INT193697

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Context Info
Confidence 0.02
First Reported 2006
Last Reported 2006
Negated 0
Speculated 0
Reported most in Body
Documents 1
Total Number 1
Disease Relevance 1.84
Pain Relevance 0.12

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

cytosol (Apaf1, CASP9) nucleus (Apaf1, CASP9) intracellular (Apaf1, CASP9)
peptidase activity (CASP9) Golgi apparatus (Apaf1) cytoplasm (Apaf1)
Apaf1 (Mus musculus)
CASP9 (Homo sapiens)
Pain Link Frequency Relevance Heat
cytokine 19 96.92 Very High Very High Very High
Inflammation 14 69.84 Quite High
chemokine 2 25.60 Quite Low
tolerance 20 12.92 Low Low
halothane 2 5.00 Very Low Very Low Very Low
Pain 1 5.00 Very Low Very Low Very Low
Bile 1 5.00 Very Low Very Low Very Low
metalloproteinase 1 5.00 Very Low Very Low Very Low
vincristine 1 5.00 Very Low Very Low Very Low
antagonist 1 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 35 99.38 Very High Very High Very High
Death 15 97.20 Very High Very High Very High
Autoimmune Disease 52 93.28 High High
Autoimmune Lymphoproliferative Syndrome 1 91.92 High High
Malignant Neoplastic Disease 10 72.88 Quite High
INFLAMMATION 14 69.84 Quite High
Lymphadenopathy 2 62.08 Quite High
Lymphoproliferative Disease 5 59.36 Quite High
Necrosis 6 45.52 Quite Low
Cancer 54 45.16 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Lack of cytokine signaling has been shown to cause an increase in mitochondrial permeability and cytochrome c release; along with apoptotic protease-activating factor 1 (APAF1), cytochrome c activates caspase-9 and downstream effector caspases.
APAF1 Positive_regulation (activates) of caspase-9 associated with apoptosis and cytokine
1) Confidence 0.02 Published 2006 Journal Theor Biol Med Model Section Body Doc Link PMC1508139 Disease Relevance 1.84 Pain Relevance 0.12

General Comments

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