INT141183

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Context Info
Confidence 0.75
First Reported 2005
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 9
Total Number 10
Disease Relevance 11.96
Pain Relevance 2.46

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

cytosol (Casp9) peptidase activity (Casp9) mitochondrion (Casp9)
nucleus (Casp9) cytoplasm (Casp9)
Anatomy Link Frequency
dorsal horn spinal cord 1
Casp9 (Mus musculus)
Pain Link Frequency Relevance Heat
chemokine 45 100.00 Very High Very High Very High
Dorsal horn 4 99.68 Very High Very High Very High
Eae 12 99.50 Very High Very High Very High
Spinal cord 10 99.20 Very High Very High Very High
allodynia 2 99.00 Very High Very High Very High
Neuropathic pain 8 98.60 Very High Very High Very High
Thermal hyperalgesia 2 98.50 Very High Very High Very High
cva 25 98.04 Very High Very High Very High
Sciatic nerve 6 96.96 Very High Very High Very High
ischemia 8 76.88 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 307 100.00 Very High Very High Very High
Carcinoma 88 99.84 Very High Very High Very High
Injury 31 99.50 Very High Very High Very High
Neuropathic Pain 10 99.00 Very High Very High Very High
Cancer 216 98.84 Very High Very High Very High
Hyperalgesia 2 98.50 Very High Very High Very High
Hemorrhage 25 98.04 Very High Very High Very High
Death 75 97.12 Very High Very High Very High
Hemorrhagic Shock 51 96.70 Very High Very High Very High
Lymphopenia 2 85.52 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
RT-PCR analysis showed increased expression of bax, apoptotic protease-activating factor-1 (apaf-1), and caspase-9 in the dorsal horn spinal cord 3 days after chronic constriction injury of sciatic nerve.
Gene_expression (expression) of caspase-9 in dorsal horn spinal cord associated with eae, injury, dorsal horn, sciatic nerve, apoptosis and spinal cord
1) Confidence 0.75 Published 2007 Journal Pharmacol. Res. Section Abstract Doc Link 17207636 Disease Relevance 1.17 Pain Relevance 0.93
Of the ten genes assayed, the expression changes for eight genes were confirmed with a change of 1.3-fold or greater: intracisternal-A particles (Iap), upstream transcription factor 1 (Usf1), potassium voltage-gated channel, subfamily Q, member 2 (Kcnq2), chemokine (C-C motif) ligand 19 (Ccl19), erythroid differentiation regulator (edr), caspase 9 (Casp9), chemokine (C-C motif) ligand 27 (Ccl27), complement and component 4 (C4).
Gene_expression (expression) of Casp9 associated with chemokine
2) Confidence 0.52 Published 2005 Journal Genome Biol Section Body Doc Link PMC1175968 Disease Relevance 0.10 Pain Relevance 0.13
Immunohistochemistry demonstrated that the expression of the active forms of caspase-3 and caspase-9 were much higher in mammary tumors treated with raloxifene (Figure 6D, F) than in the untreated control tumors (Figure 6C, E), suggesting that mitochondria-mediated apoptosis occurred in mammary tumor tissues exposed to raloxifene in vivo, too.
Gene_expression (expression) of caspase-9 associated with cancer and apoptosis
3) Confidence 0.35 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2978204 Disease Relevance 1.38 Pain Relevance 0
Immunohistochemistry was conducted using the LSAB method, and CSA II amplification (Dako) was additionally applied to detect cleaved caspase-9.


Gene_expression (detect) of caspase-9
4) Confidence 0.32 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2978204 Disease Relevance 0.79 Pain Relevance 0
Administration of phenyl-N-tert-butylnitrone (PBN), a potent ROS scavenger, reduced the development of thermal hyperalgesia and mechanical allodynia at 1 and 3 days post-CCI, and decreased the mRNA levels of bax, apaf-1, and caspase-9.
Gene_expression (levels) of caspase-9 associated with allodynia, eae and thermal hyperalgesia
5) Confidence 0.26 Published 2007 Journal Pharmacol. Res. Section Abstract Doc Link 17207636 Disease Relevance 1.42 Pain Relevance 1.14
Our observation of significantly increased cytosolic expression of cytochrome C and pro-caspase-9 in ethanol-treated mice depicts an essential role of the mitochondrial death pathway in ethanol-induced apoptosis.
Gene_expression (expression) of pro-caspase-9 associated with apoptosis and death
6) Confidence 0.13 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2807457 Disease Relevance 1.60 Pain Relevance 0.07
A rapid activation of splenic apoptosis in HS mice was observed at t = 0 hours and t = 72 hours after hemorrhage and predominantly confirmed by increased DNA fragmentation, elevated caspase-3/7, caspase-8, and caspase-9 activities, and enhanced expression of intrinsic mitochondrial proteins.
Gene_expression (expression) of caspase-9 associated with cva, hemorrhagic shock and apoptosis
7) Confidence 0.10 Published 2008 Journal Crit Care Section Abstract Doc Link PMC2374615 Disease Relevance 1.94 Pain Relevance 0.12
Neither ethanol nor ADH affected the expression of ANP, total pro-caspase-9, cytosolic and total pro-caspase-8, TNF-?
Gene_expression (expression) of pro-caspase-9
8) Confidence 0.10 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2807457 Disease Relevance 0.66 Pain Relevance 0.07
Immunoblot analysis indicated increased active, cleaved caspase-9 levels solely in non-adherent CXCL12-expressing cells compared to active caspase-8, suggesting an intrinsic apoptotic mechanism driving anoikis of those cells (Figure 4A).
Gene_expression (levels) of caspase-9 associated with apoptosis
9) Confidence 0.08 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 1.40 Pain Relevance 0
As a first step, we examined activity levels of the extrinsic apoptotic initiator, caspase-8, and intrinsic apoptotic initiator caspase-9 levels in carcinoma cells secreting varying amounts of CXCL12 (Hi, Med, Low) [24].
Gene_expression (levels) of caspase-9 associated with carcinoma and apoptosis
10) Confidence 0.08 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 1.50 Pain Relevance 0

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