INT303277

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Context Info
Confidence 0.94
First Reported 2010
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 3
Total Number 4
Disease Relevance 0.31
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.

cytosol (Map1lc3a) cytoskeleton (Map1lc3a) cytoplasm (Map1lc3a)
Anatomy Link Frequency
face 2
Map1lc3a (Mus musculus)
Pain Link Frequency Relevance Heat
medulla 6 5.28 Low Low
Clonidine 9 5.00 Very Low Very Low Very Low
Spinal cord 7 5.00 Very Low Very Low Very Low
Hippocampus 5 5.00 Very Low Very Low Very Low
midbrain 2 5.00 Very Low Very Low Very Low
Substantia nigra 2 5.00 Very Low Very Low Very Low
antagonist 2 5.00 Very Low Very Low Very Low
carbamazepine 2 5.00 Very Low Very Low Very Low
withdrawal 2 5.00 Very Low Very Low Very Low
agonist 2 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Injury 4 72.08 Quite High
Death 18 65.72 Quite High
Disease 93 58.64 Quite High
Motor Neuron Diseases 70 50.88 Quite High
Toxicity 21 50.00 Quite Low
Apoptosis 14 45.64 Quite Low
Neuroblastoma 1 39.60 Quite Low
Dementia 18 37.48 Quite Low
Weight Loss 4 20.56 Low Low
Tremor 11 20.04 Low Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
This also allowed us to demonstrate that this increase in LC3-II levels results from an increase in synthesis rather than a decrease in degradation of autophagosomes, as increased levels were also seen in the presence of bafilomycin A1, an autophagy inhibitor that blocks autophagosome-lysosome fusion and therefore LC3-II degradation (27) (Fig. 1E and F).
Protein_catabolism (degradation) of LC3-II
1) Confidence 0.94 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2865373 Disease Relevance 0.06 Pain Relevance 0
LC3-II is bound to both sides of the membrane, and it remains membrane bound even after fusion with lysosomes, after which LC3-II on the cytosolic face of autophagosomes can be recycled (to LC3-I) by Atg4 [10], while the LC3-II on the inner face of the membrane is degraded.


Protein_catabolism (degraded) of LC3 in face
2) Confidence 0.31 Published 2010 Journal Seminars in Cell & Developmental Biology Section Body Doc Link PMC2938570 Disease Relevance 0 Pain Relevance 0
LC3-II is bound to both sides of the membrane, and it remains membrane bound even after fusion with lysosomes, after which LC3-II on the cytosolic face of autophagosomes can be recycled (to LC3-I) by Atg4 [10], while the LC3-II on the inner face of the membrane is degraded.


Protein_catabolism (degraded) of LC3 in face
3) Confidence 0.23 Published 2010 Journal Seminars in Cell & Developmental Biology Section Body Doc Link PMC2938570 Disease Relevance 0 Pain Relevance 0
Autophagosomes sequester the target organelle/protein and fuse with lysosomes, where the contents – and the LC3-II present on the luminal side of the autophagosome – are degraded [67].
Protein_catabolism (degraded) of LC3
4) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844426 Disease Relevance 0.25 Pain Relevance 0

General Comments

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