INT174158

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Context Info
Confidence 0.55
First Reported 2003
Last Reported 2010
Negated 2
Speculated 0
Reported most in Body
Documents 23
Total Number 24
Disease Relevance 13.74
Pain Relevance 0.72

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

extracellular space (Cxadr) extracellular region (Cxadr) cell adhesion (Cxadr)
mitochondrion organization (Cxadr) plasma membrane (Cxadr) nucleus (Cxadr)
Anatomy Link Frequency
CAR 16
ventricle 3
atrium 2
myocardium 1
neurons 1
Cxadr (Mus musculus)
Pain Link Frequency Relevance Heat
Dopamine 36 98.76 Very High Very High Very High
anesthesia 128 91.68 High High
midbrain 6 88.92 High High
addiction 25 80.64 Quite High
Substantia nigra 36 72.16 Quite High
Central nervous system 18 72.08 Quite High
cytokine 11 36.00 Quite Low
fibrosis 21 33.28 Quite Low
imagery 30 5.00 Very Low Very Low Very Low
isoflurane 23 5.00 Very Low Very Low Very Low
Disease Link Frequency Relevance Heat
Targeted Disruption 1621 100.00 Very High Very High Very High
Cancer 156 99.86 Very High Very High Very High
Infection 52 99.68 Very High Very High Very High
Disease 156 99.16 Very High Very High Very High
Arrhythmia Under Development 399 98.98 Very High Very High Very High
Pressure And Volume Under Development 42 97.92 Very High Very High Very High
Arrhythmias 2 Under Development 84 97.72 Very High Very High Very High
Heart Rate Under Development 105 96.60 Very High Very High Very High
Coronary Heart Disease 21 95.88 Very High Very High Very High
Body Weight 42 94.72 High High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
We extended the expression analysis to cardiac ventricle (where differences in coupling were documented) and found that RNA levels of both cell–cell contact and adaptor proteins were altered secondary to loss of CAR (Fig. 6).
Negative_regulation (loss) of CAR in cardiac ventricle
1) Confidence 0.55 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.44 Pain Relevance 0
In parallel with the reduction of CAR protein levels, cellular exchange of the fluorescein dye increased from weeks 2–4 (Fig. 5, A and B).
Negative_regulation (reduction) of CAR in CAR
2) Confidence 0.55 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.35 Pain Relevance 0
Although the loss of CAR is well compensated in the myocardium, the altered electrical properties of the AV node result in a progressive AV block.
Negative_regulation (loss) of CAR in myocardium
3) Confidence 0.55 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.72 Pain Relevance 0
Toward understanding the molecular basis of the isolated AV block, we would envision a mechanism where the loss of CAR results in an altered protein composition of the tight junction, as documented by our expression and immunofluorescence analysis (Figs. 6 and 7).
Negative_regulation (loss) of CAR in CAR
4) Confidence 0.48 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.38 Pain Relevance 0
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).
Negative_regulation (loss) of CAR in CAR
5) Confidence 0.48 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.56 Pain Relevance 0
Furthermore, our preliminary expression profiling analysis indicated that the regulation of connexin expression in response to the loss of CAR differs between atrium and ventricle.
Negative_regulation (loss) of CAR in atrium
6) Confidence 0.48 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.65 Pain Relevance 0
We have generated a heart-specific inducible CAR knockout (KO) and found impaired electrical conduction between atrium and ventricle that increased with progressive loss of CAR.
Negative_regulation (loss) of CAR in ventricle associated with targeted disruption
7) Confidence 0.48 Published 2008 Journal The Journal of Experimental Medicine Section Abstract Doc Link PMC2556793 Disease Relevance 0.37 Pain Relevance 0
In the heart, this virus-induced disruption of CAR dimers would be expected to produce the same effect as the loss of CAR and, thus, ultimately lead to uncoupling and electrical conduction defects, which can accompany viral myocarditis (32).
Negative_regulation (loss) of CAR in CAR associated with arrhythmias 2 under development and coronary heart disease
8) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.79 Pain Relevance 0
At this time, there is no genetic defect of CAR associated with human disease, but our findings would suggest tight junction proteins as potential disease genes in genetic forms of isolated AV block.
Neg (no) Negative_regulation (defect) of CAR in CAR associated with disease
9) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.77 Pain Relevance 0
In conclusion, we have identified a novel mechanism for cardiac arrhythmia that involves the tight junction and results from loss of CAR, which is required to maintain functional gap junctions at the intercalated disc.
Negative_regulation (loss) of CAR in CAR associated with arrhythmia under development
10) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.87 Pain Relevance 0
Ultrastructure of the KO cardiac sarcomere and intercalated disc is not significantly altered upon loss of CAR (Fig.
Negative_regulation (loss) of CAR in CAR associated with targeted disruption
11) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.19 Pain Relevance 0
CAR mRNA levels declined to <10% from 1 wk after injections.
Negative_regulation (declined) of CAR mRNA in CAR
12) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.58 Pain Relevance 0.06
Loss of the tight junction protein CAR leads to severe AV block but leaves the electrical properties of the atrial and ventricular myocardium remarkably unaffected.
Negative_regulation (Loss) of CAR in ventricular myocardium
13) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.59 Pain Relevance 0
CAR deficiency results in midembryonic lethality with pericardial edema that is related to altered organization of myofibrils and increased proliferation of cardiomyocytes (14–16).
Negative_regulation (deficiency) of CAR in CAR associated with pressure and volume under development
14) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.58 Pain Relevance 0
To determine which genes contribute to the development of the AV block phenotype, we have obtained preliminary expression profiling data from mouse atria that show the expected down-regulation of CAR (>10-fold down in the KO) and suggest a specific role of connexin 43.
Negative_regulation (regulation) of CAR in CAR associated with targeted disruption
15) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.34 Pain Relevance 0
Thus, CAR deficiency resulted in binodal disease in 50% of CAR KO mice.
Negative_regulation (deficiency) of CAR in CAR associated with targeted disruption and disease
16) Confidence 0.41 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 1.07 Pain Relevance 0.09
The altered protein levels of Cx45 and Cx43 (both >40% reduction) in KO hearts compared with Cx40, which was unchanged (Fig. 6 D), indicate a selective effect of CAR on a subset of connexins.
Negative_regulation (effect) of CAR in CAR associated with targeted disruption
17) Confidence 0.40 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.37 Pain Relevance 0
This indicates that CAR KO cardiomyocytes, unlike AV nodal cells are not limited by GAP junction activity, a feature which could derive both from altered expression of connexins and differential localization of CAR between the cell types (Fig. 3).
Neg (not) Negative_regulation (limited) of CAR in CAR associated with targeted disruption
18) Confidence 0.40 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.83 Pain Relevance 0.04
Although the structure of the intercalated discs was maintained, protein composition changed in response to the loss of CAR.
Negative_regulation (loss) of CAR in CAR
19) Confidence 0.35 Published 2008 Journal The Journal of Experimental Medicine Section Body Doc Link PMC2556793 Disease Relevance 0.41 Pain Relevance 0
These findings demonstrate that CAR deficiency limits infection of wild type DA neurons by Ad5 and provide a rationale for the development of tropism-modified, CAR-independent Ad-vectors for use in gene therapy of human PD.



Negative_regulation (deficiency) of CAR in CAR associated with parkinson's disease, dopamine and infection
20) Confidence 0.28 Published 2010 Journal PLoS ONE Section Abstract Doc Link PMC2941453 Disease Relevance 0.67 Pain Relevance 0.34

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