INT98130

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Context Info
Confidence 0.67
First Reported 2001
Last Reported 2011
Negated 4
Speculated 1
Reported most in Abstract
Documents 79
Total Number 82
Disease Relevance 65.29
Pain Relevance 10.08

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

cytosol (CASP8) peptidase activity (CASP8) mitochondrion (CASP8)
nucleolus (CASP8) cytoskeleton (CASP8) nucleus (CASP8)
Anatomy Link Frequency
cleavage 9
Hep G2 2
HL-60 2
apoptotic cell 2
Hep 3B 2
CASP8 (Homo sapiens)
Pain Link Frequency Relevance Heat
cINOD 119 99.96 Very High Very High Very High
diclofenac 20 99.78 Very High Very High Very High
amygdala 17 99.78 Very High Very High Very High
Morphine 10 99.50 Very High Very High Very High
COX-2 inhibitor 115 99.44 Very High Very High Very High
Paracetamol 18 99.28 Very High Very High Very High
dexamethasone 387 98.24 Very High Very High Very High
rheumatoid arthritis 90 98.08 Very High Very High Very High
Hippocampus 19 94.00 High High
ischemia 81 93.48 High High
Disease Link Frequency Relevance Heat
Apoptosis 2989 100.00 Very High Very High Very High
Death 829 99.68 Very High Very High Very High
Lung Cancer 51 99.62 Very High Very High Very High
Stress 236 99.04 Very High Very High Very High
Reprotox - General 1 27 98.72 Very High Very High Very High
Leukemia 104 98.62 Very High Very High Very High
Hepatocellular Cancer 50 98.56 Very High Very High Very High
Cancer 1618 98.44 Very High Very High Very High
Colon Cancer 267 98.40 Very High Very High Very High
Breast Cancer 102 98.16 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
These include inhibition of expression of the cellular inhibitor of apoptosis protein-2, potentiation of the activities of other apoptosis inducers such as TNF-related apoptosis-inducing ligand (TRAIL), increased sensitivity to Fas induction, and enhanced caspase 8 activation.78 Caspase 8, an integral component of Fas-mediated apoptosis, is sharply upregulated by lenalidomide (Figure 3).63 In addition, dexamethasone activates caspase 9 indicating that the two drugs in combination generate dual signals capable of enhanced cell death.71 Lenalidomide has been associated with direct antiproliferative activity against MM cells in the absence of immune cells or proapoptotic mechanisms by inducing G1 growth arrest.74,78 Importantly, lenalidomide inhibits the proliferation of malignant B cells while protecting normal CD34+ progenitor cells.75 The various mechanisms of action of lenalidomide are summarized in Figure 4.


Positive_regulation (upregulated) of Caspase 8 in B cells associated with malignant neoplastic disease, multiple myeloma, apoptosis, dexamethasone and death
1) Confidence 0.67 Published 2010 Journal Core evidence Section Body Doc Link PMC2899783 Disease Relevance 1.02 Pain Relevance 0.05
Codeinone did not activate caspase-8 or caspase-9 in these cells.
Neg (not) Positive_regulation (activate) of caspase-8
2) Confidence 0.67 Published 2005 Journal Anticancer Res. Section Abstract Doc Link 16309196 Disease Relevance 0.40 Pain Relevance 0.19
Nimesulide, a selective COX-2 inhibitor, acts synergistically with ionizing radiation against A549 human lung cancer cells through the activation of caspase-8 and caspase-3.
Positive_regulation (activation) of caspase-8 in lung associated with lung cancer and cox-2 inhibitor
3) Confidence 0.51 Published 2009 Journal Int. J. Oncol. Section Title Doc Link 19360361 Disease Relevance 0.59 Pain Relevance 0.33
Morphinone did not activate caspase-8 or -9 in these cells.
Neg (not) Positive_regulation (activate) of caspase-8
4) Confidence 0.48 Published 2006 Journal Anticancer Res. Section Abstract Doc Link 17094451 Disease Relevance 0.87 Pain Relevance 0.15
has been suggested to be an inducer of apoptotic cell death via TNF-R1 occupancy in a caspase-mediated pathway, which includes the activation of caspase-8 [30].
Positive_regulation (activation) of caspase-8 in apoptotic cell associated with apoptosis and death
5) Confidence 0.45 Published 2010 Journal Molecular Vision Section Body Doc Link PMC2994763 Disease Relevance 0.91 Pain Relevance 0.25
Fluorometric assay showed that codeinone time-dependently activated caspase 3 and caspase 9, but not caspase 8, suggesting the activation of intrinsic apoptotic signaling pathway via mitochondria.
Positive_regulation (activated) of caspase 8 associated with apoptosis
6) Confidence 0.38 Published 2003 Journal Anticancer Res. Section Abstract Doc Link 12894543 Disease Relevance 1.01 Pain Relevance 0.26
Strikingly, we showed for the first time that CF also sensitized the metastatic and resistant colon cancer SW620 to TRAIL-induced apoptosis and the mechanisms involved at least enhanced activation of caspase-8 and -3.
Positive_regulation (activation) of caspase-8 in SW620 associated with colon cancer and apoptosis
7) Confidence 0.37 Published 2009 Journal Biochem. Pharmacol. Section Abstract Doc Link 19426686 Disease Relevance 1.09 Pain Relevance 0
However, the caspase-3 inhibitor z-DEVD-fmk failed to suppress activation of the caspase-8/Bid pathway, indicating that caspase-3 activation occurred downstream of caspase-8 activation in our experiments.
Positive_regulation (activation) of caspase-8
8) Confidence 0.37 Published 2009 Journal Int. J. Oncol. Section Abstract Doc Link 19360361 Disease Relevance 0.59 Pain Relevance 0.22
However, the caspase-3 inhibitor z-DEVD-fmk failed to suppress activation of the caspase-8/Bid pathway, indicating that caspase-3 activation occurred downstream of caspase-8 activation in our experiments.
Positive_regulation (activation) of caspase-8
9) Confidence 0.37 Published 2009 Journal Int. J. Oncol. Section Abstract Doc Link 19360361 Disease Relevance 0.57 Pain Relevance 0.21
Sulindac sulfide up-regulated DR5 and activated the proximal caspase 8 in various different colon and prostate cancer cell lines.
Positive_regulation (activated) of caspase 8 in colon associated with reprotox - general 1
10) Confidence 0.35 Published 2001 Journal Cancer Res. Section Abstract Doc Link 11559570 Disease Relevance 1.47 Pain Relevance 0.08
The combined nimesulide-radiation treatment increased apoptosis, induced the cleavage of caspase-3, caspase-9, and poly(ADP-ribose) polymerase (PARP), activated caspase-8, and induced cleavage of Bid.
Positive_regulation (induced) of caspase-8 in cleavage associated with apoptosis
11) Confidence 0.34 Published 2009 Journal Int. J. Oncol. Section Abstract Doc Link 19360361 Disease Relevance 0.60 Pain Relevance 0.30
In addition, z-IETD-fmk, a selective caspase-8 inhibitor, suppressed the nimesulide- and radiation-induced cleavage activation of caspase-9, caspase-3, caspase-8, and Bid, and suppressed the concomitant apoptosis, indicating that the nimesulide-induced increase in radiosensitivity was initiated by caspase-8.
Positive_regulation (activation) of caspase-8 in cleavage associated with apoptosis
12) Confidence 0.34 Published 2009 Journal Int. J. Oncol. Section Abstract Doc Link 19360361 Disease Relevance 0.63 Pain Relevance 0.25
We also demonstrate that treatment with sulindac sulfide, but not sulindac, results in a very early robust activation of both caspase-8 and -9.
Positive_regulation (activation) of caspase-8
13) Confidence 0.33 Published 2006 Journal Int. J. Oncol. Section Abstract Doc Link 16685448 Disease Relevance 0.33 Pain Relevance 0.06
Caspase-8 activation was a postmictochondrial event and occurred in a Fas-independent manner.
Positive_regulation (activation) of Caspase-8
14) Confidence 0.33 Published 2002 Journal Pharmacol. Toxicol. Section Abstract Doc Link 12005112 Disease Relevance 0.54 Pain Relevance 0.83
Given that sulindac sulfide activated caspase-8 and increased membrane death receptor (DR4 and DR5) protein levels, we evaluated its combination with the endogenous death receptor ligand tumor necrosis factor-related apoptosis-inducing ligand (TRAIL).
Positive_regulation (activated) of caspase-8 associated with necrosis, cancer, apoptosis and death
15) Confidence 0.32 Published 2005 Journal Mol. Cancer Ther. Section Abstract Doc Link 16227396 Disease Relevance 1.39 Pain Relevance 0.13
These results suggest the sequential mechanism of diclofenac-induced apoptosis of HL-60 cells: ROS generation suppresses Akt activity, thereby activating caspase-8, which stimulates Bid cleavage and induces cytochrome c release and the activation of caspase-9 and-3 in a CsA-insensitive mechanism.
Positive_regulation (activating) of caspase-8 in HL-60 associated with apoptosis and diclofenac
16) Confidence 0.31 Published 2004 Journal Free Radic. Biol. Med. Section Abstract Doc Link 15451068 Disease Relevance 0.48 Pain Relevance 0.39
We report that diclofenac, a NSAID, induces growth inhibition and apoptosis of HL-60 cells through modulation of mitochondrial functions regulated by reactive oxygen species (ROS), Akt, caspase-8, and Bid.
Positive_regulation (induces) of caspase-8 in HL-60 associated with cinod, apoptosis and diclofenac
17) Confidence 0.31 Published 2004 Journal Free Radic. Biol. Med. Section Abstract Doc Link 15451068 Disease Relevance 0.53 Pain Relevance 0.42
In this study, justicidin A activated caspase-8 to increase tBid, disrupted mitochondrial membrane potential (Delta psi(m)), and caused the release of cytochrome c and Smac/DIABLO in Hep 3B and Hep G2 cells.
Positive_regulation (activated) of caspase-8 in Hep G2
18) Confidence 0.31 Published 2006 Journal FEBS Lett. Section Abstract Doc Link 16684533 Disease Relevance 0.69 Pain Relevance 0.09
In this study, justicidin A activated caspase-8 to increase tBid, disrupted mitochondrial membrane potential (Delta psi(m)), and caused the release of cytochrome c and Smac/DIABLO in Hep 3B and Hep G2 cells.
Positive_regulation (increase) of caspase-8 in Hep G2
19) Confidence 0.31 Published 2006 Journal FEBS Lett. Section Abstract Doc Link 16684533 Disease Relevance 0.69 Pain Relevance 0.09
N-Acetyl-L-cysteine, an antioxidant, suppresses ROS generation, Akt inactivation, caspase-8 activation, and DNA fragmentation.
Positive_regulation (activation) of caspase-8
20) Confidence 0.29 Published 2004 Journal Free Radic. Biol. Med. Section Abstract Doc Link 15451068 Disease Relevance 0.54 Pain Relevance 0.40

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