INT80220

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Context Info
Confidence 0.58
First Reported 1999
Last Reported 2011
Negated 3
Speculated 1
Reported most in Body
Documents 71
Total Number 72
Disease Relevance 57.73
Pain Relevance 7.86

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

mitochondrion (Bcl2) cell morphogenesis (Bcl2) endoplasmic reticulum (Bcl2)
intracellular (Bcl2) cytoplasm (Bcl2) cell proliferation (Bcl2)
Anatomy Link Frequency
brain 4
head 2
liver 2
endothelial cell 2
cleft 1
Bcl2 (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 325 99.40 Very High Very High Very High
Paracetamol 58 99.40 Very High Very High Very High
Spinal cord 21 99.18 Very High Very High Very High
ischemia 47 98.88 Very High Very High Very High
cva 51 97.84 Very High Very High Very High
Leflunomide 20 97.52 Very High Very High Very High
Hippocampus 15 96.76 Very High Very High Very High
anesthesia 57 93.28 High High
antagonist 23 91.84 High High
cINOD 62 90.08 High High
Disease Link Frequency Relevance Heat
Apoptosis 1988 100.00 Very High Very High Very High
Targeted Disruption 614 99.96 Very High Very High Very High
Death 280 99.92 Very High Very High Very High
Injury 424 99.88 Very High Very High Very High
Hyperplasia 18 99.74 Very High Very High Very High
Chronic Lymphoid Leukemia 98 99.70 Very High Very High Very High
Aging 30 99.64 Very High Very High Very High
Hepatotoxicity 22 99.48 Very High Very High Very High
Repression 12 99.44 Very High Very High Very High
Fibrosis 50 99.42 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In conclusion, GrTP supplementation attenuated hepatotoxicity by normalizing Cox-2 and Bcl-2 activation, suggesting a potential use for GrTP in treatng APAP toxicity.
Positive_regulation (activation) of Bcl-2 associated with toxicity, paracetamol and hepatotoxicity
1) Confidence 0.58 Published 2008 Journal Dig. Dis. Sci. Section Abstract Doc Link 18373199 Disease Relevance 0.68 Pain Relevance 0.62
GrTP supplementation normalized APAP induced Cox-2 expression and Bcl-2 activation (P < 0.01), as evidenced by immunohistochemistry and Western blot analyses.
Positive_regulation (activation) of Bcl-2 associated with paracetamol
2) Confidence 0.58 Published 2008 Journal Dig. Dis. Sci. Section Abstract Doc Link 18373199 Disease Relevance 0.66 Pain Relevance 0.85
The second type involved the activation of BCL-2 (Gascoyne et al 1997).
Positive_regulation (activation) of BCL-2
3) Confidence 0.49 Published 2007 Journal Biologics : Targets & Therapy Section Body Doc Link PMC2721318 Disease Relevance 1.36 Pain Relevance 0
Cytoplasmic and nuclear beta-catenin are overexpressed in many of these lesions and Bcl-2, which inhibits apoptosis, may also be elevated during the course of intestinal tumorigenesis.
Spec (may) Positive_regulation (elevated) of Bcl-2 associated with apoptosis
4) Confidence 0.49 Published 1999 Journal Carcinogenesis Section Abstract Doc Link 10223192 Disease Relevance 0.75 Pain Relevance 0.25
AS Bcl-2-mediated downregulation of Bcl-2 augments anticancer drug-induced signal transduction pathways leading to apoptosis, which is associated with the activation of proapoptotic proteins such as Bax and the suppression of antiapoptotic proteins such as Bcl-2 and pAkt.
Positive_regulation (activation) of Bcl-2 associated with apoptosis
5) Confidence 0.46 Published 2005 Journal Breast Cancer Res Section Body Doc Link PMC1410745 Disease Relevance 0.88 Pain Relevance 0
B–mediated upregulation of antiapoptotic bcl-2, bcl-xL, and bfl-1/A1 genes [7,9].
Positive_regulation (upregulation) of bcl-2
6) Confidence 0.45 Published 2007 Journal PLoS Pathogens Section Body Doc Link PMC1781481 Disease Relevance 0.51 Pain Relevance 0
Upregulation of Bcl-2 and downregulation of Fas in injured fB-/- brains
Positive_regulation (Upregulation) of Bcl-2 in brains
7) Confidence 0.43 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1540436 Disease Relevance 0.94 Pain Relevance 0.09
In addition, increased sensitivity to anticancer drugs after treatment with AS Bcl-2 is observed in solid tumors, such as breast, prostate, lung, and gastric cancer [11-14].
Positive_regulation (increased) of Bcl-2 in lung associated with solid tumor and stomach cancer
8) Confidence 0.43 Published 2005 Journal Breast Cancer Res Section Body Doc Link PMC1410745 Disease Relevance 0.98 Pain Relevance 0
B functions in mature B cells as a survival factor by mediating the upregulation of several antiapoptotic proteins, including A1, Bcl-2, and Bcl-xL [7,57].
Positive_regulation (upregulation) of Bcl-2 in mature B cells
9) Confidence 0.42 Published 2007 Journal PLoS Pathogens Section Body Doc Link PMC1781481 Disease Relevance 0.35 Pain Relevance 0
Chemically damaged cells undergo a p53-dependent apoptotic pathway that involves upregulation of p53 transcripts such as the pro-apoptotic Bcl2 family members and p53 translocation to the mitochondria, resulting in neutralization of the anti-apoptotic members Bcl-xL and Bcl-2 [26].
Positive_regulation (upregulation) of Bcl2 associated with apoptosis
10) Confidence 0.41 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2944824 Disease Relevance 1.11 Pain Relevance 0
AS Bcl-2 ODNs induced splenomegaly in association with increased serum IL-12, which was attenuated by methylation of the CpG motifs of AS Bcl-2; however, methylated CpG failed to negate the increased antitumor effect of AS Bcl-2.
Positive_regulation (increased) of Bcl-2 associated with splenomegaly
11) Confidence 0.40 Published 2005 Journal Breast Cancer Res Section Abstract Doc Link PMC1410745 Disease Relevance 0.26 Pain Relevance 0
Hypothyroid rats display increased caspase 3 activity and increased levels of pro-apoptotic Bcl2 members and decreased Bcl2 family members in the cortex [7] cerebellum [8], and hippocampus [9].
Positive_regulation (increased) of Bcl2 in cerebellum associated with hippocampus and apoptosis
12) Confidence 0.35 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2944824 Disease Relevance 1.21 Pain Relevance 0.05
The proliferative phase is marked by high mitotic index, and Ki-67 indicative of rapid cellular proliferation, as well as elevated levels of BCL2, an anti-apoptotic factor, presumably involved in stabilizing the cells during this period and allowing for normal physiologic growth in preparation for implantation and pregnancy (153).
Positive_regulation (elevated) of BCL2 associated with apoptosis and hyperplasia
13) Confidence 0.35 Published 2006 Journal Nucleic Acids Research Section Body Doc Link PMC1361617 Disease Relevance 0.66 Pain Relevance 0
COX-2 appears to: (a) play a key role in the release and activity of proangiogenic proteins; (b) result in the production of eicosanoid products TXA2, PGI2, PGE2 that directly stimulate endothelial cell migration and angiogenesis in vivo, and (c) result in enhanced tumor cell, and possibly, vascular endothelial cell survival by upregulation of the antiapoptotic proteins Bcl-2 and/or activation of PI3K-Akt.
Positive_regulation (activation) of Bcl-2 in endothelial cell associated with cancer
14) Confidence 0.33 Published 2003 Journal Prog Exp Tumor Res Section Abstract Doc Link 12795055 Disease Relevance 0.33 Pain Relevance 0
COX-2 appears to: (a) play a key role in the release and activity of proangiogenic proteins; (b) result in the production of eicosanoid products TXA2, PGI2, PGE2 that directly stimulate endothelial cell migration and angiogenesis in vivo, and (c) result in enhanced tumor cell, and possibly, vascular endothelial cell survival by upregulation of the antiapoptotic proteins Bcl-2 and/or activation of PI3K-Akt.
Positive_regulation (upregulation) of Bcl-2 in endothelial cell associated with cancer
15) Confidence 0.33 Published 2003 Journal Prog Exp Tumor Res Section Abstract Doc Link 12795055 Disease Relevance 0.34 Pain Relevance 0
In bright contrast, splenocytes of HS mice showed remarkably divergent values in their Bax and Bcl-2 protein expression levels at t = 0 hours, t = 24 hours, and t = 72 hours after hemorrhage (Figure 4b, left and middle).
Positive_regulation (levels) of Bcl-2 associated with cva and hemorrhagic shock
16) Confidence 0.30 Published 2008 Journal Crit Care Section Body Doc Link PMC2374615 Disease Relevance 0.85 Pain Relevance 0.11
HV68 latency in splenocytes requires the vBcl-2-mediated inhibition of the host autophagy machinery.
Positive_regulation (requires) of vBcl-2
17) Confidence 0.29 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.22 Pain Relevance 0
However, by 28 days postinfection, the titers of vBcl-2 mutant viruses, including the independently derived vBcl-2??
Neg (independently) Positive_regulation (derived) of vBcl-2
18) Confidence 0.29 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.30 Pain Relevance 0
HV68 in cultured cells (Figure 6A and S4), suggesting that the vBcl-2-mediated inhibition of autophagy and apoptosis are not required for lytic replication in vitro, which is consistent with the previous reports that ?
Neg (not) Positive_regulation (required) of vBcl-2 associated with apoptosis
19) Confidence 0.29 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.54 Pain Relevance 0
1-7) of vBcl-2 forms a globular structure, where helices 2, 3, 4, and 5 define an extended hydrophobic surface cleft allowing vBcl-2 to associate with BH3 domains, especially those of Bak and Bax [25],[28].
Positive_regulation (allowing) of vBcl-2 in cleft
20) Confidence 0.29 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.70 Pain Relevance 0

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