INT15542

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Context Info
Confidence 0.41
First Reported 1992
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 20
Total Number 20
Disease Relevance 17.30
Pain Relevance 5.63

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 2
lymph node 1
CASP8 (Homo sapiens)
Pain Link Frequency Relevance Heat
halothane 33 100.00 Very High Very High Very High
narcan 12 99.18 Very High Very High Very High
Morphine 9 98.66 Very High Very High Very High
diclofenac 12 94.76 High High
Intracerebroventricular 3 91.64 High High
Endogenous opioid 6 88.40 High High
Inflammation 42 87.48 High High
cINOD 22 85.76 High High
cytokine 27 81.52 Quite High
antagonist 55 80.16 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 840 99.76 Very High Very High Very High
Infection 188 99.62 Very High Very High Very High
Death 132 99.04 Very High Very High Very High
Cancer 260 98.48 Very High Very High Very High
Chronic Lymphoid Leukemia 30 91.08 High High
Stress 16 91.08 High High
Colon Cancer 31 89.72 High High
Mycobacterial Infection 143 89.40 High High
Inflammatory Breast Neoplasms 1 88.04 High High
Breast Cancer 73 85.88 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Cellular FLICE inhibitory
Negative_regulation (inhibitory) of FLICE
1) Confidence 0.41 Published 2008 Journal PPAR Research Section Body Doc Link PMC2442903 Disease Relevance 1.50 Pain Relevance 0
Additional intracellular factors leading to TRAIL-resistance affect the caspase 8/c-FLIP ratio, such as loss of caspase 8 and caspase 10 due to mutations or gene methylation, CARP-dependent degradation of active caspase 8 and changes in caspase 8 or c-FLIP expression levels.
Negative_regulation (loss) of caspase 8
2) Confidence 0.37 Published 2004 Journal Drug Resist. Updat. Section Abstract Doc Link 15790545 Disease Relevance 1.05 Pain Relevance 0.07
Ac-IETD-CHO, a caspase-8 inhibitor, suppresses Bid cleavage and DNA fragmentation. z-VAD-fmk, a universal caspase inhibitor, but not cyclosporin A (CsA), an inhibitor of mitochondrial membrane permeability transition, suppresses DNA fragmentation.
Negative_regulation (inhibitor) of caspase-8 in cleavage
3) Confidence 0.36 Published 2004 Journal Free Radic. Biol. Med. Section Abstract Doc Link 15451068 Disease Relevance 0.52 Pain Relevance 0.39
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.
Negative_regulation (inhibitor) of caspase-8 in cleavage associated with apoptosis
4) Confidence 0.32 Published 2009 Journal Int. J. Oncol. Section Abstract Doc Link 19360361 Disease Relevance 0.63 Pain Relevance 0.26
Finally, the icv administration of a 15-micrograms naloxone dose appeared to reverse completely the MACH reduction elicited by TCES (n = 8, P less than 0.01).
Negative_regulation (reduction) of MACH associated with narcan and halothane
5) Confidence 0.29 Published 1992 Journal Anesthesiology Section Abstract Doc Link 1736702 Disease Relevance 0 Pain Relevance 0.69
MACH was decreased markedly in stimulated animals (TCES, n = 10) in comparison with sham-operated nonstimulated rats (controls, n = 10): MACH = 0.60 +/- 0.15, mean +/- SD, versus 1.07 +/- 0.05 vol%, P less than 0.001.
Negative_regulation (decreased) of MACH associated with halothane
6) Confidence 0.29 Published 1992 Journal Anesthesiology Section Abstract Doc Link 1736702 Disease Relevance 0 Pain Relevance 0.85
The magnitude of MACH reduction was significantly increased with the cumulative duration of stimulation.
Negative_regulation (reduction) of MACH associated with halothane
7) Confidence 0.29 Published 1992 Journal Anesthesiology Section Abstract Doc Link 1736702 Disease Relevance 0 Pain Relevance 0.88
N-Acetyl-L-cysteine, an antioxidant, suppresses ROS generation, Akt inactivation, caspase-8 activation, and DNA fragmentation.
Negative_regulation (suppresses) of caspase-8
8) Confidence 0.26 Published 2004 Journal Free Radic. Biol. Med. Section Abstract Doc Link 15451068 Disease Relevance 0.55 Pain Relevance 0.40
The initiator caspase-8 was not altered, but FLIP(L) (Fas-associated protein with death domain-like interleukin-1beta-converting enzyme-inhibitory protein), a dominant inhibitor of caspase-8, was increased in LT addicts (19%).
Negative_regulation (inhibitor) of caspase-8 associated with death
9) Confidence 0.25 Published 2008 Journal Neuroscience Section Abstract Doc Link 18834930 Disease Relevance 1.22 Pain Relevance 0.43
However, blockade of morphine-induced cell death by beta-arrestin2 seems to be dependent on the inhibition of caspase-8, as inhibition of beta-arrestin2 and morphine treatment significantly enhanced the levels of cleaved caspase-8.
Negative_regulation (inhibition) of caspase-8 associated with death and morphine
10) Confidence 0.23 Published 2009 Journal Neoplasma Section Abstract Doc Link 19239323 Disease Relevance 1.11 Pain Relevance 1.31
Without excluding alternative possibilities, the anti-apoptotic property of HMW-HA in our model system appears to be mediated by the inhibition of the extrinsic pathway, notably by caspase-8 inhibition.
Negative_regulation (inhibition) of caspase-8 associated with apoptosis
11) Confidence 0.19 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2660376 Disease Relevance 0.89 Pain Relevance 0.15
A number of new targets such as hypothetical proteins, CAP4, SALL1, ZONAB, and SUMO1 were identified.
Negative_regulation (number) of CAP4
12) Confidence 0.16 Published 2008 Journal Mol Cancer Section Body Doc Link PMC2263075 Disease Relevance 0.78 Pain Relevance 0.04
inhibitor of the extrinsic apoptotic pathway by preventing caspase-8
Negative_regulation (preventing) of caspase-8 associated with apoptosis
13) Confidence 0.09 Published 2008 Journal PPAR Research Section Body Doc Link PMC2442903 Disease Relevance 1.63 Pain Relevance 0.03
affected the levels of an endogenous caspase-8 inhibitor, c-FLIP (caspase-8
Negative_regulation (inhibitor) of caspase-8
14) Confidence 0.09 Published 2008 Journal PPAR Research Section Body Doc Link PMC2408681 Disease Relevance 1.45 Pain Relevance 0
affected the levels of an endogenous caspase-8 inhibitor, c-FLIP (caspase-8
Negative_regulation (inhibitor) of caspase-8
15) Confidence 0.06 Published 2008 Journal PPAR Research Section Body Doc Link PMC2408681 Disease Relevance 1.45 Pain Relevance 0
To determine whether apoptosis was mediated by extrinsic or intrinsic pathways we exposed lymph node cells from progressor animals taken at week 12 post infection to small molecule inhibitors of caspase-8 or caspase-9, respectively.
Negative_regulation (inhibitors) of caspase-8 in lymph node associated with apoptosis and infection
16) Confidence 0.06 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC3009592 Disease Relevance 1.36 Pain Relevance 0
Z-DEVD-FMK (a caspase-3 inhibitor), Z-IETD-FMK (a caspase-8 inhibitor) and Z-LEHD-FMK (a caspase-9 inhibitor) were purchased from R&D Systems, Inc.
Negative_regulation (inhibitor) of caspase-8
17) Confidence 0.06 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC373449 Disease Relevance 0.52 Pain Relevance 0.13
These results indicate that mitochondrial-mediated apoptosis in HepG2 cells, triggered by DLS, is predominantly associated with down-regulation of the Bcl-2/Bax expression ratio.Fig. 3Western blot analysis of the expression levels of caspase3, caspase9, Bcl-2, Bax, caspase8 and DR5 with the treatment of DLS for 24 h (All the experiments were repeated four times.)Fig. 4Bcl-2, Bax, DR5 protein expression in HepG2 cells (×200). a, c, e Immunocytochemistry of Bcl-2, Bax and DR5 staining in HepG2 cells for 24 h of treatment without DLS. b, d, f Immunocytochemistry of Bcl-2, Bax and DR5 staining in HepG2 cells for 24 h of treatment with 25 ?
Negative_regulation (regulation) of caspase8 associated with apoptosis
18) Confidence 0.05 Published 2009 Journal Mol Biol Rep Section Body Doc Link PMC2941086 Disease Relevance 0.64 Pain Relevance 0
BIRC2 encodes cIAP1, which is involved in inhibiting caspase-8 activation [39].
Negative_regulation (inhibiting) of caspase-8
19) Confidence 0.04 Published 2010 Journal BMC Genomics Section Body Doc Link PMC2996966 Disease Relevance 0.52 Pain Relevance 0
In order to determine if the nuoG mutant induces apoptosis via the extrinsic (i.e., death receptor mediated), or the intrinsic (i.e., mitochondrial) pathway [29], cells were treated with Caspase-8 and Caspase-9 inhibitors, respectively.
Negative_regulation (inhibitors) of Caspase-8 associated with apoptosis and death
20) Confidence 0.03 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2858756 Disease Relevance 1.48 Pain Relevance 0

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