INT158329

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Context Info
Confidence 0.32
First Reported 2006
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 9
Total Number 10
Disease Relevance 7.53
Pain Relevance 0.54

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

cell differentiation (Mcl1) mitochondrion (Mcl1) nucleus (Mcl1)
cytoplasm (Mcl1)
Mcl1 (Mus musculus)
Pain Link Frequency Relevance Heat
cva 50 99.40 Very High Very High Very High
Inflammation 52 81.32 Quite High
cINOD 12 78.84 Quite High
chemokine 49 71.68 Quite High
tolerance 22 68.84 Quite High
rheumatoid arthritis 52 56.20 Quite High
Arthritis 5 49.92 Quite Low
Inflammatory mediators 2 39.12 Quite Low
COX-2 inhibitor 3 27.88 Quite Low
cytokine 57 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 309 100.00 Very High Very High Very High
Hemorrhagic Shock 102 100.00 Very High Very High Very High
Repression 10 99.42 Very High Very High Very High
Hemorrhage 50 99.40 Very High Very High Very High
Death 50 92.64 High High
Injury 35 89.48 High High
Cancer 213 87.08 High High
Acute Renal Failure 1 85.92 High High
Toxicity 19 84.92 Quite High
INFLAMMATION 63 81.32 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Solely at t = 24 hours, expression of the anti-apoptotic Mcl-1 protein shows a significant increase when compared with sham-operated and control animals.
Positive_regulation (increase) of Gene_expression (expression) of Mcl-1 associated with apoptosis
1) Confidence 0.32 Published 2008 Journal Crit Care Section Abstract Doc Link PMC2374615 Disease Relevance 1.67 Pain Relevance 0.08
In contrast, Mcl-1 expression in splenocytes of HS-treated animals was significantly enhanced at t = 24 hours after hemorrhage when compared with t = 0 hours and t = 72 hours, supporting our hypothesis that splenic cells are rescued from apoptosis by potential involvement of Mcl-1 (Figure 4b,c, right).
Positive_regulation (enhanced) of Gene_expression (expression) of Mcl-1 associated with cva, apoptosis and hemorrhagic shock
2) Confidence 0.32 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 1.04 Pain Relevance 0.16
Enhanced Mcl-1 but not Bcl-2 expression alleviated indomethacin-increased caspase-3 activity.
Positive_regulation (Enhanced) of Gene_expression (expression) of Mcl-1
3) Confidence 0.19 Published 2009 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 19250643 Disease Relevance 0.72 Pain Relevance 0.16
PGE2 may reduce apoptotic rates by increasing levels of antiapoptotic proteins like Bcl-2 (Sheng et al. 1998), Mcl-1 or other key mediators as NF-?
Positive_regulation (mediators) of Gene_expression (levels) of Mcl-1 associated with apoptosis
4) Confidence 0.18 Published 2007 Journal Cancer Informatics Section Body Doc Link PMC2675840 Disease Relevance 0.90 Pain Relevance 0.04
Interestingly, Bim repression resulted in the concomitant increase in Mcl-1 and Bcl-2 levels in CXCL12-producing, but not wild-type, cells mirroring our results seen in HT29 cells (Figure 4D).
Positive_regulation (increase) of Gene_expression (levels) of Mcl-1 associated with repression
5) Confidence 0.17 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.45 Pain Relevance 0
Studies of the phenotypic cell signaling profiles of rituximab sensitive and resistant cell clones demonstrate that rituximab failed to chemosensitize rituximab-resistant clones which exhibited constitutively hyperactivation of NF-kB and ERK1/2 pathways, which leads to overexpression of resistance factors such as Bcl-2, Bcl-xL, and Mcl-1 (Jazirehi et al 2004, 2005, 2007).
Positive_regulation (hyperactivation) of Gene_expression (overexpression) of Mcl-1
6) Confidence 0.15 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721318 Disease Relevance 0.07 Pain Relevance 0
Studies of the phenotypic cell signaling profiles of rituximab sensitive and resistant cell clones demonstrate that rituximab failed to chemosensitize rituximab-resistant clones which exhibited constitutively hyperactivation of NF-kB and ERK1/2 pathways, which leads to overexpression of resistance factors such as Bcl-2, Bcl-xL, and Mcl-1 (Jazirehi et al 2004, 2005, 2007).
Positive_regulation (overexpression) of Gene_expression (overexpression) of Mcl-1
7) Confidence 0.15 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721318 Disease Relevance 0.06 Pain Relevance 0
As shown in Figure 4D, immunoblot analysis showed a marked loss of Mcl-1 and Bcl-2 expression coincident with the marked increase in Bim protein levels in anoikis sensitive CXCL12- expressing cells.
Positive_regulation (increase) of Gene_expression (expression) of Mcl-1
8) Confidence 0.12 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.58 Pain Relevance 0.04
Overexpression of Bcl-2, Bcl-xL or Mcl-1 has been shown to prevent drug-induced apoptosis in several cell lines [6,7].


Positive_regulation (Overexpression) of Gene_expression (Overexpression) of Mcl-1 associated with apoptosis
9) Confidence 0.08 Published 2006 Journal Theor Biol Med Model Section Body Doc Link PMC1508139 Disease Relevance 1.03 Pain Relevance 0.03
The expression of Mcl-1 could be induced by treatment with TNF-?
Positive_regulation (induced) of Gene_expression (expression) of Mcl-1
10) Confidence 0.06 Published 2007 Journal Arthritis Res Ther Section Body Doc Link PMC2246247 Disease Relevance 1.01 Pain Relevance 0.03

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