INT249774

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Context Info
Confidence 0.41
First Reported 2008
Last Reported 2010
Negated 0
Speculated 0
Reported most in Abstract
Documents 2
Total Number 2
Disease Relevance 0.25
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 (Plk1) mitosis (Plk1) chromosome (Plk1)
nucleus (Plk1) cytoskeleton (Plk1) cell cycle (Plk1)
Plk1 (Mus musculus)
Pain Link Frequency Relevance Heat
isoflurane 4 5.00 Very Low Very Low Very Low
tolerance 3 5.00 Very Low Very Low Very Low
anesthesia 3 5.00 Very Low Very Low Very Low
cytokine 2 5.00 Very Low Very Low Very Low
analgesia 1 5.00 Very Low Very Low Very Low
Buprenorphine 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Stress 1 72.88 Quite High
Injury 7 63.92 Quite High
Targeted Disruption 17 63.76 Quite High
Hyperglycemia 2 51.60 Quite High
Diabetes Mellitus 6 5.00 Very Low Very Low Very Low
Hyperplasia 3 5.00 Very Low Very Low Very Low
Impaired Glucose Tolerance 3 5.00 Very Low Very Low Very Low
Necrosis 2 5.00 Very Low Very Low Very Low
Polyploidy 2 5.00 Very Low Very Low Very Low
Cancer 2 5.00 Very Low Very Low Very Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Additionally, we observed significant upregulation of known FoxM1 targets, including Plk1, Cenp-a, Birc5/survivin, and Ccnb1 (Fig. 2).
Positive_regulation (upregulation) of Plk1
1) Confidence 0.41 Published 2008 Journal Diabetes Section Body Doc Link PMC2570403 Disease Relevance 0.12 Pain Relevance 0
Upstream signaling pathways involved in the blockage of G2/M transition included lack of persistent Erk1/2 activation and inability to up-regulate the levels of Cdk1, Plk1, Aurora A and B, and Mad2 along with a defective histone 3 phosphorylation and lack of chromatin condensation.
Positive_regulation (activation) of Plk1
2) Confidence 0.35 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2940888 Disease Relevance 0.14 Pain Relevance 0

General Comments

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