INT228129

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Context Info
Confidence 0.58
First Reported 2008
Last Reported 2010
Negated 0
Speculated 1
Reported most in Body
Documents 10
Total Number 16
Disease Relevance 11.08
Pain Relevance 1.93

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

cytosol (Bcl2l11) mitochondrion (Bcl2l11) cytoplasm (Bcl2l11)
Anatomy Link Frequency
T cells 7
Bcl2l11 (Mus musculus)
Pain Link Frequency Relevance Heat
Kinase C 38 99.98 Very High Very High Very High
cytokine 96 99.26 Very High Very High Very High
substance P 66 99.04 Very High Very High Very High
nav1.8 65 98.36 Very High Very High Very High
chemokine 147 96.68 Very High Very High Very High
withdrawal 24 91.88 High High
Pain 11 78.08 Quite High
Peripheral sensitization 1 77.76 Quite High
calcitonin gene related peptide 1 69.32 Quite High
Neuropeptide 2 68.04 Quite High
Disease Link Frequency Relevance Heat
Repression 35 100.00 Very High Very High Very High
Lymphadenopathy 104 99.96 Very High Very High Very High
Adhesions 245 99.62 Very High Very High Very High
Infection 192 99.36 Very High Very High Very High
Cold Sores 144 99.10 Very High Very High Very High
Colon Cancer 175 98.70 Very High Very High Very High
Apoptosis 618 98.60 Very High Very High Very High
Death 305 97.20 Very High Very High Very High
Cancer 158 97.10 Very High Very High Very High
Herpes Simplex Virus 144 96.96 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Some studies showed that deletion of SEB-activated T cells in mice was in part FasL-Fas dependent (Mogil et al., 1995; Renno et al., 1996), whereas others found that Fas deficiency (in Faslpr/lpr mutant mice) had no impact but that loss of Bim provided profound protection (Hildeman et al., 2002).
Negative_regulation (loss) of Bim in T cells
1) Confidence 0.58 Published 2008 Journal Immunity Section Body Doc Link PMC2270348 Disease Relevance 0.31 Pain Relevance 0
Interestingly, the death of antigen-activated CD8+ T cells during shutdown of and acute immune response to a viral (HSV-1) infection was substantially inhibited by loss of Bim but was not affected by Fas deficiency (Pellegrini et al., 2003).
Negative_regulation (loss) of Bim in T cells associated with cold sores, infection and death
2) Confidence 0.43 Published 2008 Journal Immunity Section Body Doc Link PMC2270348 Disease Relevance 0.58 Pain Relevance 0
Indeed, Bim and Puma doubly deficient T cells survive better in culture in the absence of cytokines than those lacking only Bim or Puma (Erlacher et al., 2006).
Negative_regulation (deficient) of Bim in T cells associated with cytokine
3) Confidence 0.43 Published 2008 Journal Immunity Section Body Doc Link PMC2270348 Disease Relevance 0.59 Pain Relevance 0.17
Combined loss of Fas and Bim also synergized in causing lymphadenopathy, demonstrating that these two pathways cooperate not only in the killing of T cells chronically activated by pathogen-borne antigens but also those stimulated by self-antigens.
Negative_regulation (loss) of Bim in T cells associated with lymphadenopathy
4) Confidence 0.43 Published 2008 Journal Immunity Section Body Doc Link PMC2270348 Disease Relevance 0.43 Pain Relevance 0.04
These unusual T cells are as sensitive as conventional T cells to cytokine deprivation but can be protected by loss of Bim, providing a likely explanation as to why their numbers are greatly increased in Bcl2l11?
Negative_regulation (loss) of Bim in T cells associated with cytokine
5) Confidence 0.43 Published 2008 Journal Immunity Section Body Doc Link PMC2270348 Disease Relevance 0.33 Pain Relevance 0.08
The mitochondrial pathway has been implicated in immune response shutdown, because Bcl-2 overexpression (Strasser et al., 1991), loss of Bim (Hildeman et al., 2002; Pellegrini et al., 2003), or Bax and Bak deficiency (Rathmell et al., 2002) inhibited death of T cells stimulated in vitro or in vivo by a single dose of SEB or in vivo after infection with human herpes simplex virus (HSV-1).
Negative_regulation (loss) of Bim in T cells associated with cold sores, herpes simplex virus, infection and death
6) Confidence 0.42 Published 2008 Journal Immunity Section Body Doc Link PMC2270348 Disease Relevance 0.83 Pain Relevance 0.06
As shown in Figure 3 and Figure 4, PKC inhibitor BIM completely blocked Sar-SP-induced potentiation of Nav1.8 currents, whereas PKC activator PMA could mimic the effects of Sar-SP on Nav1.8 currents.
Negative_regulation (inhibitor) of BIM associated with kinase c, nav1.8 and substance p
7) Confidence 0.41 Published 2009 Journal Mol Pain Section Body Doc Link PMC2715383 Disease Relevance 0.21 Pain Relevance 1.46
Loss of either Bim or Fas both lead to marked lymphadenopathy.
Negative_regulation (Loss) of Bim associated with lymphadenopathy
8) Confidence 0.37 Published 2008 Journal Immunity Section Body Doc Link PMC2270348 Disease Relevance 0.90 Pain Relevance 0
Loss of Bim resulted in a significant (p < 0.05), albeit relatively small, increase in MHV-OVA-specific CD8+ T cells on days 40 and 60, which was particularly prominent in the spleen (Figures 3E and 3G).
Negative_regulation (Loss) of Bim in T cells associated with herpes simplex virus
9) Confidence 0.37 Published 2008 Journal Immunity Section Body Doc Link PMC2270348 Disease Relevance 1.11 Pain Relevance 0
Repression of Bim protein levels by RNAi rescued anoikis resistance in CXCL12-expressing cells describing Bim as a critical physiological step for colorectal carcinoma anchorage-independent survival and tumor metastasis.
Negative_regulation (Repression) of Bim associated with colon cancer, repression and metastasis
10) Confidence 0.21 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.83 Pain Relevance 0.04
CXCL12 expression and adhesion are unaffected by Bim repression
Negative_regulation (repression) of Bim associated with repression and adhesions
11) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.51 Pain Relevance 0
Furthermore, depletion of Bim enhances anchorage-independent survival in both transformed and non-transformed cells [9], [10].
Negative_regulation (depletion) of Bim
12) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 1.00 Pain Relevance 0
Mirroring our previous findings (Figure 8D), net tumor burden was slightly decreased, but not statistically different, over time in CXCL12-Luc mice compared to GFP-Luc controls and was unaffected by Bim depletion [13].
Negative_regulation (depletion) of Bim associated with cancer
13) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 1.15 Pain Relevance 0.03
Having demonstrated Bim expression was upregulated in non-adherent colorectal carcinoma cells expressing CXCL12, we next examined whether RNAi-mediated repression of Bim would reverse anoikis sensitivity in those cells.
Spec (whether) Negative_regulation (repression) of Bim associated with repression and colon cancer
14) Confidence 0.16 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.51 Pain Relevance 0
Further, our data indicate that Bim depletion had little effect on formation or stability of focal adhesion proteins, with FAK levels decreasing equally in Bim knockdown and Bim-competent CXCL12 cells.
Negative_regulation (knockdown) of Bim associated with adhesions
15) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 1.19 Pain Relevance 0
Consistent with soft-agar survival, knockdown of Bim in CXCL12-expressing cells significantly decreased executioner caspase-3/7 activity (Figure 7C) and DNA degradation (Figure 7D) in HCT116 cells cultured in suspension.
Negative_regulation (knockdown) of Bim
16) Confidence 0.15 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2943927 Disease Relevance 0.58 Pain Relevance 0.05

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