INT122485

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Context Info
Confidence 0.46
First Reported 2004
Last Reported 2010
Negated 1
Speculated 0
Reported most in Body
Documents 18
Total Number 18
Disease Relevance 15.78
Pain Relevance 1.12

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

cytosol (CASP9) peptidase activity (CASP9) nucleus (CASP9)
intracellular (CASP9)
Anatomy Link Frequency
lymph node 1
poly 1
B-cell 1
CASP9 (Homo sapiens)
Pain Link Frequency Relevance Heat
Arthritis 6 96.56 Very High Very High Very High
licofelone 7 94.24 High High
rheumatoid arthritis 105 92.52 High High
aspirin 24 77.32 Quite High
Rheumatism 2 64.80 Quite High
agonist 34 63.44 Quite High
cINOD 27 55.32 Quite High
Inflammation 49 50.00 Quite Low
lidocaine 5 50.00 Quite Low
cytokine 32 41.44 Quite Low
Disease Link Frequency Relevance Heat
Apoptosis 675 99.76 Very High Very High Very High
Mouth Cancer 3 99.72 Very High Very High Very High
Infection 162 99.62 Very High Very High Very High
Death 127 99.38 Very High Very High Very High
Experimental Arthritis 1 96.56 Very High Very High Very High
Colon Cancer 32 95.04 Very High Very High Very High
Rheumatoid Arthritis 105 92.52 High High
Pancreatic Cancer 31 91.56 High High
Mycobacterial Infection 141 88.84 High High
Immunotherapy Of Cancer 4 88.60 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Inhibition of caspase-3 prevented the activation of caspase 8, while the inhibition of caspase-9 inhibitor blocked activation of both caspase 3 and 8 by the derivatives.
Negative_regulation (inhibitor) of caspase-9
1) Confidence 0.46 Published 2005 Journal Int. J. Cancer Section Abstract Doc Link 15499625 Disease Relevance 1.02 Pain Relevance 0
Survivin is a 142-amino-acid protein that belongs to the IAP family, and it inhibits the activity of caspase 3, caspase 7, and caspase 9, but not of the upstream initiator protease caspase 8.
Negative_regulation (inhibits) of caspase 9
2) Confidence 0.42 Published 2005 Journal Arthritis Res Ther Section Body Doc Link PMC1065333 Disease Relevance 1.11 Pain Relevance 0.28
These results indicate that the second generation celecoxib derivatives induce apoptosis in human oral cancer lines by the disruption of mitochondrial membrane potential activating caspase 9 and downstream caspase 3 and 8.
Negative_regulation (disruption) of activating caspase 9 associated with mouth cancer and apoptosis
3) Confidence 0.34 Published 2005 Journal Int. J. Cancer Section Abstract Doc Link 15499625 Disease Relevance 0.92 Pain Relevance 0
Inhibitors of caspase-3 and caspase-9 and cyclosporin A, a mitochondrial membrane potential stabilizer, attenuated derivative induced apoptosis.
Negative_regulation (Inhibitors) of caspase-9 associated with apoptosis
4) Confidence 0.34 Published 2005 Journal Int. J. Cancer Section Abstract Doc Link 15499625 Disease Relevance 1.26 Pain Relevance 0.11
Caspase-9 activation was quite similar in both PBS and HMW-HA treatments, except at the dose 75 mJ/cm2 of UVB, which indicated a significant caspase-9 decrease (?
Negative_regulation (decrease) of caspase-9
5) Confidence 0.21 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2660376 Disease Relevance 0.19 Pain Relevance 0
HCE cells treated with HMW-HA exhibited a significant decrease in UVB-induced capase-8 activation but few or no decrease in caspase-9 activation.
Neg (no) Negative_regulation (decrease) of caspase-9
6) Confidence 0.21 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2660376 Disease Relevance 1.25 Pain Relevance 0
Apoptosis by lidocaine was strongly reduced by B-cell lymphoma-2 protein overexpression or caspase-9 deficiency, whereas cells lacking the death receptor pathway components caspase 8 and Fas-associated protein with death domain were not protected and displayed similar apoptotic alterations as the parental cells.
Negative_regulation (deficiency) of caspase-9 in B-cell
7) Confidence 0.19 Published 2007 Journal Anesthesiology Section Body Doc Link 17585225 Disease Relevance 0.07 Pain Relevance 0
Next, we assessed the enzymatic activity of caspase-9 by using a fluorescence based assay in the presence or absence of LEHD-CHO, a specific inhibitor for the caspase-9.
Negative_regulation (inhibitor) of caspase-9
8) Confidence 0.15 Published 2006 Journal Mol Cancer Section Body Doc Link PMC1762018 Disease Relevance 0.63 Pain Relevance 0
It blocks common downstream elements of both the mitochondrial pathway and the death receptor pathway, by directly inhibiting terminal effector caspase-3, caspase-7, and caspase-9 activity[1,2].
Negative_regulation (inhibiting) of caspase-9 associated with death
9) Confidence 0.09 Published 2005 Journal BMC Cancer Section Body Doc Link PMC1266027 Disease Relevance 0.89 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-9
10) Confidence 0.06 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC373449 Disease Relevance 0.47 Pain Relevance 0.13
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-9
11) Confidence 0.06 Published 2004 Journal BMC Pharmacol Section Body Doc Link PMC373449 Disease Relevance 0.52 Pain Relevance 0.13
mainly suppress the intrinsic apoptotic pathway by inhibiting caspase-9 as well
Negative_regulation (inhibiting) of caspase-9 associated with apoptosis
12) Confidence 0.06 Published 2008 Journal PPAR Research Section Body Doc Link PMC2442903 Disease Relevance 1.76 Pain Relevance 0.03
Instead, as can be seen in Figure 3(b), A-beta oligomers activate caspase 9 and this activation is noticeably reduced by the presence of insulin, indicating, once again, that insulin is able to produce a positive protective effect.
Negative_regulation (reduced) of caspase 9
13) Confidence 0.05 Published 2010 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC2871552 Disease Relevance 0.61 Pain Relevance 0
M concentration of caspase-9 inhibitor (Fig. 4D).
Negative_regulation (inhibitor) of caspase-9
14) Confidence 0.05 Published 2005 Journal J Transl Med Section Body Doc Link PMC549525 Disease Relevance 0.75 Pain Relevance 0.04
Induction of apoptosis was related to the recruitment of the intrinsic mitochondrial apoptotic pathway, as shown by loss in mitochondrial membrane potential, cytochrome c release, caspase-9 and 3 activation and poly-(ADP-ribose)polymerase-1 cleavage.
Negative_regulation (loss) of caspase-9 in poly associated with apoptosis
15) Confidence 0.05 Published 2008 Journal Carcinogenesis Section Abstract Doc Link 18033773 Disease Relevance 0.78 Pain Relevance 0.40
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-9 in lymph node associated with apoptosis and infection
16) Confidence 0.04 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC3009592 Disease Relevance 1.42 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-9 associated with apoptosis and death
17) Confidence 0.03 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC2858756 Disease Relevance 1.47 Pain Relevance 0
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 caspase9 associated with apoptosis
18) Confidence 0.01 Published 2009 Journal Mol Biol Rep Section Body Doc Link PMC2941086 Disease Relevance 0.64 Pain Relevance 0

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