INT168396

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Context Info
Confidence 0.72
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 12
Total Number 13
Disease Relevance 7.69
Pain Relevance 8.74

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

signal transduction (Cnr2) plasma membrane (Cnr2) signal transducer activity (Cnr2)
Anatomy Link Frequency
brain 4
NOS1 2
spinal cord 2
microglial cells 2
macrophages 1
Cnr2 (Mus musculus)
Cnr2 - Q63R (1)
Pain Link Frequency Relevance Heat
Spinal cord 128 100.00 Very High Very High Very High
opioid receptor 18 100.00 Very High Very High Very High
Neuropathic pain 46 99.68 Very High Very High Very High
Central nervous system 18 99.38 Very High Very High Very High
qutenza 36 98.60 Very High Very High Very High
imagery 10 98.36 Very High Very High Very High
Lasting pain 24 98.32 Very High Very High Very High
Inflammation 79 98.06 Very High Very High Very High
agonist 200 98.04 Very High Very High Very High
Peripheral nerve injury 4 97.64 Very High Very High Very High
Disease Link Frequency Relevance Heat
Stress 192 100.00 Very High Very High Very High
Neuropathic Pain 70 99.68 Very High Very High Very High
Pain 72 98.32 Very High Very High Very High
INFLAMMATION 87 98.06 Very High Very High Very High
Nervous System Injury 6 97.64 Very High Very High Very High
Drug Dependence 84 97.08 Very High Very High Very High
Targeted Disruption 66 96.72 Very High Very High Very High
Depression 222 96.28 Very High Very High Very High
Vomiting 6 95.00 High High
Multiple Sclerosis 18 86.08 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We then hypothesized that if CB2-Rs are present in the brain, then antisense oligonucleotides complementary to CB2 mRNA transcript will block translation of or stimulate degradation of CB2 mRNA.
Transcription (transcript) of CB2 in brain
1) Confidence 0.72 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2241668 Disease Relevance 0.75 Pain Relevance 0.52
In the mouse model, the CB2 gene transcripts were present in whole brain preparations following CMS and CB2-R protein was enhanced by CMS and prenatal capsaicin exposure.
Transcription (transcripts) of CB2 gene in brain associated with stress and qutenza
2) Confidence 0.69 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2241668 Disease Relevance 0.58 Pain Relevance 0.78
A significant association was found between the CB2 Q63R polymorphism and Japanese depressed subjects (p?
Transcription (polymorphism) of CB2 (Q63R)
3) Confidence 0.69 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2241668 Disease Relevance 0.36 Pain Relevance 0.42
Results show that CB2 mRNA is constitutively expressed in primary cultured microglial cells (Figure. 2A) and, more importantly, is significantly increased following IFN-?
Transcription (expressed) of CB2 in microglial cells
4) Confidence 0.65 Published 2005 Journal J Neuroinflammation Section Body Doc Link PMC1352348 Disease Relevance 0 Pain Relevance 0.06
In the mouse model, the CB2 gene transcripts were present in whole brain preparations following CMS and CB2-R protein was enhanced by CMS and prenatal capsaicin exposure.
Transcription (present) of CB2-R in brain associated with stress and qutenza
5) Confidence 0.60 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2241668 Disease Relevance 0.58 Pain Relevance 0.79
Thus, in the brain areas analyzed CB2-R immunoreactivity was detected in mice and rat brains, and this is supported by reports of identification of neuronal CB2-Rs in the brain stem involved in emesis [21].


Transcription (detected) of CB2-R in brains associated with vomiting
6) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2241668 Disease Relevance 0.16 Pain Relevance 0.36
The absence of CB2 mRNA in CB2-R deficient mice and presence in wild type controls has also been demonstrated by others [21].
Neg (absence) Transcription (absence) of CB2
7) Confidence 0.53 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2241668 Disease Relevance 0.17 Pain Relevance 0.14
Results suggest that inactivation of the nitric oxide-cGMP-PKG peripheral pathway triggered by NOS1 and NOS2 enhanced the peripheral actions of DOPr and CB2R agonists and that nitric oxide synthesized by NOS1 is implicated in the peripheral regulation of DOPr and CB2R gene transcription during neuropathic pain.
Transcription (transcription) of CB2R in NOS1 associated with neuropathic pain, agonist and opioid receptor
8) Confidence 0.43 Published 2010 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 20498253 Disease Relevance 0.81 Pain Relevance 0.74
Expression of DOPr and CB2R mRNA in the spinal cord and dorsal root ganglia of naive and nerve-injured WT, NOS1-knockout (KO), and NOS2-KO mice, also was assessed.
Transcription (Expression) of CB2R in NOS1 associated with targeted disruption, opioid receptor and spinal cord
9) Confidence 0.41 Published 2010 Journal J. Pharmacol. Exp. Ther. Section Abstract Doc Link 20498253 Disease Relevance 0.83 Pain Relevance 0.99
Chronic pain models (CCI or Bennett and Chung models, sciatic nerve and spinal nerve ligation, respectively) associated with peripheral nerve injury but not inflammatory chronic pain models (Freund's complete adjuvant injection in the paw) have been shown to induce CB2 mRNA expression in rat lumbar spinal cord on activated microglial cells/macrophages, in regions undergoing neuronal damage [49].
Transcription (expression) of CB2 in macrophages associated with nervous system injury, inflammation, spinal nerve ligature, lasting pain, sciatic nerve, spinal cord and peripheral nerve injury
10) Confidence 0.27 Published 2006 Journal BMC Neurol Section Body Doc Link PMC1413551 Disease Relevance 1.30 Pain Relevance 0.94
Although early studies failed to identify CB2 receptors in the central nervous system, recent work has reported the presence of CB2 mRNA in the spinal cord of control rats [34] and CB2 receptor protein in brain tissue [35,36].
Transcription (presence) of CB2 in spinal cord associated with central nervous system and spinal cord
11) Confidence 0.23 Published 2009 Journal Mol Pain Section Body Doc Link PMC2770047 Disease Relevance 0.43 Pain Relevance 1.00
Although early studies failed to identify CB2 receptors in the central nervous system, recent work has reported the presence of CB2 mRNA in the spinal cord of control rats [34] and CB2 receptor protein in brain tissue [35,36].
Transcription (presence) of CB2 in spinal cord associated with central nervous system and spinal cord
12) Confidence 0.23 Published 2009 Journal Mol Pain Section Body Doc Link PMC2770047 Disease Relevance 0.43 Pain Relevance 1.05
Chronic pain models (CCI or Bennett and Chung models, sciatic nerve and spinal nerve ligation, respectively) associated with peripheral nerve injury but not inflammatory chronic pain models (Freund's complete adjuvant injection in the paw) have been shown to induce CB2 mRNA expression in rat lumbar spinal cord on activated microglial cells/macrophages, in regions undergoing neuronal damage [49].
Transcription (expression) of CB2 in microglial cells associated with nervous system injury, inflammation, spinal nerve ligature, lasting pain, sciatic nerve, spinal cord and peripheral nerve injury
13) Confidence 0.09 Published 2006 Journal BMC Neurol Section Body Doc Link PMC1413551 Disease Relevance 1.30 Pain Relevance 0.94

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