INT172855

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.32
First Reported 2003
Last Reported 2010
Negated 3
Speculated 2
Reported most in Body
Documents 37
Total Number 39
Disease Relevance 23.41
Pain Relevance 1.09

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
groove 2
tail 1
spleens 1
cleft 1
Bcl2 (Mus musculus)
Pain Link Frequency Relevance Heat
antagonist 13 100.00 Very High Very High Very High
Chronic pancreatitis 1 97.12 Very High Very High Very High
dexamethasone 94 93.36 High High
withdrawal 2 91.92 High High
Inflammatory mediators 4 91.84 High High
Multiple sclerosis 17 88.80 High High
Inflammation 46 88.68 High High
Spinal cord 98 87.68 High High
cytokine 29 85.68 High High
imagery 22 72.92 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 2505 100.00 Very High Very High Very High
Death 160 100.00 Very High Very High Very High
Wrinkles 10 100.00 Very High Very High Very High
Infection 984 99.36 Very High Very High Very High
Pancreatic Cancer 125 99.04 Very High Very High Very High
Epstein-barr Virus 48 98.96 Very High Very High Very High
Adhesions 14 98.60 Very High Very High Very High
Starvation 64 98.08 Very High Very High Very High
Spinal Cord Injury 122 98.00 Very High Very High Very High
Viral Infection 248 97.16 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
As shown in Fig. 5, treatment with AS Bcl-2 and DOX markedly suppressed Bcl-2 expression from that observed after treatment with DOX alone.
Bcl-2 Binding (treatment) of
1) Confidence 0.32 Published 2005 Journal Breast Cancer Res Section Body Doc Link PMC1410745 Disease Relevance 0.42 Pain Relevance 0
Effect of combined treatment with AS Bcl-2 and various anticancer drugs in vivo
Bcl-2 Binding (treatment) of
2) Confidence 0.32 Published 2005 Journal Breast Cancer Res Section Body Doc Link PMC1410745 Disease Relevance 0.51 Pain Relevance 0
Combined treatment with AS Bcl-2 and DOX enhanced the expression of Bax, which is a proapoptotic protein, and inhibited phosphorylated Akt (pAkt), which is an antiapoptotic protein.
Bcl-2 Binding (treatment) of
3) Confidence 0.32 Published 2005 Journal Breast Cancer Res Section Body Doc Link PMC1410745 Disease Relevance 0.48 Pain Relevance 0
1 helix of vBcl-2 abolished Beclin1 binding, as also seen with the AAA mutant of vBcl-2 (Figure 2A).
vBcl-2 Binding (binding) of
4) Confidence 0.28 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0 Pain Relevance 0
It is also possible that the autophagy induced when Beclin1 is unchecked by vBcl-2 can trigger cell death of latently infected cells, such a scenario is supported by the fact that a Beclin1 mutant unable to bind to Bcl-2 induces caspase-independent autophagic cell death [12].
Bcl-2 Neg (unable) Binding (bind) of associated with death
5) Confidence 0.25 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.45 Pain Relevance 0
In fact, the anti-autophagic action of Bcl-2 closely mirrors its capacity to bind and inhibit Beclin1 [12].
Bcl-2 Binding (bind) of
6) Confidence 0.24 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.72 Pain Relevance 0
To clarify this, we tested whether the mutants of vBcl-2 retain the ability to associate with other BH3-domain-containing molecules.
vBcl-2 Binding (associate) of
7) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.09 Pain Relevance 0
1 helix deletion has been previously shown not affecting the overall folding of Bcl-2 family proteins [28],[34], it remains possible that the inability of the vBcl-2 ??
vBcl-2 Spec (possible) Binding (inability) of
8) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.07 Pain Relevance 0
Since the BH2 domain is involved in the ability of vBcl-2 to inhibit apoptosis but not autophagy, this result thus suggests that the inhibition of host apoptosis by vBcl-2 is required for efficient ex vivo reactivation from the latent state particularly at later time points after infection, which is consistent with the previous report that the ?
vBcl-2 Neg (inhibition) Binding (inhibition) of associated with apoptosis and infection
9) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.75 Pain Relevance 0
1 helix abolished vBcl-2's anti-autophagic activity but retained its anti-apoptotic function, the impaired latency associated with the vBcl-2??
vBcl-2 Binding (associated) of associated with apoptosis
10) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.44 Pain Relevance 0
In contrast, a vBcl-2 mutant with a triple alanine substitution at the conserved residues of Ser85, Gly86, and Arg87 (hereafter termed as vBcl-2 AAA) within the BH3 binding groove that has been shown to abrogate BH3 peptide binding of vBcl-2, lost the ability to interact with Beclin1 (Figure 1).
vBcl-2 Binding (binding) of in groove
11) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.13 Pain Relevance 0
Our results thus indicate that the loss-of-function mutations of vBcl-2 in autophagy or apoptosis inhibition, or both, have no appreciable impact on the establishment of viral latency in spleens, consistent with earlier finding that vBcl-2 is not required for the establishment of latency by ?
vBcl-2 Binding (finding) of in spleens associated with apoptosis
12) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.39 Pain Relevance 0
It also points to the unique protective activities of vBcl-2 mutants in apoptosis and autophagy with respect to distinct phases of viral infection, and also their coordinated effects on ?
vBcl-2 Binding (points) of associated with viral infection and apoptosis
13) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.41 Pain Relevance 0
Specifically, vBcl-2 ??
vBcl-2 Binding (Specifically) of
14) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.11 Pain Relevance 0
HV68 vBcl-2 mutant suggests a complex nature of ?
vBcl-2 Binding (complex) of
15) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.61 Pain Relevance 0
7 or BH2, one of the central components of the vBcl-2 hydrophobic cleft, had no significant effect on the interaction between vBcl-2 and Beclin1, as was seen with the deletion mutation of the C-terminal hydrophobic ‘tail’ (?
vBcl-2 Neg (no) Binding (interaction) of in tail
16) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0 Pain Relevance 0
Indeed, the vBcl-2?
vBcl-2 Binding (Indeed) of
17) Confidence 0.22 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.47 Pain Relevance 0
Whereas Sag exposure did not induce alterations in the expression of Bcl-2, TRAIL or TNFR1, interaction of Sags with the cognate V?
Bcl-2 Binding (interaction) of
18) Confidence 0.21 Published 2010 Journal PLoS ONE Section Body Doc Link PMC3008744 Disease Relevance 1.05 Pain Relevance 0
, nitrotyrosine, S-100, PAR, Fas Ligand (FasL), Bax and Bcl-2
Bcl-2 Binding (nitrotyrosine) of
19) Confidence 0.21 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2935363 Disease Relevance 0.64 Pain Relevance 0.07
We show that removing the BH2 domain from vBcl-2 does not affect vBcl-2's capacity to bind and suppress Beclin1, but it significantly dampens its anti-apoptotic activity.
vBcl-2 Binding (bind) of associated with apoptosis
20) Confidence 0.21 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2752191 Disease Relevance 0.71 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox