB isoform expression is regulated during development when the dominant trkB isoform expression in the brain switches from trkB.FL to trkB.T1 [39].
Gene_expression (expression) of T1 in brain
4) Confidence 0.32 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.66 Pain Relevance 0.19
Moreover, altered trkB.T1 expression can affect synaptic plasticity.
Gene_expression (expression) of T1
5) Confidence 0.32 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.73 Pain Relevance 0.19
We have shown that neurons from a mouse model of neurodegeneration over-express trkB.T1, resulting in a significant increase in resting intracellular calcium; reducing trkB.T1 expression in those neurons reduced intracellular calcium to wildtype levels [23].
Gene_expression (expression) of T1 in neurons
6) Confidence 0.32 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.47 Pain Relevance 0.40
We and others have recently described the identification, isolation, and characterization of the novel mouse ESC-derived cardiac progenitor cells (CPCs) on the basis of Brachyury/Flk1 [11], Isl1/Flk1/Nkx2-5 [12], cKit/Nkx2-5 [13], or Nkx2-5 [14] expression.
Gene_expression (expression) of Brachyury
7) Confidence 0.28 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2902505 Disease Relevance 0.22 Pain Relevance 0
Detection of the described markers was achieved with FAM/MGB probes (Applied Biosystems): Nkx2.5 (Mm00657783_m1), Myh6 (Mm00440354_m1), Brachyury (Mm00436877_m1).
Gene_expression (achieved) of Brachyury
8) Confidence 0.28 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2902505 Disease Relevance 0 Pain Relevance 0
For example, neurons express both isoforms [33] while astrocytes only express trkB.T1 [23,40].
Gene_expression (express) of T1 in astrocytes
9) Confidence 0.28 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.73 Pain Relevance 0.35
Next, we asked whether genetic deletion of trkB.T1 would provide a benefit for mice treated with capsaicin, an agonist of TRPV1 receptors that are expressed in BDNF-immunoreactive nociceptors.
Gene_expression (expressed) of T1 in nociceptors associated with qutenza, nociceptor and agonist
10) Confidence 0.28 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.96 Pain Relevance 0.65
Over-expression of trkB.T1 in hippocampal neurons leads to the inhibition of synaptic potentiation [34] and over-expressing trkB.T1 at neuromuscular synapses results in disassembly of acetylcholine receptor clustering [18].
Gene_expression (expressing) of T1 in synapses
11) Confidence 0.28 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.81 Pain Relevance 0.29
Over-expression of trkB.T1 in hippocampal neurons leads to the inhibition of synaptic potentiation [34] and over-expressing trkB.T1 at neuromuscular synapses results in disassembly of acetylcholine receptor clustering [18].
Gene_expression (expression) of T1 in neurons
12) Confidence 0.28 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.79 Pain Relevance 0.26
Generation of trkB.T1 wildtype and knockout mice
Gene_expression (wildtype) of T1 associated with targeted disruption
13) Confidence 0.28 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.37 Pain Relevance 0.07
Here, we demonstrate that trkB.T1 mRNA and protein are both significantly up-regulated in the spinal dorsal horn following systemic antiretroviral drug administration and hind paw inflammation (Figure 1).
Gene_expression (mRNA) of T1 in dorsal horn associated with inflammation and spinal dorsal horn
14) Confidence 0.28 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.87 Pain Relevance 0.41
In addition to trkB.FL, the Ntrk2 (trkB) locus encodes for several alternatively-spliced isoforms of the receptor [15], including trkB.T1, the predominant isoform expressed in the adult mammalian nervous system.
Gene_expression (expressed) of T1 in nervous system
15) Confidence 0.25 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.56 Pain Relevance 0.29
If trkB.T1 were functioning solely as a dominant negative inhibitor of signaling in the dorsal horn, the prediction would be that deletion of trkB.T1 would result in more, not less pain.
Gene_expression (deletion) of T1 in dorsal horn associated with pain and dorsal horn
16) Confidence 0.24 Published 2009 Journal Mol Pain Section Body Doc Link PMC2777863 Disease Relevance 0.53 Pain Relevance 0.38
Although this is the most G-rich amplicon of those tested, and T1 ribonuclease cuts 3?
Gene_expression (cuts) of T1
17) Confidence 0.11 Published 2007 Journal PLoS Biology Section Body Doc Link PMC1808499 Disease Relevance 0.05 Pain Relevance 0
Anti-T1/ST2 also induces the selective expression of IL-4 but not IFN-?
Gene_expression (/) of T1
18) Confidence 0.11 Published 2008 Journal J Occup Med Toxicol Section Body Doc Link PMC2259400 Disease Relevance 0.14 Pain Relevance 0.12

General Comments

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