INT20603
From wiki-pain
(Difference between revisions)
Latest revision as of 02:13, 24 September 2012
| Context
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Info
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| Confidence
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0.67
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| First Reported
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1983
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| Last Reported
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2010
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| Negated
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0
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| Speculated
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0
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| Reported most in
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Abstract
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| Documents
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40
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| Total Number
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40
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| Disease Relevance
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32.61
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| Pain Relevance
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11.44
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[edit] Sentences Mentioned In
| Key:
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Protein
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Mutation
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Event
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Anatomy
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Negation
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Speculation
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Pain term
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Disease term
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| Sulindac sulfide up-regulated DR5 and activated the proximal caspase 8 in various different colon and prostate cancer cell lines.
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| 1)
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Confidence
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0.67
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Published
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2001
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Journal
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Cancer Res.
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Section
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Abstract
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Doc Link
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11559570
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Disease Relevance
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1.39
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Pain Relevance
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0.08
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| Induction of apoptosis by pectenotoxin-2 is mediated with the induction of DR4/DR5, Egr-1 and NAG-1, activation of caspases and modulation of the Bcl-2 family in p53-deficient Hep3B hepatocellular carcinoma cells.
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| 2)
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Confidence
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0.67
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Published
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2008
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Journal
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Oncol. Rep.
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Section
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Title
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Doc Link
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18202802
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Disease Relevance
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0.94
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Pain Relevance
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0.05
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| SC-'236 also upregulates DR5 in both Bax-proficient and Bax-deficient cells but Apo2L/TRAIL potentiates SC-'236-mediated apoptosis and caspases-8 and -3 activation in both Bax-proficient and Bax-deficient cells.
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| 3)
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Confidence
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0.67
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Published
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2002
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Journal
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Oncogene
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Section
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Abstract
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Doc Link
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12203115
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Disease Relevance
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1.12
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Pain Relevance
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0.36
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| We further show that sulindac sulfide and SC-'236-induced DR5 upregulation occurs independent of the COX inhibitory effects of these NSAIDs.
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| 4)
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Confidence
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0.67
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Published
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2002
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Journal
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Oncogene
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Section
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Abstract
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Doc Link
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12203115
|
Disease Relevance
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1.06
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Pain Relevance
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0.46
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| We show that sulindac sulfide and SC-'236-induced apoptosis is coupled with upregulation of DR5, caspase 8 activation and Bid cleavage.
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| 5)
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Confidence
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0.67
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Published
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2002
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Journal
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Oncogene
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Section
|
Abstract
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Doc Link
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12203115
|
Disease Relevance
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1.02
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Pain Relevance
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0.46
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| For example, sulindac sulfide upregulates DR5 in both Bax-deficient and proficient cells, but Apo2L/TRAIL efficiently potentiates sulindac sulfide-induced apoptosis as well as activation of caspase-8, -9 and -3 only in Bax-proficient cells.
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| 6)
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Confidence
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0.58
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Published
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2002
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Journal
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Oncogene
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Section
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Abstract
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Doc Link
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12203115
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Disease Relevance
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1.08
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Pain Relevance
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0.40
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| Sulindac sulfide specifically up-regulated the DR5 levels but had no effect on the levels of other DRs including DR4, Fas, and tumor necrosis factor receptor 1.
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| 7)
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Confidence
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0.49
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Published
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2001
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Journal
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Cancer Res.
|
Section
|
Abstract
|
Doc Link
|
11559570
|
Disease Relevance
|
1.59
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Pain Relevance
|
0.07
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|
| The salient points of various stages of this study are: low frequency of HLA-B14 antigen with, in contrast, high frequency of the HLA-DR5 antigen of the major histocompatibility system.
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| These findings demonstrate that b-end enhances NK activity and IFN production of purified LGL, and suggests that b-end might bind to an opioid receptor on LGL that can be blocked by naloxone.
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| 9)
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Confidence
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0.49
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Published
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1986
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Journal
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J. Immunol.
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Section
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Abstract
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Doc Link
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2934481
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Disease Relevance
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0
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Pain Relevance
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0.26
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| At effector:target cell ratios of 100:1, 33:1 and 11:1 leucine-enkephalin significantly (p less than 0.05) enhanced NK activity at dilutions of 10(-6), 10(-8), 10(-10), and 10(-14) mg/ml.
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| The enhancement of NK activity with beta-endorphin increased at all E:T ratios tested.
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| 11)
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Confidence
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0.49
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Published
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1983
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Journal
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J. Immunol.
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Section
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Abstract
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Doc Link
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6300232
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Disease Relevance
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0
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Pain Relevance
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0.68
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| At effector:target cell ratios of 11:1 methionine-enkephalin significantly (P less than 0.05) enhanced NK activity at dilutions of 10(-6), 10(-8), 10(-10), and 10(-14) mg/ml, while leucine-enkephalin significantly (P less than 0.05) enhanced NK activity at dilutions of 10(-4), 10(-6), 10(-8), 10(-10), and 10(-14) mg/ml.
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| In fact, both doses of tramadol were able to prevent surgery-induced NK activity suppression, while the drug significantly increased NK activity in normal non-operated animals.
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| At effector:target cell ratios of 11:1 methionine-enkephalin significantly (P less than 0.05) enhanced NK activity at dilutions of 10(-6), 10(-8), 10(-10), and 10(-14) mg/ml, while leucine-enkephalin significantly (P less than 0.05) enhanced NK activity at dilutions of 10(-4), 10(-6), 10(-8), 10(-10), and 10(-14) mg/ml.
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| It was suggested that the clinical response would be expected in case of increasing of CD16 cells or CD25 cells and augmentation of NK or LAK activity.
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| indicating a critical role of DR5 induction in this death process.
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| ligands to induce DR5 or downregulate c-FLIP [34].
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| 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).
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| Overexpression of DR5 receptor and its ligand (TRAIL) in chondrocyte-like cells suggested activation of programmed cell death, as also demonstrated by TUNEL-positive cells.
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| Figure 6 shows that although wild-type DREAM causes activation of the DR3- and DR5-containing promoters, DREAM mutants bearing the mutations L47,52V in the first LCD or L155V in the second LCD did not activate basal or ligand-dependent expression of the DR3 and RAR?
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This test has worked.
