INT102752

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Context Info
Confidence 0.67
First Reported 2002
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 14
Total Number 14
Disease Relevance 13.80
Pain Relevance 2.19

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
HT-29 2
cleavage 2
keratinocytes 2
BCL2L1 (Homo sapiens)
Pain Link Frequency Relevance Heat
dexamethasone 78 99.20 Very High Very High Very High
aspirin 12 97.92 Very High Very High Very High
Paracetamol 12 97.88 Very High Very High Very High
Inflammation 30 92.48 High High
cytokine 18 92.04 High High
antagonist 41 91.12 High High
cINOD 8 81.36 Quite High
rheumatoid arthritis 35 79.92 Quite High
metalloproteinase 25 78.64 Quite High
withdrawal 3 73.80 Quite High
Disease Link Frequency Relevance Heat
Apoptosis 555 100.00 Very High Very High Very High
Nasopharynx Cancer 149 99.96 Very High Very High Very High
Acquired Immune Deficiency Syndrome Or Hiv Infection 92 99.40 Very High Very High Very High
Stress 74 98.36 Very High Very High Very High
Cancer 292 98.08 Very High Very High Very High
Death 159 97.88 Very High Very High Very High
Glioblastoma 49 97.60 Very High Very High Very High
Toxicity 67 97.36 Very High Very High Very High
Disease 169 93.72 High High
INFLAMMATION 33 92.48 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Nevertheless, celecoxib at both concentrations induced a strong NFkappaB activation, with increased expression of NFkappaB-dependent genes, such as bcl-2, bcl-XL and survivin.
Positive_regulation (increased) of Gene_expression (expression) of bcl-XL
1) Confidence 0.67 Published 2007 Journal Oncol. Rep. Section Abstract Doc Link 17342322 Disease Relevance 0.99 Pain Relevance 0.28
Overexpression of the antiapoptotic protein Bcl-XL prevented these various apoptotic events induced by acetaminophen in Jurkat cells.
Positive_regulation (Overexpression) of Gene_expression (Overexpression) of Bcl-XL associated with paracetamol and apoptosis
2) Confidence 0.55 Published 2002 Journal Pharmacol. Toxicol. Section Abstract Doc Link 12005112 Disease Relevance 0.60 Pain Relevance 0.85
Nevertheless, celecoxib at both concentrations induced a strong NFkappaB activation, with increased expression of NFkappaB-dependent genes, such as bcl-2, bcl-XL and survivin.
Positive_regulation (increased) of Gene_expression (expression) of bcl-XL
3) Confidence 0.49 Published 2007 Journal Oncol. Rep. Section Abstract Doc Link 17342322 Disease Relevance 0.99 Pain Relevance 0.28
Knockdown of bcl-xL expression with RNAi induced NPC cells apoptosis, suggesting that the siRNA technique could provide a new method for anti-NPC gene therapy [34].
Positive_regulation (induced) of Gene_expression (expression) of bcl-xL associated with nasopharynx cancer and apoptosis
4) Confidence 0.33 Published 2007 Journal Mol Cancer Section Body Doc Link PMC1774581 Disease Relevance 1.34 Pain Relevance 0
Activation of the apoptotic/survival machinery was also observed, whereby celecoxib treatment induced expression of genes encoding such products as cytochrome C oxidase subunit VIII, BAX, BCLxs, presenillin 2 (structural protein from cleavage of death substrate), apoptotic chromatin condensation inducer, and PDCD5 (programmed cell death 5).
Positive_regulation (induced) of Gene_expression (expression) of BCLxs in cleavage associated with apoptosis and death
5) Confidence 0.29 Published 2006 Journal Breast Cancer Res Section Body Doc Link PMC1797025 Disease Relevance 0.51 Pain Relevance 0.07
Moreover, Bcl-X(L) transfection into HCC cells abrogated apoptosis induced by both substances, indicating that modulation of intracellular pro- and anti-apoptotic proteins is a key event in VPA or ITF2357 induced tumor-cell death.
Positive_regulation (transfection) of Gene_expression (transfection) of Bcl-X
6) Confidence 0.26 Published 2005 Journal J. Hepatol. Section Body Doc Link 15664246 Disease Relevance 0.14 Pain Relevance 0
DXM has been shown to inhibit apoptosis by induction of transcriptional expression of anti-apoptotic proteins Bcl-2 and Bcl-xL [37,38].
Positive_regulation (induction) of Gene_expression (expression) of Bcl-xL associated with apoptosis and dexamethasone
7) Confidence 0.20 Published 2004 Journal Mol Cancer Section Body Doc Link PMC544397 Disease Relevance 0.96 Pain Relevance 0.20
This phenotype has been associated with the overexpression of two intracellular molecules, Bcl-2 and Bcl-xl [3,6,7], capable of blocking mitochondria-induced apoptosis.
Positive_regulation (overexpression) of Gene_expression (overexpression) of Bcl-xl associated with apoptosis
8) Confidence 0.16 Published 2008 Journal Arthritis Res Ther Section Body Doc Link PMC2656252 Disease Relevance 1.06 Pain Relevance 0.24
Moreover, Bcl-XL overexpression protected LNCaP cells from troglitazone- and ?
Positive_regulation (overexpression) of Gene_expression (overexpression) of Bcl-XL
9) Confidence 0.09 Published 2008 Journal PPAR Research Section Body Doc Link PMC2442903 Disease Relevance 0.93 Pain Relevance 0
These mechanisms may, amongst others, involve expression of genes different from c-Myc, which is suggested by the fact that plakoglobin deficiency resulted in protection of keratinocytes from apoptosis, possibly via overexpression of the anti-apoptotic molecule Bcl-XL (Dusek et al. 2007a).
Positive_regulation (overexpression) of Gene_expression (overexpression) of Bcl-XL in keratinocytes associated with apoptosis
10) Confidence 0.08 Published 2008 Journal Histochem Cell Biol Section Body Doc Link PMC2413110 Disease Relevance 1.37 Pain Relevance 0
Using HIV-1 isolates, cell lines which overexpress Bcl-2 or Bcl-xL are protected from damage whereas the wild-type cells are significantly compromised [51].
Positive_regulation (overexpress) of Gene_expression (overexpress) of Bcl-xL associated with acquired immune deficiency syndrome or hiv infection
11) Confidence 0.08 Published 2006 Journal Journal of Biomedicine and Biotechnology Section Body Doc Link PMC1510947 Disease Relevance 1.25 Pain Relevance 0.08
Although the mechanism for activating the expression and function of Bcl-2, Bcl-XL and Bax is not fully understood, it is possible that the p53 molecule plays a role in this process [30].
Positive_regulation (activating) of Gene_expression (expression) of Bcl-XL
12) Confidence 0.07 Published 2010 Journal Cancer Cell Int Section Body Doc Link PMC2873331 Disease Relevance 1.04 Pain Relevance 0.11
Introduction of Bcl-2 into HT-29 cells caused caspase-3 activation, changed the Bcl-XL expression pattern, increased the apoptosis ratio with no effect on overall toxicity, and supported arrest in the G2/M-phase of cell cycle.
Positive_regulation (changed) of Gene_expression (expression) of Bcl-XL in HT-29 associated with toxicity and apoptosis
13) Confidence 0.07 Published 2010 Journal International Journal of Molecular Sciences Section Body Doc Link PMC2852855 Disease Relevance 1.27 Pain Relevance 0.03
The Bcl-2 family includes pro-apoptotic (Bax and Bad) and anti-apoptotic (Bcl-2 and Bcl-XL) proteins, whose expression and activity is regulated through different signaling pathways including trophic factors deprivation, A?
Positive_regulation (apoptotic) of Gene_expression (expression) of Bcl-XL associated with apoptosis
14) Confidence 0.05 Published 2006 Journal BMC Neurosci Section Body Doc Link PMC1775042 Disease Relevance 1.34 Pain Relevance 0.05

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