INT106413

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Context Info
Confidence 0.53
First Reported 2002
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 8
Total Number 8
Disease Relevance 3.35
Pain Relevance 1.52

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

mitochondrion (Bcl2l1) intracellular (Bcl2l1) response to stress (Bcl2l1)
cytoplasm (Bcl2l1) cytosol (Bcl2l1) cell proliferation (Bcl2l1)
Anatomy Link Frequency
retina 1
cleavage 1
brain 1
optic nerve 1
hippocampus 1
Bcl2l1 (Rattus norvegicus)
Pain Link Frequency Relevance Heat
Clonidine 6 99.76 Very High Very High Very High
Hippocampus 9 99.68 Very High Very High Very High
agonist 9 99.56 Very High Very High Very High
antagonist 6 98.52 Very High Very High Very High
ischemia 96 92.40 High High
cytokine 7 75.60 Quite High
Inflammation 9 75.20 Quite High
Mechanotransduction 1 63.60 Quite High
anesthesia 10 55.76 Quite High
Neurotransmitter 3 53.20 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 167 100.00 Very High Very High Very High
Fistula 21 96.44 Very High Very High Very High
Cv General 4 Under Development 12 92.40 High High
Disease 43 80.24 Quite High
Death 26 80.16 Quite High
Neurodegenerative Disease 10 79.92 Quite High
Necrosis 7 78.56 Quite High
Cancer 3 78.20 Quite High
INFLAMMATION 12 75.20 Quite High
Ganglion Cysts 9 72.64 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Administration of clonidine 20 min after yohimbine administration abolished its effect on Bcl-XL mRNA level in the hippocampus.
Transcription (level) of Bcl-XL in hippocampus associated with hippocampus and clonidine
1) Confidence 0.53 Published 2008 Journal Izv. Akad. Nauk. Ser. Biol. Section Abstract Doc Link 18491567 Disease Relevance 0.07 Pain Relevance 0.45
The effects of antagonist of alpha2-adrenoceptors yohimbine and their agonist clonidine on Bax and Bcl-XL mRNA levels in neonatal rat brain were studied.
Transcription (levels) of Bcl-XL in brain associated with antagonist, agonist and clonidine
2) Confidence 0.53 Published 2008 Journal Izv. Akad. Nauk. Ser. Biol. Section Abstract Doc Link 18491567 Disease Relevance 0.07 Pain Relevance 0.42
Our results are in agreement with the moderate decrease in Bcl-xL mRNA expression in the retina observed after optic nerve crush [25].
Transcription (expression) of Bcl-xL in optic nerve
3) Confidence 0.50 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2765238 Disease Relevance 0.28 Pain Relevance 0.03
As for mRNA, the Bax:Bcl-2 and Bax:Bcl-xL protein ratios did not reveal any modulation (1.144±0.238 and 0.970±0.129, respectively; Figure 2E-F).


Transcription (ratios) of Bcl-xL
4) Confidence 0.48 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2765238 Disease Relevance 0 Pain Relevance 0.06
However, our results showing a time-related decrease in Bcl-xL expression in the retina following I/R are in conflict with a publication on hippocampal neurons, where no alteration of the abundance of Bcl-xL was observed following I/R [27].
Transcription (abundance) of Bcl-xL in retina
5) Confidence 0.48 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2765238 Disease Relevance 0.46 Pain Relevance 0.05
For example, the mRNA levels of Bcl-xS were initially decreased at 1 day, 3 days and 1 week followed by returning to base line level after 2 weeks.
Transcription (levels) of Bcl-xS
6) Confidence 0.31 Published 2002 Journal BMC Cardiovasc Disord Section Body Doc Link PMC119850 Disease Relevance 0.64 Pain Relevance 0.06
Clonidine upregulated the expression of mRNA encoding an anti-apoptotic factor Bcl-xL.
Transcription (expression) of anti-apoptotic factor Bcl-xL associated with apoptosis and clonidine
7) Confidence 0.20 Published 2002 Journal Neuropharmacology Section Abstract Doc Link 12423672 Disease Relevance 0.49 Pain Relevance 0.46
As for possible mechanisms underlying its anti-apoptotic action, EGb761 may maintain the integrity of the mitochondrial membrane; prevent cytochrome c release from the mitochondria, thereby blocking the formation of the apoptosome and the apoptotic caspase cascade; enhance the transcription of antiapoptotic Bcl-2-like protein; attenuate the transcription of pro-apoptotic caspase-12; inactivate pro-apoptotic c-Jun N-terminal kinase (JNK), thereby “turning off” downstream target c-Jun; inhibit the cleavage of the key effector protease caspase-3, thereby blocking the execution of apoptosis and prevent nuclear DNA fragmentation, the molecular hallmark of apoptosis [3,7,50].
Transcription (transcription) of Bcl-2-like in cleavage associated with apoptosis
8) Confidence 0.07 Published 2010 Journal International Journal of Molecular Sciences Section Body Doc Link PMC2820992 Disease Relevance 1.34 Pain Relevance 0

General Comments

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