INT267216

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Context Info
Confidence 0.36
First Reported 2009
Last Reported 2009
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 6
Disease Relevance 9.29
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.

cytoplasm (Cryab, Hspb8) nucleus (Cryab, Hspb8) unfolded protein binding (Cryab)
mitochondrion (Cryab) Golgi apparatus (Cryab) intracellular (Hspb8)
Anatomy Link Frequency
cardiomyocytes 1
Cryab (Mus musculus)
Hspb8 (Mus musculus)
Cryab - R120G (5)
Pain Link Frequency Relevance Heat
Central nervous system 6 43.04 Quite Low
fibrosis 30 13.20 Low Low
anesthesia 6 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Alzheimer's Dementia 192 100.00 Very High Very High Very High
Coronary Heart Disease 180 99.16 Very High Very High Very High
Death 72 97.52 Very High Very High Very High
Targeted Disruption 576 95.72 Very High Very High Very High
Apoptosis 30 91.32 High High
Toxicity 24 87.00 High High
Muscular Atrophy 36 82.28 Quite High
Disease 42 79.28 Quite High
Neurodegenerative Disease 24 76.32 Quite High
Injury 6 51.92 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We have shown that HSPB8 can directly interact with HSPB5 R120G and inhibit amyloid oligomer and aggresome formation [15].
HSPB5 (R120G) Binding (interact) of HSPB8 associated with alzheimer's dementia
1) Confidence 0.36 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 0.99 Pain Relevance 0
HSPB8 interacts with HSPB5 R120G and functions as a chaperone, assisting in the folding of the mutant protein [27], [28].
HSPB5 (R120G) Binding (interacts) of HSPB8
2) Confidence 0.36 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.09 Pain Relevance 0
In our previous study, we showed that recombinant HSPB8 or HSPB1 protein could directly interrupt HSPB5 R120G-mediated amyloid oligomer formation although amyloid oligomer is still present in the mixture of wild-type (WT) HSPB5 and mutant HSPB5 R120G [15].
HSPB5 (R120G) Binding (interrupt) of HSPB8 associated with alzheimer's dementia
3) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.97 Pain Relevance 0
In our previous study, we showed that recombinant HSPB8 or HSPB1 protein could directly interrupt HSPB5 R120G-mediated amyloid oligomer formation although amyloid oligomer is still present in the mixture of wild-type (WT) HSPB5 and mutant HSPB5 R120G [15].
HSPB5 (R120G) Binding (interrupt) of HSPB8 associated with alzheimer's dementia
4) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.85 Pain Relevance 0
In our previous study, we showed that recombinant HSPB8 or HSPB1 protein could directly interrupt HSPB5 R120G-mediated amyloid oligomer formation although amyloid oligomer is still present in the mixture of wild-type (WT) HSPB5 and mutant HSPB5 R120G [15].
HSPB5 Binding (interrupt) of HSPB8 associated with alzheimer's dementia
5) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.96 Pain Relevance 0
Our previous in vitro study showed that HSPB8 and HSPB1, which can bind to HSPB5 R120G, inhibited amyloid oligomer formation and reduced cell death in the R120G transfected cardiomyocytes [15].
HSPB5 (R120G) Binding (bind) of HSPB8 in cardiomyocytes associated with alzheimer's dementia and death
6) Confidence 0.28 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2670514 Disease Relevance 1.42 Pain Relevance 0

General Comments

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