INT303241

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Context Info
Confidence 0.42
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 7
Disease Relevance 0
Pain Relevance 0

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

intracellular (Trim3) cytoplasm (Trim3)
Anatomy Link Frequency
spine 4
neurons 2
brain 2
Trim3 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
tetrodotoxin 28 38.00 Quite Low
Glutamate receptor 14 5.00 Very Low Very Low Very Low
imagery 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Syndrome 14 5.00 Very Low Very Low Very Low
Anxiety Disorder 7 5.00 Very Low Very Low Very Low
Attention Deficit Hyperactivity Disorder 7 5.00 Very Low Very Low Very Low
Intellectual Impairment 7 5.00 Very Low Very Low Very Low
Cognitive Disorder 7 5.00 Very Low Very Low Very Low
Disease 7 5.00 Very Low Very Low Very Low
Autism 7 5.00 Very Low Very Low Very Low
Angelman Syndrome 7 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In addition, the loss of GKAP with TRIM3 cotransfection was blocked by addition of the proteasome inhibitors MG-132 or lactacystin (Figure 3F).
Negative_regulation (loss) of Gene_expression (cotransfection) of TRIM3
1) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
As expected, the TRIM3/264 RNAi construct also decreased the expression of cotransfected TRIM3 protein in COS7 cells, while having no effect on the related protein TRIM2 (Figure S1C).


Negative_regulation (decreased) of Gene_expression (expression) of TRIM3
2) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
In addition, the loss of GKAP with TRIM3 cotransfection was blocked by addition of the proteasome inhibitors MG-132 or lactacystin (Figure 3F).
Negative_regulation (blocked) of Gene_expression (cotransfection) of TRIM3
3) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
By immunoblotting, TRIM3 was expressed in the brain at low levels at embryonic day 15 (E15) and then increased during the first two postnatal weeks before decreasing through adulthood (Figure 2A, B).
Negative_regulation (decreasing) of Gene_expression (expressed) of TRIM3 in brain
4) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
In neurons overexpressing TRIM3, levels of dendritic GKAP were significantly reduced (Figure 4A, quantified in C).
Negative_regulation (reduced) of Gene_expression (overexpressing) of TRIM3 in neurons
5) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
RNAi knockdown of TRIM3 did not greatly influence spine length (Figure S3B) or density (spines/10 µm; pSUPER: 5.34±0.18; TRIM3/264 6.18±0.24; TRIM3/2756 5.02±0.29; TRIM3/2756 ?
Negative_regulation (0.29) of Gene_expression (/) of TRIM3 in spine
6) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0
RNAi knockdown of TRIM3 did not greatly influence spine length (Figure S3B) or density (spines/10 µm; pSUPER: 5.34±0.18; TRIM3/264 6.18±0.24; TRIM3/2756 5.02±0.29; TRIM3/2756 ?
Negative_regulation (0.24) of Gene_expression (/) of TRIM3 in spine
7) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844417 Disease Relevance 0 Pain Relevance 0

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