INT297181

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Context Info
Confidence 0.52
First Reported 2010
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 1
Total Number 7
Disease Relevance 2.30
Pain Relevance 0.07

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

Anatomy Link Frequency
Heart 2
mesenchyme 1
keratinocytes 1
Ppp3r1 (Mus musculus)
Pain Link Frequency Relevance Heat
imagery 7 69.16 Quite High
fibrosis 28 60.88 Quite High
agonist 14 5.00 Very Low Very Low Very Low
anesthesia 7 5.00 Very Low Very Low Very Low
isoflurane 7 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Hyperplasia 35 99.40 Very High Very High Very High
Death 21 92.84 High High
Arrhythmia Under Development 91 92.56 High High
Targeted Disruption 63 91.40 High High
Infection 21 87.64 High High
Respiratory Failure 7 87.60 High High
Cardiovascular Disorder Under Development 14 84.56 Quite High
Hypertrophy 14 81.44 Quite High
Sudden Death 28 68.52 Quite High
Cancer 14 64.08 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
To determine whether loss of CnB1 truly cripples CnA function in vivo, we analyzed CnA protein stability and NFAT-luciferase activity in CnB1-deleted MEFs.
Spec (whether) Negative_regulation (loss) of CnB1
1) Confidence 0.52 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2825466 Disease Relevance 0.29 Pain Relevance 0
By comparison, deletion of CnB1 from keratinocytes altered their differentiated state, resulting in severe skin defects (22).
Negative_regulation (deletion) of CnB1 in keratinocytes
2) Confidence 0.38 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2825466 Disease Relevance 0.54 Pain Relevance 0
Analysis of cell cycle activity in these hearts by examination of phosphorylated histone H3 in 3-day-old mice revealed significantly less reactivity in CnB1fl/flcTnT-Cre mice when compared with controls, again suggesting that loss of CnB1 from the heart negatively affected cellular proliferation (Fig. 6, H and I).



Negative_regulation (loss) of CnB1 in heart associated with hyperplasia
3) Confidence 0.38 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2825466 Disease Relevance 0.18 Pain Relevance 0
Deletion of CnB1 from the ?
Negative_regulation (Deletion) of CnB1
4) Confidence 0.38 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2825466 Disease Relevance 0.47 Pain Relevance 0
Deletion of CnB1 from the Early Heart Results in Perinatal Lethality
Negative_regulation (Deletion) of CnB1 in Heart
5) Confidence 0.38 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2825466 Disease Relevance 0.21 Pain Relevance 0.07
For example, deletion of CnB1 from the mesenchyme of the developing urinary tract reduced proliferation of smooth muscle cells and other cell types in the urinary tract, leading to multiple defects in development (25).
Negative_regulation (deletion) of CnB1 in mesenchyme
6) Confidence 0.38 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2825466 Disease Relevance 0.41 Pain Relevance 0
These results suggest that loss of CnB1 blocks all CnA-NFAT activity.
Negative_regulation (loss) of CnB1
7) Confidence 0.38 Published 2010 Journal The Journal of Biological Chemistry Section Body Doc Link PMC2825466 Disease Relevance 0.20 Pain Relevance 0

General Comments

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