INT176445

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.76
First Reported 2004
Last Reported 2010
Negated 0
Speculated 0
Reported most in Body
Documents 23
Total Number 23
Disease Relevance 7.57
Pain Relevance 0.75

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

transport (Gopc) Golgi apparatus (Gopc) plasma membrane (Gopc)
cytoplasm (Gopc)
Anatomy Link Frequency
neuronal 2
liver 1
muscle 1
osteoclasts 1
articular cartilage 1
Gopc (Mus musculus)
Pain Link Frequency Relevance Heat
Inflammation 127 94.72 High High
carbamazepine 18 92.88 High High
Arthritis 44 74.96 Quite High
imagery 37 63.36 Quite High
cva 1 59.72 Quite High
dexamethasone 18 53.20 Quite High
methotrexate 18 52.00 Quite High
Angina 2 47.60 Quite Low
Neuropathic pain 12 46.96 Quite Low
cytokine 29 39.68 Quite Low
Disease Link Frequency Relevance Heat
Frailty 61 100.00 Very High Very High Very High
Hypertrophy 9 100.00 Very High Very High Very High
Synovitis 8 99.34 Very High Very High Very High
Diabetes Mellitus 306 99.32 Very High Very High Very High
Acquired Immune Deficiency Syndrome Or Hiv Infection 300 99.18 Very High Very High Very High
Metastasis 61 98.92 Very High Very High Very High
Shock 13 98.78 Very High Very High Very High
Hematological Disease 11 97.44 Very High Very High Very High
Disease 58 95.52 Very High Very High Very High
INFLAMMATION 138 95.24 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Repeated presentation of the CS-UCS contingency directly to BALB test mice engendered progressive HR deceleration (Fig. 8a, maximum HR decrease±s.e.m.; ?
Protein_catabolism (deceleration) of Fig
1) Confidence 0.76 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2633046 Disease Relevance 0 Pain Relevance 0
Fig. 2Environcam™ system diagram
Protein_catabolism (diagram) of Fig
2) Confidence 0.76 Published 2007 Journal Bioprocess Biosyst Eng Section Body Doc Link PMC2214824 Disease Relevance 0 Pain Relevance 0
Fig. 1Environcam™ shroud diagram
Protein_catabolism (diagram) of Fig
3) Confidence 0.76 Published 2007 Journal Bioprocess Biosyst Eng Section Body Doc Link PMC2214824 Disease Relevance 0 Pain Relevance 0
Elastic lamellae and collagenous matrix were degraded (Fig. 3A).
Protein_catabolism (degraded) of Fig
4) Confidence 0.46 Published 2010 Journal J Cardiothorac Surg Section Body Doc Link PMC2933604 Disease Relevance 0.53 Pain Relevance 0.21
Out of several signaling molecules in the downstream of AT1R, the phosphorylation of ERK, but not Akt or STAT3, was required for synaptophysin degradation (Fig. 5), suggesting that the UPS-dependent synaptophysin degradation is mediated by ERK activation.
Protein_catabolism (degradation) of Fig
5) Confidence 0.38 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.05 Pain Relevance 0
Angiotensin II–induced neuronal ERK activation, also observed in the diabetic retina (Fig. 1), resulted in the degradation of synaptophysin protein in vitro (Fig. 5).
Protein_catabolism (degradation) of Fig in neuronal associated with diabetes mellitus
6) Confidence 0.38 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.82 Pain Relevance 0
Interestingly, angiotensin II/AT1R signaling proved to cause the activation of the UPS, leading to synaptophysin degradation in neuronal cells (Fig. 4G–I).
Protein_catabolism (degradation) of Fig in neuronal
7) Confidence 0.38 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.14 Pain Relevance 0
Application with the proteasome inhibitor MG132 or lactacystin, but not the lysosome inhibitor E64, led to significant (P < 0.05) suppression of angiotensin II–induced degradation of synaptophysin (Fig. 4H and I).
Protein_catabolism (degradation) of Fig
8) Confidence 0.38 Published 2008 Journal Diabetes Section Body Doc Link PMC2494692 Disease Relevance 0.18 Pain Relevance 0
This unstable epoxide is not toxic, in contrast to other epoxides that are formed after enzymatic degradation in the liver (Fig. 4).
Protein_catabolism (degradation) of Fig in liver
9) Confidence 0.36 Published 2008 Journal Perspectives in Medicinal Chemistry Section Body Doc Link PMC2746576 Disease Relevance 0.24 Pain Relevance 0.23
On the basis of these results, we conclude that Ozz-E3 ligase promotes the ubiquitination and the degradation of sarcomeric MyHCemb (Fig. 8).
Protein_catabolism (degradation) of Fig
10) Confidence 0.33 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2844429 Disease Relevance 0 Pain Relevance 0
However, because HOXA3 has been previously shown to promote angiogenesis and endothelial cell migration, we chose to focus on factors from this gene set that directly promote EPC mobilization and EPC/endothelial cell migration (Fig. 6E).
Protein_catabolism (migration) of Fig in endothelial cell
11) Confidence 0.31 Published 2009 Journal Stem Cells (Dayton, Ohio) Section Body Doc Link PMC2733377 Disease Relevance 0.47 Pain Relevance 0.06
Retrograde tracing from the RPa (Fig. 5A) or DMH (not shown) show labeled neurons in the POA.
Protein_catabolism (Retrograde) of Fig in neurons
12) Confidence 0.23 Published 2010 Journal Diabetes Section Body Doc Link PMC2797943 Disease Relevance 0.25 Pain Relevance 0.03
In contrast, incubation with EndoN did not remove PSA from PC but specifically degraded PSA-NCAM (Fig.
Protein_catabolism (degraded) of Fig
13) Confidence 0.20 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2919383 Disease Relevance 0 Pain Relevance 0
Interestingly, administration of diacerein at 2–60 mg/kg daily in Tg197 mice resulted in a significant reduction (P < 0.05) in all three analytical histopathologic scores as compared with those of control Tg197 mice, which all developed synovitis with severe articular cartilage degradation and bone erosions (Fig. 3).
Protein_catabolism (degradation) of Fig in articular cartilage associated with synovitis
14) Confidence 0.18 Published 2004 Journal Arthritis Res Ther Section Body Doc Link PMC400419 Disease Relevance 0.60 Pain Relevance 0.17
Bone-associated osteoclasts were often observed in areas adjacent to bone metastases indicating increased osteoclastogenesis and elevated degradation of bone in these areas (Fig. 6).
Protein_catabolism (degradation) of Fig in osteoclasts associated with metastasis
15) Confidence 0.17 Published 2008 Journal BMC Cancer Section Body Doc Link PMC2529338 Disease Relevance 1.30 Pain Relevance 0.03
The UPS includes concerted actions of enzymes that link ubiquitin (Ub), a member of the heat-shock protein family, to protein substrates that are destined for degradation (Fig. 1).
Protein_catabolism (degradation) of Fig associated with shock
16) Confidence 0.11 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.39 Pain Relevance 0.03
Cells expressing wild type HIV-1 Gag-GFP exhibited attenuated HA-CXCR4 degradation (Fig 2A).
Protein_catabolism (degradation) of Fig associated with acquired immune deficiency syndrome or hiv infection
17) Confidence 0.09 Published 2008 Journal Virol J Section Body Doc Link PMC2262066 Disease Relevance 0.51 Pain Relevance 0
COS-1 cells overexpressing TSG101 also exhibited attenuated HA-CXCR4 degradation (Fig. 1A).
Protein_catabolism (degradation) of Fig
18) Confidence 0.08 Published 2008 Journal Virol J Section Body Doc Link PMC2262066 Disease Relevance 0.22 Pain Relevance 0
Fig. 1The ubiquitin–proteasome pathway of protein degradation.
Protein_catabolism (degradation) of Fig
19) Confidence 0.07 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.25 Pain Relevance 0
Fig. 2The balance between muscle hypertrophy and atrophy depends on whether protein synthesis is more active than degradation or vice versa.
Protein_catabolism (degradation) of Fig in muscle associated with hypertrophy and frailty
20) Confidence 0.07 Published 2007 Journal Pediatr Nephrol Section Body Doc Link PMC2259254 Disease Relevance 0.64 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox