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[title] => [Absence of the SRC-2 coactivator results in a glycogenopathy resembling Von Gierke's disease.]
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<div class="biblio_authors"><h3>Authors:</h3> <a href="/biblio/author/Chopra+AR">Chopra AR , Louet JF , Saha P , An J , Demayo F , Xu J , York B , Karpen S , Finegold M , Moore D , Chan L , Newgard CB , O'Malley BW ,</a></div>
<div class="biblio_source"><h3>Source: </h3> Science (New York, N.Y.), Volume 322, p.1395-9 (2008)</div>
<h3>URL:</h3><a href="http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=19039140">http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=19039140</a>
<h3>Abstract:</h3> <p>Hepatic glucose production is critical for basal brain function and survival when dietary glucose is unavailable. Glucose-6-phosphatase (G6Pase) is an essential, rate-limiting enzyme that serves as a terminal gatekeeper for hepatic glucose release into the plasma. Mutations in G6Pase result in Von Gierke's disease (glycogen storage disease-1a), a potentially fatal genetic disorder. We have identified the transcriptional coactivator SRC-2 as a regulator of fasting hepatic glucose release, a function that SRC-2 performs by controlling the expression of hepatic G6Pase. SRC-2 modulates G6Pase expression directly by acting as a coactivator with the orphan nuclear receptor RORalpha. In addition, SRC-2 ablation, in both a whole-body and liver-specific manner, resulted in a Von Gierke's disease phenotype in mice. Our results position SRC-2 as a critical regulator of mammalian glucose production.</p>
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[biblio_authors] => [Chopra AR , Louet JF , Saha P , An J , Demayo F , Xu J , York B , Karpen S , Finegold M , Moore D , Chan L , Newgard CB , O'Malley BW ,]
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[biblio_abst_e] => [<p>Hepatic glucose production is critical for basal brain function and survival when dietary glucose is unavailable. Glucose-6-phosphatase (G6Pase) is an essential, rate-limiting enzyme that serves as a terminal gatekeeper for hepatic glucose release into the plasma. Mutations in G6Pase result in Von Gierke's disease (glycogen storage disease-1a), a potentially fatal genetic disorder. We have identified the transcriptional coactivator SRC-2 as a regulator of fasting hepatic glucose release, a function that SRC-2 performs by controlling the expression of hepatic G6Pase. SRC-2 modulates G6Pase expression directly by acting as a coactivator with the orphan nuclear receptor RORalpha. In addition, SRC-2 ablation, in both a whole-body and liver-specific manner, resulted in a Von Gierke's disease phenotype in mice. Our results position SRC-2 as a critical regulator of mammalian glucose production.</p>]
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<div class="biblio_authors"><h3>Authors:</h3> <a href="/biblio/author/Chopra+AR">Chopra AR , Louet JF , Saha P , An J , Demayo F , Xu J , York B , Karpen S , Finegold M , Moore D , Chan L , Newgard CB , O'Malley BW ,</a></div>
<div class="biblio_source"><h3>Source: </h3> Science (New York, N.Y.), Volume 322, p.1395-9 (2008)</div>
<h3>URL:</h3><a href="http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=19039140">http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=19039140</a>
<h3>Abstract:</h3> <p>Hepatic glucose production is critical for basal brain function and survival when dietary glucose is unavailable. Glucose-6-phosphatase (G6Pase) is an essential, rate-limiting enzyme that serves as a terminal gatekeeper for hepatic glucose release into the plasma. Mutations in G6Pase result in Von Gierke's disease (glycogen storage disease-1a), a potentially fatal genetic disorder. We have identified the transcriptional coactivator SRC-2 as a regulator of fasting hepatic glucose release, a function that SRC-2 performs by controlling the expression of hepatic G6Pase. SRC-2 modulates G6Pase expression directly by acting as a coactivator with the orphan nuclear receptor RORalpha. In addition, SRC-2 ablation, in both a whole-body and liver-specific manner, resulted in a Von Gierke's disease phenotype in mice. Our results position SRC-2 as a critical regulator of mammalian glucose production.</p>
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<div class="biblio_authors"><h3>Authors:</h3> <a href="/biblio/author/Chopra+AR">Chopra AR , Louet JF , Saha P , An J , Demayo F , Xu J , York B , Karpen S , Finegold M , Moore D , Chan L , Newgard CB , O'Malley BW ,</a></div>
<div class="biblio_source"><h3>Source: </h3> Science (New York, N.Y.), Volume 322, p.1395-9 (2008)</div>
<h3>URL:</h3><a href="http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=19039140">http://www.sciencemag.org/cgi/pmidlookup?view=long&pmid=19039140</a>
<h3>Abstract:</h3> <p>Hepatic glucose production is critical for basal brain function and survival when dietary glucose is unavailable. Glucose-6-phosphatase (G6Pase) is an essential, rate-limiting enzyme that serves as a terminal gatekeeper for hepatic glucose release into the plasma. Mutations in G6Pase result in Von Gierke's disease (glycogen storage disease-1a), a potentially fatal genetic disorder. We have identified the transcriptional coactivator SRC-2 as a regulator of fasting hepatic glucose release, a function that SRC-2 performs by controlling the expression of hepatic G6Pase. SRC-2 modulates G6Pase expression directly by acting as a coactivator with the orphan nuclear receptor RORalpha. In addition, SRC-2 ablation, in both a whole-body and liver-specific manner, resulted in a Von Gierke's disease phenotype in mice. Our results position SRC-2 as a critical regulator of mammalian glucose production.</p>
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