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Context Info
Confidence 0.69
First Reported 2009
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 5
Total Number 5
Disease Relevance 3.76
Pain Relevance 0.34

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

cytosol (BCL2L1) mitochondrion (BCL2L1) growth (BCL2L1)
cytoskeleton (BCL2L1) nucleus (BCL2L1) intracellular (BCL2L1)
Anatomy Link Frequency
lymphocytes 1
BCL2L1 (Homo sapiens)
Pain Link Frequency Relevance Heat
withdrawal 3 91.12 High High
Inflammation 103 77.60 Quite High
Inflammatory mediators 14 71.00 Quite High
peripheral neuropathy 1 69.24 Quite High
Central nervous system 35 67.92 Quite High
Inflammatory response 7 60.40 Quite High
intrathecal 1 39.88 Quite Low
antagonist 5 36.84 Quite Low
chemokine 37 27.16 Quite Low
Multiple sclerosis 10 9.36 Low Low
Disease Link Frequency Relevance Heat
Apoptosis 297 100.00 Very High Very High Very High
Neuromyelitis Optica 81 91.28 High High
Adhesions 7 91.08 High High
Death 48 89.92 High High
Sarcoma 4 88.40 High High
Fever 41 83.28 Quite High
Lung Cancer 8 80.40 Quite High
Cancer 168 79.52 Quite High
INFLAMMATION 129 77.60 Quite High
Disease 34 77.12 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
In vivo, Bcl-xS mRNA is expressed at high levels in cells that undergo a high rate of turnover, such as developing lymphocytes.
Transcription (expressed) of Bcl-xS in lymphocytes
1) Confidence 0.69 Published 2010 Journal Journal of Carcinogenesis Section Body Doc Link PMC2862505 Disease Relevance 0.57 Pain Relevance 0.05
It had been reported that STAT3 might regulate the transcription of anti-apoptotic proteins such as BCL-XL that control cell growth and survival [29,30].
Transcription (transcription) of BCL-XL associated with apoptosis
2) Confidence 0.21 Published 2009 Journal Molecular Vision Section Body Doc Link PMC2730746 Disease Relevance 1.35 Pain Relevance 0.19
Apoptosis can be inhibited because STAT3 regulates the transcription of Bcl-XL, a well-known anti-apoptotic protein [53].
Transcription (transcription) of Bcl-XL associated with apoptosis
3) Confidence 0.19 Published 2010 Journal International Journal of Cell Biology Section Body Doc Link PMC2841246 Disease Relevance 0.94 Pain Relevance 0
This conclusion was founded on the observed upregulation in transcripts for AKT1 and Bcl-XL, paired with decreased gene expression for DRAM.
Transcription (transcripts) of Bcl-XL
4) Confidence 0.07 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2771360 Disease Relevance 0.55 Pain Relevance 0.10
In cultures containing only SY cells and B. burgdorferi, there were prominent increases in transcript for the cell survival and anti-apoptotic molecules protein kinase B (AKT1) and BCL2-like (Bcl-XL) genes, combined with a decrease in transcript for pro-apoptotic damage-regulated autophagy modulator (DRAM) (Table 6-left, Figure 4A).
Transcription (transcript) of Bcl-XL associated with apoptosis
5) Confidence 0.05 Published 2009 Journal PLoS Pathogens Section Body Doc Link PMC2771360 Disease Relevance 0.35 Pain Relevance 0

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