INT181818

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Context Info
Confidence 0.78
First Reported 2005
Last Reported 2011
Negated 0
Speculated 0
Reported most in Body
Documents 50
Total Number 57
Disease Relevance 24.33
Pain Relevance 2.71

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

cytosol (Ppargc1a) RNA binding (Ppargc1a) mitochondrion organization (Ppargc1a)
nucleus (Ppargc1a) DNA binding (Ppargc1a) transcription factor binding (Ppargc1a)
Anatomy Link Frequency
cardiac myocytes 3
skeletal muscle 2
ventricle 1
neuronal 1
liver 1
Ppargc1a (Mus musculus)
Pain Link Frequency Relevance Heat
electroacupuncture 656 98.86 Very High Very High Very High
Acupuncture 80 95.52 Very High Very High Very High
fibrosis 70 95.40 Very High Very High Very High
alcohol 34 94.28 High High
tolerance 265 92.68 High High
medulla 20 91.52 High High
cerebral cortex 50 91.08 High High
Hippocampus 14 88.04 High High
cOX1 8 74.28 Quite High
adenocard 4 69.24 Quite High
Disease Link Frequency Relevance Heat
Targeted Disruption 261 99.98 Very High Very High Very High
Hyperglycemia 47 99.88 Very High Very High Very High
Insulin Resistance 505 99.34 Very High Very High Very High
Diabetes Mellitus 393 99.12 Very High Very High Very High
Stress 171 98.88 Very High Very High Very High
Obesity 988 98.52 Very High Very High Very High
Lifespan 43 96.88 Very High Very High Very High
Hypertension 100 96.72 Very High Very High Very High
Congenital Anomalies 188 95.76 Very High Very High Very High
Fibrosis 70 95.40 Very High Very High Very High

Sentences Mentioned In

Key: Protein Mutation Event Anatomy Negation Speculation Pain term Disease term
Meanwhile, decreased expression of PPARGC1A in skeletal muscle has been associated with an increased risk for type II diabetes.
Gene_expression (expression) of PPARGC1A in skeletal muscle associated with diabetes mellitus
1) Confidence 0.78 Published 2008 Journal BMC Cardiovasc Disord Section Body Doc Link PMC2637232 Disease Relevance 0.70 Pain Relevance 0
Forced expression of PPARGC1A has been demonstrated to activate mitochondrial biogenesis and metabolism in cardiac myocytes in vitro, and cardiac-specific over-expression of PPARGC1A in transgenic mice has led to mitochondrial proliferation and loss of sarcomeric structure in cardiac myocytes, leading to a dilated cardiomyopathy [20].
Gene_expression (expression) of PPARGC1A in cardiac myocytes associated with targeted disruption and dilated cardiomyopathy
2) Confidence 0.78 Published 2008 Journal BMC Cardiovasc Disord Section Body Doc Link PMC2637232 Disease Relevance 0.88 Pain Relevance 0
Forced expression of PPARGC1A has been demonstrated to activate mitochondrial biogenesis and metabolism in cardiac myocytes in vitro, and cardiac-specific over-expression of PPARGC1A in transgenic mice has led to mitochondrial proliferation and loss of sarcomeric structure in cardiac myocytes, leading to a dilated cardiomyopathy [20].
Gene_expression (expression) of PPARGC1A in cardiac myocytes associated with targeted disruption and dilated cardiomyopathy
3) Confidence 0.78 Published 2008 Journal BMC Cardiovasc Disord Section Body Doc Link PMC2637232 Disease Relevance 0.91 Pain Relevance 0
A previous study indicated that the expression level of PGC-1?
Gene_expression (expression) of PGC
4) Confidence 0.75 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.07 Pain Relevance 0
The expression of PGC-1?
Gene_expression (expression) of PGC
5) Confidence 0.75 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.41 Pain Relevance 0.04
These results indicate that high ROS levels activate CREB phosphorylation and result in increased expression of PGC-1?.
Gene_expression (expression) of PGC
6) Confidence 0.75 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.07 Pain Relevance 0
This result indicates that the reduced expression of PGC-1?
Gene_expression (expression) of PGC
7) Confidence 0.75 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.08 Pain Relevance 0
In response to glucagon, protein kinase A phosphorylates transcription factor CREB at Ser133 and increases its transcriptional activity (23), which activates the expression of PGC-1?
Gene_expression (expression) of PGC
8) Confidence 0.75 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.09 Pain Relevance 0.03
Biochemical analysis of these cells also revealed an
                       increase in the expression of PGC-1? 
Gene_expression (expression) of PGC
9) Confidence 0.75 Published 2010 Journal Aging (Albany NY) Section Body Doc Link PMC2837205 Disease Relevance 0.17 Pain Relevance 0
Direct support for this proposition comes from the observation that over-expression of PGC-1?
Gene_expression (over) of PGC
10) Confidence 0.75 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2716517 Disease Relevance 0.81 Pain Relevance 0
Several studies reported that insulin reduces the expression of PGC-1?
Gene_expression (expression) of PGC
11) Confidence 0.75 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.37 Pain Relevance 0.09
Lastly, forced expression of PGC-1?
Gene_expression (expression) of PGC-1
12) Confidence 0.74 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1064854 Disease Relevance 0.37 Pain Relevance 0
Third, studies in primary cardiac myocytes in culture and in the hearts of transgenic mice have demonstrated that overexpression of PGC-1?
Gene_expression (overexpression) of PGC-1 in cardiac myocytes associated with targeted disruption
13) Confidence 0.74 Published 2005 Journal PLoS Biology Section Body Doc Link PMC1064854 Disease Relevance 0.37 Pain Relevance 0
It is plausible that PPARGC1A levels and PPARGC1A gene polymorphisms could be associated with cardiac function, as PPARGC1A is an important regulator of metabolic pathways, and as heart failure and diastolic dysfunction can be caused by metabolic disturbances, such as diabetes and insulin resistance [40-42], obesity [8,9] and hypertension [1].
Gene_expression (levels) of PPARGC1A in heart associated with diabetes mellitus, hypertension, obesity, insulin resistance, coronary heart disease and myocardial infarction
14) Confidence 0.67 Published 2008 Journal BMC Cardiovasc Disord Section Body Doc Link PMC2637232 Disease Relevance 1.26 Pain Relevance 0
MAPK are upstream of the Pgc-1?
Gene_expression (upstream) of Pgc
15) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775956 Disease Relevance 0.09 Pain Relevance 0
Insulin suppresses the expression of the PGC-1?
Gene_expression (expression) of PGC
16) Confidence 0.65 Published 2008 Journal Diabetes Section Body Doc Link PMC2494675 Disease Relevance 0.09 Pain Relevance 0.05
CONCLUSIONS—Our results indicate that the reduction of ROS is a potential therapeutic target of liver insulin resistance, at least partly by the reduced expression of PGC-1?.



Gene_expression (expression) of PGC in liver associated with insulin resistance
17) Confidence 0.65 Published 2008 Journal Diabetes Section Abstract Doc Link PMC2494675 Disease Relevance 0.41 Pain Relevance 0
 ; loxP-flanked Pgc1?
Gene_expression (flanked) of Pgc
18) Confidence 0.65 Published 2009 Journal PLoS ONE Section Body Doc Link PMC2775956 Disease Relevance 0.08 Pain Relevance 0
This is somewhat supported by our current data of upregulated PGC-1?
Gene_expression (data) of PGC
19) Confidence 0.65 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890411 Disease Relevance 0.25 Pain Relevance 0
, anti-PGC1?
Gene_expression (anti) of PGC
20) Confidence 0.65 Published 2010 Journal PLoS ONE Section Body Doc Link PMC2890411 Disease Relevance 0 Pain Relevance 0

General Comments

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