INT154938

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.62
First Reported 2008
Last Reported 2010
Negated 0
Speculated 2
Reported most in Body
Documents 11
Total Number 16
Disease Relevance 8.08
Pain Relevance 2.03

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

cytosol (MAP1LC3A) cytoskeleton (MAP1LC3A) cytoplasm (MAP1LC3A)
Anatomy Link Frequency
HeLa 2
neuronal 1
HT-29 1
neurons 1
MAP1LC3A (Homo sapiens)
Pain Link Frequency Relevance Heat
Fibrositis 174 94.44 High High
chemokine 28 92.04 High High
cytokine 47 86.52 High High
Inflammation 20 86.12 High High
imagery 4 85.44 High High
qutenza 27 75.00 Quite High
Neurobehavioral 28 70.92 Quite High
Pain 8 19.84 Low Low
ketamine 4 11.52 Low Low
anesthesia 4 10.08 Low Low
Disease Link Frequency Relevance Heat
Hepatitis C Virus Infection 756 99.84 Very High Very High Very High
Disease 216 94.52 High High
Sleep Disorders 174 94.44 High High
Death 37 90.56 High High
Necrosis 12 88.88 High High
Cancer 82 88.52 High High
Drug Induced Neurotoxicity 48 88.24 High High
INFLAMMATION 28 86.12 High High
Acquired Immune Deficiency Syndrome Or Hiv Infection 292 83.28 Quite High
Targeted Disruption 80 80.24 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
And the expression of LC3-II changes in parallel with AVOs.
Gene_expression (expression) of LC3
1) Confidence 0.62 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2914703 Disease Relevance 0.27 Pain Relevance 0
The expression of both MAP-LC3 and BECLIN 1 genes in BMCs was analyzed with SYBR Green quantitative PCR by using mRNA extracts and primers.
Spec (analyzed) Gene_expression (expression) of MAP-LC3
2) Confidence 0.50 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2875645 Disease Relevance 0.09 Pain Relevance 0.05
-galactosidase, cathepsin, LC3, and Lyso Tracker) and enhanced expression of autophagic genes at both transcriptional and translational levels, indicating the presence of autophagy [9].
Gene_expression (expression) of LC3
3) Confidence 0.50 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2875645 Disease Relevance 0.71 Pain Relevance 0.32
Then, to confirm autophagy induction by 5-FU, and the inhibition by CQ, the expression of LC3-II was investigated in HT-29 cells treated with 5-FU at 5 ?
Gene_expression (expression) of LC3 in HT-29
4) Confidence 0.48 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2914703 Disease Relevance 0 Pain Relevance 0
In addition, we analyzed the expression of genes involved in autophagic processes, such as BECLIN 1 and MAP-LC3.
Spec (analyzed) Gene_expression (expression) of MAP-LC3
5) Confidence 0.44 Published 2010 Journal Arthritis Res Ther Section Body Doc Link PMC2875645 Disease Relevance 0.32 Pain Relevance 0.16
Additionally, LC3 was highly expressed in Gal-exposed neurons (Figure 5Bi, inset).
Gene_expression (expressed) of LC3 in neurons
6) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943470 Disease Relevance 1.22 Pain Relevance 0.03
Western blot analysis of neuronal lysates showed a reduction of LC3-II expression in HCV core-exposed HFNs compared with control HFNs (Figure 5C, p<0.05), indicating that HCV core protein inhibited LC3-I to LC3-II conversion.
Gene_expression (expression) of LC3 in neuronal associated with hepatitis c virus infection
7) Confidence 0.44 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943470 Disease Relevance 1.31 Pain Relevance 0.08
-III-tubulin and lipidated LC3-II expression (p<0.05).
Gene_expression (expression) of LC3
8) Confidence 0.38 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2943470 Disease Relevance 2.45 Pain Relevance 0.20
Crude protein lysates were separated by 16% SDS-PAGE and the membrane were blotted for LC3 and ?
Gene_expression (blotted) of LC3
9) Confidence 0.33 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943470 Disease Relevance 0.26 Pain Relevance 0.04
The catalase inhibitor 3-amino-1,2,4-triazole (3AT) abrogated DHC-induced expression of LC3-II, overexpression of the catalase gene increased expression of LC3-II protein, and knockdown decreased it.
Gene_expression (expression) of LC3-II
10) Confidence 0.14 Published 2008 Journal Autophagy Section Abstract Doc Link 18818525 Disease Relevance 0.33 Pain Relevance 0.37
DHC attenuated basal ROS levels through catalase induction; this effect was enhanced by antioxidants, which increased both LC3-II expression and caspase-3 activation.
Gene_expression (expression) of LC3-II
11) Confidence 0.14 Published 2008 Journal Autophagy Section Abstract Doc Link 18818525 Disease Relevance 0.36 Pain Relevance 0.40
The catalase inhibitor 3-amino-1,2,4-triazole (3AT) abrogated DHC-induced expression of LC3-II, overexpression of the catalase gene increased expression of LC3-II protein, and knockdown decreased it.
Gene_expression (expression) of LC3-II
12) Confidence 0.14 Published 2008 Journal Autophagy Section Abstract Doc Link 18818525 Disease Relevance 0.34 Pain Relevance 0.38
We used a HeLa cell line constitutively expressing LC3 tagged to both green fluorescent protein (GFP) and red fluorescent protein (RFP).
Gene_expression (expressing) of LC3 in HeLa
13) Confidence 0.10 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2916709 Disease Relevance 0 Pain Relevance 0
HeLa cells expressing RFP and GFP tagged LC3-II as described in Materials and Methods were treated as shown (NAC 10 mm), before being fixed and subjected to automated counting of red and green dots.
Gene_expression (expressing) of LC3 in HeLa
14) Confidence 0.10 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2916709 Disease Relevance 0.05 Pain Relevance 0
We found that N-acetyl cysteine (NAC), cystamine [a drug proposed for use in HD, with pleiotropic effects including transglutaminase inhibition, but which is also metabolized to the antioxidant l-cysteine (19)] and glutathione were all able to significantly ameliorate the induction of autophagy by trehalose in a dose-dependent fashion, as measured by levels of the autophagy marker, microtubule-associated protein 1 light chain 3 II (LC3-II) (Fig. 2A–C).
Gene_expression (levels) of LC3 associated with disease
15) Confidence 0.08 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2916709 Disease Relevance 0.18 Pain Relevance 0
We found that N-acetyl cysteine (NAC), cystamine [a drug proposed for use in HD, with pleiotropic effects including transglutaminase inhibition, but which is also metabolized to the antioxidant l-cysteine (19)] and glutathione were all able to significantly ameliorate the induction of autophagy by trehalose in a dose-dependent fashion, as measured by levels of the autophagy marker, microtubule-associated protein 1 light chain 3 II (LC3-II) (Fig. 2A–C).
Gene_expression (levels) of chain 3 II associated with disease
16) Confidence 0.07 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2916709 Disease Relevance 0.18 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox