INT232840

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Context Info
Confidence 0.44
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 10
Disease Relevance 4.51
Pain Relevance 0.42

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

structural molecule activity (Krt8) nucleus (Krt8) cytoplasm (Krt8)
Krt8 (Mus musculus)
Krt8 - G61C (1)
Pain Link Frequency Relevance Heat
fibrosis 80 89.60 High High
Bile 30 80.44 Quite High
alcohol 30 66.00 Quite High
Inflammation 30 62.40 Quite High
Paracetamol 40 35.76 Quite Low
Potency 10 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 140 99.90 Very High Very High Very High
Disease 170 97.64 Very High Very High Very High
Aging 20 95.12 Very High Very High Very High
Stress 180 94.48 High High
Liver Disease 150 91.24 High High
Cirrhosis 80 89.60 High High
Nash(non-alcoholic Steatohepatitis) 70 87.96 High High
Apoptosis 230 87.32 High High
Parkinson's Disease 10 86.92 High High
Chronic Hepatitis 40 83.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Griseofulvin/DDC feeding leads to rapid induction of K8/K18 expression with disproportional K8 > K18 levels (Denk et al. 2000).
Positive_regulation (induction) of Gene_expression (expression) of K8
1) Confidence 0.44 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.71 Pain Relevance 0
This is supported by studies in transgenic mice, where K8 overexpression accelerates and K18 excess inhibits not only MDB, but also cross-link formation (Strnad et al. 2007).
Positive_regulation (overexpression) of Gene_expression (overexpression) of K8 associated with targeted disruption
2) Confidence 0.44 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.20 Pain Relevance 0
The recently established transgenic mouse lines overexpressing the naturally occurring K8 G61C and R340H variants will likely offer valuable insights in this respect (Ku and Omary 2006; Zhou et al., unpublished data).


Positive_regulation (overexpressing) of Gene_expression (overexpressing) of K8 G61C (G61C) associated with targeted disruption
3) Confidence 0.44 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.79 Pain Relevance 0.11
Dysbalanced K8/K18 expression precedes MDB formation, likely increases keratin misfolding and predisposes to posttranslational modifications, which may interfere with keratin refolding and/or repair.
Positive_regulation (increases) of Gene_expression (expression) of K8
4) Confidence 0.32 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.30 Pain Relevance 0
MDBs also arise in cell culture after transfection with K8/K18, ubiquitin, and p62.
Positive_regulation (transfection) of Gene_expression (transfection) of K8
5) Confidence 0.32 Published 2008 Journal Histochem Cell Biol Section Abstract Doc Link PMC2386529 Disease Relevance 1.00 Pain Relevance 0.04
The elevated K8/K18 ratio is crucial for MDB formation as shown in K18-knockout and K8 overexpressing animals, who are predisposed to MDB formation already upon short exposure to DDC and even form MDBs spontaneously during aging (Magin et al. 1998; Nakamichi et al. 2005).
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of K8 associated with targeted disruption and aging
6) Confidence 0.28 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.69 Pain Relevance 0
Furthermore, autophagic degradation is upregulated in DDC-fed mice and its further stimulation with rapamycin attenuates spontaneous MDB formation in K8 overexpressing mice (Harada et al. 2008).
Positive_regulation (overexpressing) of Gene_expression (overexpressing) of K8
7) Confidence 0.28 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.14 Pain Relevance 0.03
Several pathogenic mechanisms were implicated in this process (Fig. 4; Dobson 2004):1.Enhanced oxidative stress2.Disproportional K8/K18 expression together with keratin modifications3.Chaperone dysfunction4.Elevated p62 levels5.Insufficient protein degradation
Positive_regulation (oxidative) of Gene_expression (expression) of K8
8) Confidence 0.28 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.22 Pain Relevance 0.08
Several pathogenic mechanisms were implicated in this process (Fig. 4; Dobson 2004):1.Enhanced oxidative stress2.Disproportional K8/K18 expression together with keratin modifications3.Chaperone dysfunction4.Elevated p62 levels5.Insufficient protein degradation
Positive_regulation (dysfunction4.Elevated) of Gene_expression (expression) of K8
9) Confidence 0.28 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.23 Pain Relevance 0.08
Several pathogenic mechanisms were implicated in this process (Fig. 4; Dobson 2004):1.Enhanced oxidative stress2.Disproportional K8/K18 expression together with keratin modifications3.Chaperone dysfunction4.Elevated p62 levels5.Insufficient protein degradation
Positive_regulation (1.Enhanced) of Gene_expression (expression) of K8
10) Confidence 0.28 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2386529 Disease Relevance 0.22 Pain Relevance 0.08

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