INT101641

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Context Info
Confidence 0.54
First Reported 2002
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 25
Total Number 26
Disease Relevance 20.30
Pain Relevance 2.23

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)
Anatomy Link Frequency
cleavage 2
poly 1
spleen 1
MDA-MB-231 1
Mcl1 (Mus musculus)
Pain Link Frequency Relevance Heat
Paracetamol 12 99.78 Very High Very High Very High
cva 175 99.40 Very High Very High Very High
antagonist 10 91.24 High High
Inflammation 72 91.12 High High
chemokine 154 87.36 High High
cINOD 31 78.48 Quite High
tolerance 21 68.84 Quite High
rheumatoid arthritis 52 56.20 Quite High
aspirin 8 55.84 Quite High
Arthritis 5 48.56 Quite Low
Disease Link Frequency Relevance Heat
Apoptosis 1003 100.00 Very High Very High Very High
Hemorrhagic Shock 357 99.40 Very High Very High Very High
Hemorrhage 175 99.40 Very High Very High Very High
Repression 36 99.18 Very High Very High Very High
Colon Cancer 187 99.04 Very High Very High Very High
Death 137 98.48 Very High Very High Very High
Adhesions 259 98.46 Very High Very High Very High
Cancer 613 98.16 Very High Very High Very High
Breast Cancer 49 97.92 Very High Very High Very High
Pancreatic Cancer 85 97.80 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Importantly, we previously reported that MCL1, IFITM1, and USP18 are co-expressed with STAT1 in the IR- and IFN-resistant nu61 tumor [17].
Gene_expression (expressed) of MCL1 associated with cancer
1) Confidence 0.54 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2688034 Disease Relevance 0.69 Pain Relevance 0
Importantly, we previously reported that MCL1, IFITM1, and USP18 are co-expressed with STAT1 in the IR- and IFN-resistant nu61 tumor [17].
Gene_expression (-) of MCL1 associated with cancer
2) Confidence 0.54 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2688034 Disease Relevance 0.69 Pain Relevance 0
To prove the involvement of mitochondria-related proteins in the downstream apoptotic signalling cascade in spleen after HS, we investigated the protein expression of pro-apoptotic Bax as well as anti-apoptotic Bcl-2 and Mcl-1 by semi-quantitative Western blot analysis.
Spec (investigated) Gene_expression (expression) of Mcl-1 in spleen associated with hemorrhagic shock and apoptosis
3) Confidence 0.53 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 1.07 Pain Relevance 0.08
and CD95, and the intrinsic mitochondria-related apoptotic pathway by the differential expression of mitochondrial Bax, Bcl-2, and Mcl-1 proteins in regard to the HS-induced risk for post-traumatic immunosuppression.


Gene_expression (expression) of Mcl-1 associated with hemorrhagic shock and apoptosis
4) Confidence 0.53 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 0.90 Pain Relevance 0
However, consistent expression levels of the Mcl-1 protein were detectable in sham-operated and control animals, except for an increased expression at t = 24 hours after hemorrhage.
Gene_expression (expression) of Mcl-1 associated with cva
5) Confidence 0.41 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 0.92 Pain Relevance 0.16
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.
Gene_expression (expression) of Mcl-1 associated with apoptosis
6) Confidence 0.41 Published 2008 Journal Crit Care Section Abstract Doc Link PMC2374615 Disease Relevance 1.66 Pain Relevance 0.08
Additionally, the time course of anti-apoptotic Mcl-1 expression is in line with the appropriate caspase-3/7 and caspase-9 activities and correlates with the HS-induced DNA fragmentation demonstrated in Figure 2.


Gene_expression (expression) of Mcl-1 associated with hemorrhagic shock and apoptosis
7) Confidence 0.41 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 1.08 Pain Relevance 0.15
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).
Gene_expression (expression) of Mcl-1 associated with cva, apoptosis and hemorrhagic shock
8) Confidence 0.41 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 1.02 Pain Relevance 0.16
However, consistent expression levels of the Mcl-1 protein were detectable in sham-operated and control animals, except for an increased expression at t = 24 hours after hemorrhage.
Neg (except) Gene_expression (detectable) of Mcl-1 associated with cva
9) Confidence 0.41 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 0.93 Pain Relevance 0.16
The proapoptotic effect of rolipram was associated with decreased levels of the prosurvival protein Mcl-1 and increased caspase-3 cleavage.
Gene_expression (levels) of Mcl-1 in cleavage
10) Confidence 0.37 Published 2010 Journal J. Leukoc. Biol. Section Abstract Doc Link 20103769 Disease Relevance 0.76 Pain Relevance 0.28
Enhanced Mcl-1 but not Bcl-2 expression alleviated indomethacin-increased caspase-3 activity.
Gene_expression (expression) of Mcl-1
11) Confidence 0.30 Published 2009 Journal Biochem. Biophys. Res. Commun. Section Abstract Doc Link 19250643 Disease Relevance 0.72 Pain Relevance 0.16
Nonetheless, co-expression of Bcl-2, Bcl-xL, Mcl-1, or A1 with Bax and Bak can suppress death induced in yeast [30], thus reconstituting key aspects of the mammalian apoptotic machinery.
Gene_expression (expression) of Mcl-1 associated with apoptosis and death
12) Confidence 0.27 Published 2010 Journal PLoS Pathogens Section Body Doc Link PMC3009601 Disease Relevance 0.43 Pain Relevance 0
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-?
Gene_expression (levels) of Mcl-1 associated with apoptosis
13) Confidence 0.24 Published 2007 Journal Cancer Informatics Section Body Doc Link PMC2675840 Disease Relevance 0.89 Pain Relevance 0.04
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).
Gene_expression (overexpression) of Mcl-1
14) Confidence 0.22 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.
Gene_expression (expression) of Mcl-1
15) Confidence 0.19 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.58 Pain Relevance 0.03
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).
Gene_expression (levels) of Mcl-1 associated with repression
16) Confidence 0.19 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.45 Pain Relevance 0
Mcl-1 and Bcl-2 expression was sustained in anoikis-resistant control cells cultured in suspension on poly-HEMA.
Gene_expression (expression) of Mcl-1 in poly
17) Confidence 0.19 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.51 Pain Relevance 0.04
Moreover, our analyses indicate focal adhesion protein loss of activity and degradation temporally precedes alterations in Mcl-1 and Bim expression levels, which themselves regulate activation of the caspase family members (Figure 9).
Gene_expression (expression) of Mcl-1 associated with adhesions
18) Confidence 0.19 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 1.30 Pain Relevance 0.03
However, no changes were found in the antiapoptotic proteins Mcl-1, IAP-1, XIAP, survivin and the proapoptotic protein Bax (Fig 5B).
Neg (no) Gene_expression (found) of Mcl-1
19) Confidence 0.18 Published 2010 Journal BMC Cancer Section Body Doc Link PMC2883966 Disease Relevance 0.35 Pain Relevance 0
To confirm that apoptosis occurs in pancreatic cancer cells following LOX inhibitor treatment, we conducted further studies that showed that LOX inhibitors reduce expression of Bcl-2 and Mcl-1 and induce activation of caspase-3 and -9 as well as cleavage of the caspase-3 target, PARP [53,54].


Gene_expression (expression) of Mcl-1 in cleavage associated with pancreatic cancer and apoptosis
20) Confidence 0.18 Published 2003 Journal Mol Cancer Section Body Doc Link PMC149414 Disease Relevance 1.12 Pain Relevance 0.03

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