INT51654

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Context Info
Confidence 0.40
First Reported 1994
Last Reported 2010
Negated 2
Speculated 1
Reported most in Body
Documents 21
Total Number 22
Disease Relevance 12.18
Pain Relevance 4.06

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

lipid binding (Bad) cell proliferation (Bad) cytosol (Bad)
mitochondrion (Bad) cytoplasm (Bad)
Anatomy Link Frequency
brain 3
E1a 2
neurons 1
PSCs 1
tail 1
Bad (Mus musculus)
Pain Link Frequency Relevance Heat
agonist 10 100.00 Very High Very High Very High
GABAergic 5 99.70 Very High Very High Very High
tail-flick 1 99.16 Very High Very High Very High
Intracerebroventricular 1 99.14 Very High Very High Very High
Dorsal horn neuron 11 98.70 Very High Very High Very High
Antinociceptive 2 98.02 Very High Very High Very High
Spinal cord 17 97.64 Very High Very High Very High
withdrawal 11 97.38 Very High Very High Very High
methadone 6 97.08 Very High Very High Very High
antagonist 19 95.44 Very High Very High Very High
Disease Link Frequency Relevance Heat
Apoptosis 304 100.00 Very High Very High Very High
Cytomegalovirus Infection 132 100.00 Very High Very High Very High
Targeted Disruption 38 99.36 Very High Very High Very High
Cancer 334 98.70 Very High Very High Very High
Sprains And Strains 5 98.60 Very High Very High Very High
Cognitive Disorder 10 98.24 Very High Very High Very High
Disease Progression 1 97.52 Very High Very High Very High
Acquired Immune Deficiency Syndrome Or Hiv Infection 3 96.60 Very High Very High Very High
Death 39 96.20 Very High Very High Very High
Chronic Hepatitis 1 92.36 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Here, we have analyzed the effects of prolonged heroin administration on sensorimotor and cognitive performance in mice, as well as the associated changes in brain expression of proteins regulating the extrinsic (FasL and Fas) and the mitochondrial (Bcl-2, Bcl-X(L), Bad and Bax) apoptotic pathways.
Regulation (regulating) of Bad in brain associated with cognitive disorder and apoptosis
1) Confidence 0.40 Published 2008 Journal Neuropharmacology Section Abstract Doc Link 18201731 Disease Relevance 0.73 Pain Relevance 0.12
OBJECTIVES: This study analyzes the effects of prolonged administration of methadone and withdrawal on sensorimotor and cognitive performance in mice and explores the associated changes in brain expression of proteins regulating the extrinsic (FasL, Fas, and caspase-8) and the mitochondrial (Bcl-2, Bcl-x(L), Bad, and Bax) apoptotic pathways.
Regulation (regulating) of Bad in brain associated with cognitive disorder, methadone, apoptosis and withdrawal
2) Confidence 0.40 Published 2007 Journal Psychopharmacology (Berl.) Section Abstract Doc Link 17384938 Disease Relevance 0.35 Pain Relevance 0.26
The purpose of the present study was to analyse the effects of naltrexone on the expression levels of proteins regulating the extrinsic (FasL and Fas) and the mitochondrial (Bcl-2, Bcl-xL, Bad and Bax) apoptotic pathways, as well as the active fragment of the executioner caspase-3 in the mouse brain.
Regulation (regulating) of Bad in brain associated with apoptosis
3) Confidence 0.36 Published 2006 Journal Neurosci. Lett. Section Abstract Doc Link 16716514 Disease Relevance 0.26 Pain Relevance 0.30
Several key molecules, including caspase-3, Bcl-2, BAD and Bax, were modulated by l-THP treatment.
Regulation (modulated) of BAD
4) Confidence 0.24 Published 2010 Journal Toxicol. Lett. Section Abstract Doc Link 20109541 Disease Relevance 0.33 Pain Relevance 0.09
BAD is a unique BH3-only family member in that its regulation is primarily mediated through its conserved phosphorylation sites (serines 112, 136, and 155 based on the mouse sequence)[11], [12].
Regulation (regulation) of BAD
5) Confidence 0.23 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2704953 Disease Relevance 1.58 Pain Relevance 0.12
It is tempting to speculate that that high BAD expression should make these tumors increasingly sensitive to inhibitors of signaling pathways that control BAD.
Regulation (control) of BAD associated with cancer
6) Confidence 0.23 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2704953 Disease Relevance 0.52 Pain Relevance 0
This neurotoxic effect was accompanied by up-regulation of the proapoptotic proteins FasL, Fas, and Bad and the active fragments of caspases-8 and -3 in cortical and hippocampal lysates.
Regulation (regulation) of Bad
7) Confidence 0.22 Published 2006 Journal J. Neurosci. Res. Section Abstract Doc Link 16496378 Disease Relevance 0.50 Pain Relevance 0.59
Both the chronic methadone and repeated withdrawal groups showed up-regulation of several pro-apoptotic proteins (FasL, the active fragment of caspase-8, and Bad) in the cortex and hippocampus, indicating activation of both the death-receptor and mitochondrial apoptotic pathways.
Regulation (regulation) of Bad in hippocampus
8) Confidence 0.21 Published 2007 Journal Psychopharmacology (Berl.) Section Body Doc Link 17384938 Disease Relevance 0.08 Pain Relevance 0
Although it is well documented that apoptosis is also regulated by the Bcl-2 family of proteins [55], we do not detect any significant changes in the levels of Bax, Bad, Bcl-2 and Bcl-xL followed by U0126 treatment (data not shown).
Neg (not) Regulation (changes) of Bad associated with apoptosis
9) Confidence 0.18 Published 2003 Journal BMC Gastroenterol Section Body Doc Link PMC317301 Disease Relevance 0.68 Pain Relevance 0
Both the chronic methadone and repeated withdrawal groups showed up-regulation of several pro-apoptotic proteins (FasL, the active fragment of caspase-8, and Bad) in the cortex and hippocampus, indicating activation of both the death-receptor and mitochondrial apoptotic pathways.
Regulation (regulation) of Bad in cortex
10) Confidence 0.07 Published 2007 Journal Psychopharmacology (Berl.) Section Body Doc Link 17384938 Disease Relevance 0.08 Pain Relevance 0
Bcl-XL and Bad protein levels were unchanged between adherent and non-adherent CXCL12 and control cells.
Neg (unchanged) Regulation (unchanged) of Bad
11) Confidence 0.05 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.49 Pain Relevance 0.04
Activation of Akt-1 by phosphrylation at serine 473 was shown to lead to survival pathway [30] via regulation of proapoptotic proteins such as Bad, caspase 9 and p53 [28].
Regulation (regulation) of Bad
12) Confidence 0.05 Published 2008 Journal PLoS ONE Section Body Doc Link PMC2515219 Disease Relevance 0.62 Pain Relevance 0
Several kinase inhibitors, vitamin A and its metabolites were applied to study the regulation of 2.2kb hGFAP promoter in PSCs.
Regulation (regulation) of hGFAP promoter in PSCs
13) Confidence 0.04 Published 2009 Journal Dig Liver Dis Section Body Doc Link 18602878 Disease Relevance 0.08 Pain Relevance 0
Transverse lumbar spinal cord slices were obtained from adult mice expressing enhanced green fluorescent protein (EGFP) in GABAergic neurons under control of the GAD67 promoter.
Regulation (control) of GAD67 promoter in GABAergic neurons associated with gabaergic and spinal cord
14) Confidence 0.02 Published 2009 Journal Pain Section Abstract Doc Link 19608344 Disease Relevance 0.33 Pain Relevance 0.57
In an inactivated state, such as that induced by the up-regulation of PTEN, Bad may become unphosphorylated, disassociate from 14-3-3 and move to displace Bax [75],[88].
Regulation (regulation) of Bad
15) Confidence 0.02 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2771360 Disease Relevance 0.37 Pain Relevance 0
The TAT72 transgene (1-72 amino acids) was placed under the control of SV40 viral promoter to provide systemic expression.
Regulation (control) of viral promoter
16) Confidence 0.01 Published 1994 Journal Int. J. Immunopharmacol. Section Abstract Doc Link 7705968 Disease Relevance 0.80 Pain Relevance 0.52
Antinociceptive evaluations in mice showed that intracerebroventricular (icv) injections of 6d produced a partial agonist effect in the 55 degrees C tail-flick assay and a full agonist effect in the acetic acid writhing assay (A(50) = 7.5 nmol).
Spec (partial) Regulation (effect) of agonist in tail associated with tail-flick, agonist, intracerebroventricular and antinociceptive
17) Confidence 0.01 Published 1999 Journal J. Med. Chem. Section Abstract Doc Link 10479286 Disease Relevance 0.09 Pain Relevance 1.03
The structures of the recombinant adenoviruses constructed for this study are presented in Figure 1A, including Ad-hTERT-E1a-Apoptin and Ad-CMV-E1a-Apoptin, in which the E1a gene is under the control of the hTERT promoter or CMV promoter, respectively, and Apoptin is controlled by a CMV promoter.
Regulation (control) of CMV promoter in E1a associated with cytomegalovirus infection
18) Confidence 0.01 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2818692 Disease Relevance 1.59 Pain Relevance 0
The structures of the recombinant adenoviruses constructed for this study are presented in Figure 1A, including Ad-hTERT-E1a-Apoptin and Ad-CMV-E1a-Apoptin, in which the E1a gene is under the control of the hTERT promoter or CMV promoter, respectively, and Apoptin is controlled by a CMV promoter.
Regulation (control) of hTERT promoter in E1a associated with cytomegalovirus infection
19) Confidence 0.01 Published 2010 Journal Mol Cancer Section Body Doc Link PMC2818692 Disease Relevance 1.53 Pain Relevance 0
The morphological, neurochemical and electrophysiological characteristics of a subpopulation of inhibitory superficial dorsal horn neurons, have been studied in transgenic mice expressing EGFP under the control of the GAD67 promoter [2,3].
Regulation (control) of GAD67 promoter in neurons associated with targeted disruption and dorsal horn neuron
20) Confidence 0.01 Published 2006 Journal Mol Pain Section Body Doc Link PMC1479315 Disease Relevance 0.30 Pain Relevance 0.33

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