INT178128

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Context Info
Confidence 0.27
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 7
Total Number 10
Disease Relevance 3.94
Pain Relevance 0.56

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) cytosol (BCL2)
BCL2 (Homo sapiens)
Pain Link Frequency Relevance Heat
withdrawal 1 95.36 Very High Very High Very High
antagonist 34 85.36 High High
Pain 16 68.04 Quite High
ischemia 110 53.04 Quite High
Angina 40 5.00 Very Low Very Low Very Low
adenocard 30 5.00 Very Low Very Low Very Low
Clonidine 28 5.00 Very Low Very Low Very Low
Kinase C 16 5.00 Very Low Very Low Very Low
bradykinin 15 5.00 Very Low Very Low Very Low
Opioid 11 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Apoptosis 296 99.66 Very High Very High Very High
Stress 74 95.44 Very High Very High Very High
Ovarian Cancer 23 92.80 High High
Death 67 85.76 High High
Cancer 87 84.56 Quite High
Starvation 60 79.92 Quite High
Disease 198 78.96 Quite High
Neurodegenerative Disease 56 78.56 Quite High
Pressure And Volume Under Development 11 76.88 Quite High
Pain 16 68.04 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Recent studies have shown that pharmacological activation of these kinases is associated with recruitment of anti-apoptotic signaling components such as the phosphorylation and inhibition of the proapoptotic proteins Bax and Bad, the inhibition of caspase 3 activation, the phosphorylation and activation of p70S6K (which acts to inhibit Bad) and the phosphorylation and activation of the antiapoptotic protein Bcl-2 (Harada et al 2001; Hausenloy and Yellon 2007).
Negative_regulation (inhibition) of Phosphorylation (phosphorylation) of Bcl-2 associated with apoptosis
1) Confidence 0.27 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.45 Pain Relevance 0.09
Recent studies have shown that pharmacological activation of these kinases is associated with recruitment of anti-apoptotic signaling components such as the phosphorylation and inhibition of the proapoptotic proteins Bax and Bad, the inhibition of caspase 3 activation, the phosphorylation and activation of p70S6K (which acts to inhibit Bad) and the phosphorylation and activation of the antiapoptotic protein Bcl-2 (Harada et al 2001; Hausenloy and Yellon 2007).
Negative_regulation (inhibit) of Phosphorylation (phosphorylation) of Bcl-2 associated with apoptosis
2) Confidence 0.27 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.39 Pain Relevance 0.06
Recent studies have shown that pharmacological activation of these kinases is associated with recruitment of anti-apoptotic signaling components such as the phosphorylation and inhibition of the proapoptotic proteins Bax and Bad, the inhibition of caspase 3 activation, the phosphorylation and activation of p70S6K (which acts to inhibit Bad) and the phosphorylation and activation of the antiapoptotic protein Bcl-2 (Harada et al 2001; Hausenloy and Yellon 2007).
Negative_regulation (inhibition) of Phosphorylation (phosphorylation) of Bcl-2 associated with apoptosis
3) Confidence 0.27 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.45 Pain Relevance 0.09
Recent studies have shown that pharmacological activation of these kinases is associated with recruitment of anti-apoptotic signaling components such as the phosphorylation and inhibition of the proapoptotic proteins Bax and Bad, the inhibition of caspase 3 activation, the phosphorylation and activation of p70S6K (which acts to inhibit Bad) and the phosphorylation and activation of the antiapoptotic protein Bcl-2 (Harada et al 2001; Hausenloy and Yellon 2007).
Negative_regulation (inhibition) of Phosphorylation (phosphorylation) of Bcl-2 associated with apoptosis
4) Confidence 0.27 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.51 Pain Relevance 0.09
Recent studies have shown that pharmacological activation of these kinases is associated with recruitment of anti-apoptotic signaling components such as the phosphorylation and inhibition of the proapoptotic proteins Bax and Bad, the inhibition of caspase 3 activation, the phosphorylation and activation of p70S6K (which acts to inhibit Bad) and the phosphorylation and activation of the antiapoptotic protein Bcl-2 (Harada et al 2001; Hausenloy and Yellon 2007).
Negative_regulation (inhibition) of Phosphorylation (phosphorylation) of Bcl-2 associated with apoptosis
5) Confidence 0.27 Published 2007 Journal Vascular Health and Risk Management Section Body Doc Link PMC2291307 Disease Relevance 0.51 Pain Relevance 0.09
Paclitaxel-induced apoptosis resulted in the phosphorylation of Bcl-2 that was suppressed by the addition of ET-1.
Negative_regulation (suppressed) of Phosphorylation (phosphorylation) of Bcl-2 associated with apoptosis
6) Confidence 0.05 Published 2004 Journal J Transl Med Section Body Doc Link PMC436068 Disease Relevance 0.94 Pain Relevance 0.12
NAC and glutathione inhibited the activation of JNK and decreased the phosphorylation of Bcl-2 (Fig. 6C and D).
Negative_regulation (decreased) of Phosphorylation (phosphorylation) of Bcl-2
7) Confidence 0.05 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2916709 Disease Relevance 0.18 Pain Relevance 0
Vitamin E has an effect on the mTOR pathway, while thiol-containing antioxidants, such as NAC, decrease the phosphorylation of JNK and Bcl-2.
Negative_regulation (decrease) of Phosphorylation (phosphorylation) of Bcl-2
8) Confidence 0.05 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2916709 Disease Relevance 0.26 Pain Relevance 0
(D) Thiol antioxidants decrease Bcl-2 phosphorylation.
Negative_regulation (decrease) of Phosphorylation (phosphorylation) of Bcl-2
9) Confidence 0.05 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2916709 Disease Relevance 0 Pain Relevance 0
Thiol ROS scavengers such as NAC inhibit mTOR (which would be expected to induce autophagy) but decrease the phosphorylation of JNK and Bcl-2 which will inhibit autophagy, while the superoxide-generating agent menadione increases levels of LC3-II and the phosphorylation of JNK and Bcl-2.


Negative_regulation (decrease) of Phosphorylation (phosphorylation) of Bcl-2
10) Confidence 0.04 Published 2010 Journal Human Molecular Genetics Section Body Doc Link PMC2916709 Disease Relevance 0.26 Pain Relevance 0

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