INT128411

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Context Info
Confidence 0.45
First Reported 2005
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 2
Total Number 5
Disease Relevance 0.81
Pain Relevance 0.95

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
Shank 1
synapses 1
dorsal horn 1
Shank1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Hyperalgesia 1 99.88 Very High Very High Very High
spinal dorsal horn 3 99.68 Very High Very High Very High
allodynia 1 99.54 Very High Very High Very High
Thermal hyperalgesia 2 92.04 High High
Dorsal horn 2 88.44 High High
Neuropathic pain 4 86.40 High High
Dorsal horn neuron 1 75.00 Quite High
Sciatic nerve 1 74.60 Quite High
Peripheral nerve injury 1 59.32 Quite High
neuralgia 2 25.00 Low Low
Disease Link Frequency Relevance Heat
Hyperalgesia 3 99.88 Very High Very High Very High
Neuropathic Pain 5 99.54 Very High Very High Very High
Angelman Syndrome 4 66.08 Quite High
Syndrome 8 65.08 Quite High
Intellectual Impairment 4 64.72 Quite High
Nervous System Injury 1 59.32 Quite High
Anxiety Disorder 4 5.00 Very Low Very Low Very Low
Attention Deficit Hyperactivity 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
These data revealed a close association between the expression and loss of allodynia and hyperalgesia with changes in the levels of Homer1b/c and Shank1a in the spinal dorsal horn.
Regulation (changes) of Shank1a in dorsal horn associated with hyperalgesia, allodynia and spinal dorsal horn
1) Confidence 0.45 Published 2005 Journal Neurosci. Lett. Section Abstract Doc Link 16002212 Disease Relevance 0.62 Pain Relevance 0.95
In addition to being itself a target of UPS degradation [3], Shank1A is localized to synapses, and its accumulation requires other scaffold proteins in the PSD, including GKAP, Homer, and PSD-95 [16], [17], [25].
Regulation (target) of Shank1A in synapses
2) Confidence 0.23 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0.20 Pain Relevance 0
The majority of pooled RNAi constructs had no effect on the pattern or fluorescence intensity levels of the GFP-Shank1A reporter.
Neg (no) Regulation (effect) of GFP-Shank1A reporter
3) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
Thus, the parallel changes in Shank1 upon manipulation of TRIM3 could be explained by decreased stabilization of Shank at the PSD secondary to GKAP loss.
Regulation (changes) of Shank1 in Shank
4) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
However, in contrast to their effect on GFP-Shank1A, none of the TRIM3 RNAi plasmids affected the pattern or intensity of overexpressed GFP-PSD-95.
Regulation (effect) of GFP-Shank1A
5) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0

General Comments

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