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Identifying the molecular mechanism ...
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Temple, Karla Ann.
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Identifying the molecular mechanism of PPARgamma transcriptional regulation.
紀錄類型:
書目-電子資源 : Monograph/item
正題名/作者:
Identifying the molecular mechanism of PPARgamma transcriptional regulation./
作者:
Temple, Karla Ann.
面頁冊數:
150 p.
附註:
Source: Dissertation Abstracts International, Volume: 65-06, Section: B, page: 2787.
Contained By:
Dissertation Abstracts International65-06B.
標題:
Biology, Molecular. -
電子資源:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3136549
ISBN:
0496837478
Identifying the molecular mechanism of PPARgamma transcriptional regulation.
Temple, Karla Ann.
Identifying the molecular mechanism of PPARgamma transcriptional regulation.
- 150 p.
Source: Dissertation Abstracts International, Volume: 65-06, Section: B, page: 2787.
Thesis (Ph.D.)--The University of Chicago, 2004.
The metabolic syndrome or syndrome X is collectivey defined as obesity/overweight, hyperlipidemia, insulin resistance, and hypertension. As one of many rapidly progressing nontransmittable diseases, obesity has become a serious public health concern. Because obesity is defined as excess adipose tissue, which expresses high levels of peroxisome proliferator-activated receptor gamma (PPARgamma), and synthetic ligands for PPARgamma improve insulin sensitivity, understanding the function of PPARgamma is of great interest in dissecting the metabolic syndrome. PPARgamma is a member of the nuclear hormone receptor superfamily of transcription factors, and regulates transcription of genes involved in glucose and lipid metabolism. As a transcription factor, PPARgamma has been shown to heterodimerize with retinoid X receptor (RXR) and bind to a direct repeat sequence on a PPAR response element (PPRE). Although positive regulation by PPARgamma is thought to occur through direct DNA binding, the mechanism for PPARgamma-mediated negative regulation is unknown. In this dissertation, the hypothesis that both positive and negative regulation of PPAR-responsive genes requires DNA binding is examined. My findings demonstrate that PPARgamma DNA binding is necessary for the in vitro positive regulation of PPARgamma responsive genes. In addition, there is strong evidence to suggest that there is promiscuity in PPARgamma binding to a PPRE, while the binding of RXR to a PPRE is highly stringent.
ISBN: 0496837478Subjects--Topical Terms:
1017719
Biology, Molecular.
Identifying the molecular mechanism of PPARgamma transcriptional regulation.
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The metabolic syndrome or syndrome X is collectivey defined as obesity/overweight, hyperlipidemia, insulin resistance, and hypertension. As one of many rapidly progressing nontransmittable diseases, obesity has become a serious public health concern. Because obesity is defined as excess adipose tissue, which expresses high levels of peroxisome proliferator-activated receptor gamma (PPARgamma), and synthetic ligands for PPARgamma improve insulin sensitivity, understanding the function of PPARgamma is of great interest in dissecting the metabolic syndrome. PPARgamma is a member of the nuclear hormone receptor superfamily of transcription factors, and regulates transcription of genes involved in glucose and lipid metabolism. As a transcription factor, PPARgamma has been shown to heterodimerize with retinoid X receptor (RXR) and bind to a direct repeat sequence on a PPAR response element (PPRE). Although positive regulation by PPARgamma is thought to occur through direct DNA binding, the mechanism for PPARgamma-mediated negative regulation is unknown. In this dissertation, the hypothesis that both positive and negative regulation of PPAR-responsive genes requires DNA binding is examined. My findings demonstrate that PPARgamma DNA binding is necessary for the in vitro positive regulation of PPARgamma responsive genes. In addition, there is strong evidence to suggest that there is promiscuity in PPARgamma binding to a PPRE, while the binding of RXR to a PPRE is highly stringent.
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