INT128413

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Context Info
Confidence 0.70
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 2
Total Number 5
Disease Relevance 0.61
Pain Relevance 1.16

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

cell differentiation (Shank1) plasma membrane (Shank1) intracellular (Shank1)
protein complex assembly (Shank1) cytoplasm (Shank1)
Anatomy Link Frequency
Neurons 2
spinal 1
Shank1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
neuralgia 2 100.00 Very High Very High Very High
nociceptor 1 100.00 Very High Very High Very High
Dorsal horn neuron 1 98.40 Very High Very High Very High
Neuropathic pain 4 96.80 Very High Very High Very High
spinal dorsal horn 3 94.28 High High
Peripheral nerve injury 1 91.16 High High
Thermal hyperalgesia 2 79.36 Quite High
Sciatic nerve 1 75.48 Quite High
Dorsal horn 2 65.68 Quite High
tetrodotoxin 16 63.60 Quite High
Disease Link Frequency Relevance Heat
Neuropathic Pain 5 96.80 Very High Very High Very High
Nervous System Injury 1 90.72 High High
Hyperalgesia 3 79.36 Quite High
Angelman Syndrome 4 47.04 Quite Low
Syndrome 8 46.04 Quite Low
Intellectual Impairment 4 45.68 Quite Low
Attention Deficit Hyperactivity Disorder 4 21.60 Low Low
Anxiety Disorder 4 5.00 Very Low Very Low Very Low
Cognitive Disorder 4 5.00 Very Low Very Low Very Low
Disease 4 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Increased levels of Homer1b/c and Shank1a in the post-synaptic density of spinal dorsal horn neurons are associated with neuropathic pain in rats.
Positive_regulation (Increased) of Shank1a in spinal associated with neuralgia, neuropathic pain and dorsal horn neuron
1) Confidence 0.70 Published 2005 Journal Neurosci. Lett. Section Title Doc Link 16002212 Disease Relevance 0.61 Pain Relevance 1.10
Thus, we reasoned that an increase of GFP-Shank1A at postsynaptic sites would reflect impaired degradation of Shank1A itself or of other proteins controlling the size of the PSD.
Positive_regulation (increase) of GFP-Shank1A
2) Confidence 0.50 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
The increase of endogenous Shank1 with TRIM3 knockdown is in keeping with the effect on exogenous GFP-Shank1A in the original RNAi screen (see Figure 1).
Positive_regulation (increase) of Shank1
3) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0.06
Neurons transfected with each of the individual TRIM3 shRNA plasmids showed increased GFP-Shank1A fluorescence; the biggest effect was seen with construct TRIM3/264.
Positive_regulation (increased) of GFP-Shank1A in Neurons
4) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
The fact that TRIM3 knockdown shows some selectivity in its effect on postsynaptic scaffold proteins, and that it increases postsynaptic accumulation of GFP-Shank1A, would argue against a non-specific toxic effect of TRIM3 RNAi in neurons.
Positive_regulation (accumulation) of GFP-Shank1A in neurons
5) Confidence 0.34 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0

General Comments

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