INT343188

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Context Info
Confidence 0.56
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 6
Disease Relevance 3.46
Pain Relevance 0.10

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mitochondrion (ACSL4) small molecule metabolic process (ACSL4) endoplasmic reticulum (ACSL4)
peroxisome (ACSL4) ligase activity (ACSL4)
Anatomy Link Frequency
MCF-7 4
MDA-MB-231 4
colon 2
ACSL4 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 6 99.80 Very High Very High Very High
COX2 6 8.48 Low Low
COX-2 inhibitor 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
INFLAMMATION 6 99.68 Very High Very High Very High
Apoptosis 72 98.84 Very High Very High Very High
Colon Cancer 54 97.88 Very High Very High Very High
Injury 126 95.72 Very High Very High Very High
Aggression 36 95.60 Very High Very High Very High
Breast Cancer 222 88.88 High High
Targeted Disruption 24 88.64 High High
Wound Healing 18 83.32 Quite High
Cancer 84 75.08 Quite High
Starvation 12 63.76 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In line with these results, inhibition of ACSL4 expression in the highly aggressive and high-level expression of ACSL4 cell line, MDA-MB-231, by transfection of a plasmid containing ACSL4-shRNA resulted in decreased aggresiveness.
Negative_regulation (inhibition) of Gene_expression (expression) of ACSL4 in MDA-MB-231
1) Confidence 0.56 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978721 Disease Relevance 0.62 Pain Relevance 0
The involvement of ACSL4 in the regulation of intramitochondrial AA levels and lipooxygenase products were confirmed by inhibition of ACSL4 expression and the use of the MCF-7 Tet-off/ACSL4 transfection approach.
Negative_regulation (inhibition) of Gene_expression (expression) of ACSL4 in MCF-7
2) Confidence 0.56 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978721 Disease Relevance 0.39 Pain Relevance 0
As expected, the MCF-7 Tet-off/ACSL4 cell line showed a significant increase in ACSL4 mRNA and protein, as compared with MCF-7 Tet-off control cells, and ACSL4 expression was completely repressed by the treatment of the cells with tetracycline, indicating that the system is fully functional in this cell line (Fig. 6A).
Negative_regulation (repressed) of Gene_expression (expression) of ACSL4 in MCF-7
3) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978721 Disease Relevance 0.21 Pain Relevance 0
In line with these results, inhibition of ACSL4 expression in the highly aggressive and high-level expression of ACSL4 cell line, MDA-MB-231, by transfection of a plasmid containing ACSL4-shRNA resulted in decreased aggresiveness.
Negative_regulation (inhibition) of Gene_expression (expression) of ACSL4 in MDA-MB-231
4) Confidence 0.42 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978721 Disease Relevance 0.63 Pain Relevance 0
Moreover, a combination of classical non-steroideal anti-inflammatory drugs aimed at inhibiting COX-2 and Triacsin C targeting ACSL4 has shown a synergistic pro-apoptotic effect in the colon cancer cell line HT29 [21].
Negative_regulation (inhibiting) of Gene_expression (targeting) of ACSL4 in colon associated with inflammation, colon cancer, cinod and apoptosis
5) Confidence 0.41 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978721 Disease Relevance 0.92 Pain Relevance 0.10
We further investigated the role of ACSL4 using small hairpin RNA (shRNA) to disrupt the expression of endogenous ACSL4 in the more aggressive cell line MD-MB-231.
Negative_regulation (disrupt) of Gene_expression (expression) of ACSL4
6) Confidence 0.36 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2978721 Disease Relevance 0.67 Pain Relevance 0

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