INT247791

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Context Info
Confidence 0.22
First Reported 2008
Last Reported 2008
Negated 0
Speculated 0
Reported most in Body
Documents 4
Total Number 4
Disease Relevance 0.96
Pain Relevance 0.03

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

cell adhesion (Cdh2) plasma membrane (Cdh2) protein complex (Cdh2)
Anatomy Link Frequency
CAR 2
cardiomyocytes 1
Cdh2 (Mus musculus)
Pain Link Frequency Relevance Heat
imagery 3 69.48 Quite High
Morphine 77 50.00 Quite Low
tolerance 25 50.00 Quite Low
Physical dependence 15 50.00 Quite Low
Central nervous system 11 50.00 Quite Low
Spinal cord 8 39.72 Quite Low
narcan 6 21.92 Low Low
anesthesia 18 19.12 Low Low
isoflurane 3 16.68 Low Low
withdrawal 23 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 276 95.72 Very High Very High Very High
Congenital Anomalies 3 84.68 Quite High
Arrhythmia Under Development 57 80.72 Quite High
Myelodysplastic Syndromes 3 70.32 Quite High
Arrhythmias 2 Under Development 12 60.44 Quite High
Disease 21 57.92 Quite High
Deafness 3 52.48 Quite High
Cancer 3 51.44 Quite High
Hypersensitivity 6 50.64 Quite High
Drug Dependence 15 50.00 Quite Low

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
N-cadherin was used as a loading control and marker for crude synaptosomal fraction, whereas ?
Localization (used) of N-cadherin
1) Confidence 0.22 Published 2008 Journal Mol Pain Section Body Doc Link PMC2576175 Disease Relevance 0 Pain Relevance 0
The primary antibodies used were the following: rat anti-HCN4 (Abcam) and anti-CAR (rabbit polyclonal, raised against the Fc fusion protein containing the CA extracellular domain), anti-CAR (rabbit polyclonal; Santa Cruz Biotechnology, Inc.), anti–N-cadherin (mouse monoclonal; Invitrogen), anti-Cx43 (mouse monoclonal; Invitrogen), and anti–?
Localization (anti) of N-cadherin in CAR
2) Confidence 0.17 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.07 Pain Relevance 0.03
Although the tight junction as a whole is not affected with normal ultrastructure and proper sublocalization of N-cadherin, we see connexins specifically respond to the loss of CAR with redistribution away from the intercalated disc and reduced protein levels (potentially a combination of reduced expression and degradation of mislocalized protein).
Localization (sublocalization) of N-cadherin in CAR
3) Confidence 0.17 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.50 Pain Relevance 0
Although the expression and localization of the adherens junction protein N-cadherin was unaffected (Fig. 7 B), the localization of the gap junction protein Connexin 43 (Cx43) was altered in KO cardiomyocytes 8 wk after induction (Fig. 7 C).
Localization (localization) of N-cadherin in cardiomyocytes associated with targeted disruption
4) Confidence 0.16 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.38 Pain Relevance 0

General Comments

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