INT274421

From wiki-pain
Jump to: navigation, search
Context Info
Confidence 0.55
First Reported 2009
Last Reported 2009
Negated 4
Speculated 1
Reported most in Body
Documents 1
Total Number 48
Disease Relevance 15.48
Pain Relevance 0

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

Anatomy Link Frequency
heart 11
fibroblasts 6
cardiomyocyte 5
embryos 4
lung 3
Mir130a (Mus musculus)
Pain Link Frequency Relevance Heat
isoflurane 48 46.56 Quite Low
anesthesia 48 44.88 Quite Low
imagery 48 31.28 Quite Low
Disease Link Frequency Relevance Heat
Targeted Disruption 1920 99.88 Very High Very High Very High
Embryonic Lethality 144 99.20 Very High Very High Very High
Heart Defects 96 97.96 Very High Very High Very High
Ventricular Heart Septal Defects 336 97.12 Very High Very High Very High
Repression 384 96.36 Very High Very High Very High
Cv General 4 Under Development 48 95.52 Very High Very High Very High
Cytomegalovirus Infection 336 92.08 High High
Hyperplasia 48 79.52 Quite High
Atrial Heart Septal Defects 48 73.20 Quite High
Disease 144 68.28 Quite High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
As a first step, we harvested transgenic embryos at embryonic day 13.5 and isolated total RNA to perform quantitative RT-PCR to confirm increased expression of miR-130a.
Gene_expression (expression) of miR-130a in embryos associated with targeted disruption
1) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 1.04 Pain Relevance 0
Quantitative RT-PCR performed with RNA prepared from hearts at embryonic day 11.5, 13.5, 15.5, neonatal (P0), and adult revealed the highest levels of miR-130a expression at birth with levels approximately 3-fold greater compared to the adult heart (compare columns 4 & 5, Fig. 1D).
Gene_expression (expression) of miR-130a in hearts
2) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0 Pain Relevance 0
As can be seen, miR-130a is predominately expressed in the heart and lung, with lower amounts in the kidney.
Gene_expression (expressed) of miR-130a in lung
3) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0 Pain Relevance 0
To study the effect of miRNA-130a on cardiac development, we generated transgenic mice with expression of the miR-130a precursor driven by the ?
Gene_expression (expression) of miR-130a associated with targeted disruption
4) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.82 Pain Relevance 0
It was our hypothesis that overexpression of miR-130a in the embryonic heart would lead to similar defects by inhibiting translation of FOG-2 mRNA.
Gene_expression (overexpression) of miR-130a in embryonic heart
5) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.54 Pain Relevance 0
As shown in figure 4D, this vector programmed expression of miR-130a in COS-7 cells in a dose-dependent fashion.
Gene_expression (expression) of miR-130a
6) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.08 Pain Relevance 0
We also demonstrate that cardiomyocytes express miR-130a and can attenuate translation of mRNAs with a FOG-2 3?
Gene_expression (express) of miR-130a in cardiomyocytes
7) Confidence 0.55 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2701631 Disease Relevance 0.24 Pain Relevance 0
When these constructs were transfected into NIH 3T3 fibroblasts (which are known to express miR-130a), we observed a 3.3-fold increase in translational efficiency when the microRNA target site was disrupted.
Gene_expression (express) of miR-130a in fibroblasts
8) Confidence 0.55 Published 2009 Journal PLoS ONE Section Abstract Doc Link PMC2701631 Disease Relevance 0.18 Pain Relevance 0
An analysis of the miRNAs that are predicted to target the FOG-2 UTR demonstrated that miR-130a was the most highly expressed (Fig. 1A).
Gene_expression (expressed) of miR-130a
9) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.07 Pain Relevance 0
Thus, expression of miR-130a and FOG-2 overlaps in the heart and lung and suggests that in these tissues miR-130a might modulate translation of the FOG-2 message.
Gene_expression (expression) of miR-130a in heart
10) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0 Pain Relevance 0
To test if expression of miR-130a would repress translation of our reporter construct containing the FOG-2 3?
Gene_expression (expression) of miR-130a
11) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.08 Pain Relevance 0
To examine expression of miR-130a in the developing heart, we took a PCR-based approach given the small amount of tissue available for RNA preparation at these early time points in development.
Spec (examine) Gene_expression (expression) of miR-130a in heart
12) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0 Pain Relevance 0
UTR, we co-transfected COS-7 fibroblasts with our miR-130a expression vector and our FOG-2 UTR reporter.
Gene_expression (transfected) of miR-130a in fibroblasts
13) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.13 Pain Relevance 0
UTR, we co-transfected COS-7 fibroblasts with our miR-130a expression vector and our FOG-2 UTR reporter.
Gene_expression (expression) of miR-130a in fibroblasts
14) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.12 Pain Relevance 0
This result demonstrates that miR-130a is present in the embryonic heart and regulated in a dynamic pattern throughout heart development.
Gene_expression (present) of miR-130a in embryonic heart
15) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0 Pain Relevance 0
To confirm that miR-130a was indeed expressed in the heart, we performed northern analysis on total RNA from several different adult mouse tissues using a radiolabeled probe specific to miR-130a (Fig. 1C).
Gene_expression (expressed) of miR-130a in heart
16) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0 Pain Relevance 0
MHC-miR-130a transgenic embryos displayed a significant increase in miR-130a expression (Fig. 5A).
Gene_expression (expression) of miR-130a in embryos associated with targeted disruption
17) Confidence 0.55 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 1.03 Pain Relevance 0
As expected, the anti-miR-130a 2?
Gene_expression (expected) of miR-130a
18) Confidence 0.48 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.28 Pain Relevance 0
Taken together with the loss of function experiments described above, these results demonstrate that miR-130a targets the FOG-2 3?
Gene_expression (targets) of miR-130a
19) Confidence 0.48 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.36 Pain Relevance 0
To demonstrate the effect of miR-130a overexpression on FOG-2 protein levels, we performed western analysis of ?
Gene_expression (overexpression) of miR-130a
20) Confidence 0.48 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2701631 Disease Relevance 0.86 Pain Relevance 0

General Comments

This test has worked.

Personal tools
Namespaces

Variants
Actions
Navigation
Toolbox