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Int J Clin Exp Pathol 2(3),275-285;2009.
Original Article
Gene profiling reveals a diverse array of pathways inhibited by nuclear receptor SHP
during adipogenesis
Guisheng Song, Kyungtae Park and Li Wang
Departments of Medicine and Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT
84112; Department of Microbiology, Molecular Genetics & Immunology, University of Kansas Medical Center, Kansas, KS 66160
Received 3 October 2008; Accepted 10 October 2008; Available online 03 November 2008
Abstract: Orphan receptor small heterodimer partner (SHP, NROB2) has been shown to be a metabolic regulator in pathways associated with
several major aspects of the metabolic syndrome. However, the significance and transcriptional regulatory role of SHP in adipocyte
differentiation remain unclear. Transcriptional profiles of 3T3-L1 preadipocytes and early differentiating preadipocytes in response to SHP were
systemically surveyed using Affymetrix Genome Array representing well-characterized 14,000 genes. Analysis revealed about 963 genes that
were up- or down-regulated by more than 2-fold during differentiation and/or by the overexpression of SHP. These genes were organized into 4
clusters that demonstrated concerted changes in expression of genes controlling various aspects of the cellular events and metabolism.
Quantitative PCR was employed to further characterize gene expression and led to the identification of several key regulators and stimulators
of the adipogenic program as potential new SHP targets. Overexpression of SHP inhibited the differentiation process as well as the
accumulation of neutral lipids within the cells. Our data suggests that SHP may function as a molecular switch that governs adipogenesis and
a potent adipogenic suppressor that maintains preadipocytes in an undifferentiated state through inhibition of the adipogenic transcription
factors and stimulators. Developing SHP agonist may promise a future treatment for obesity. (IJCEP810002).
Key Words: nuclear receptor, SHP, adipocyte differentiation
Full text PDF , Supplemental figure 1 and figure 2, Supplemental table 1 and table 2-9
Address all correspondence to: Li Wang, PhD, Departments of Medicine and Oncological Sciences, Huntsman Cancer Institute, University of
Utah School of Medicine, Salt Lake City, UT 84112Tel: 801-587-4616; Fax: 801-587-9415; E-mail: l.wang@hsc.utah.edu
Original Article
Gene profiling reveals a diverse array of pathways inhibited by nuclear receptor SHP
during adipogenesis
Guisheng Song, Kyungtae Park and Li Wang
Departments of Medicine and Oncological Sciences, Huntsman Cancer Institute, University of Utah School of Medicine, Salt Lake City, UT
84112; Department of Microbiology, Molecular Genetics & Immunology, University of Kansas Medical Center, Kansas, KS 66160
Received 3 October 2008; Accepted 10 October 2008; Available online 03 November 2008
Abstract: Orphan receptor small heterodimer partner (SHP, NROB2) has been shown to be a metabolic regulator in pathways associated with
several major aspects of the metabolic syndrome. However, the significance and transcriptional regulatory role of SHP in adipocyte
differentiation remain unclear. Transcriptional profiles of 3T3-L1 preadipocytes and early differentiating preadipocytes in response to SHP were
systemically surveyed using Affymetrix Genome Array representing well-characterized 14,000 genes. Analysis revealed about 963 genes that
were up- or down-regulated by more than 2-fold during differentiation and/or by the overexpression of SHP. These genes were organized into 4
clusters that demonstrated concerted changes in expression of genes controlling various aspects of the cellular events and metabolism.
Quantitative PCR was employed to further characterize gene expression and led to the identification of several key regulators and stimulators
of the adipogenic program as potential new SHP targets. Overexpression of SHP inhibited the differentiation process as well as the
accumulation of neutral lipids within the cells. Our data suggests that SHP may function as a molecular switch that governs adipogenesis and
a potent adipogenic suppressor that maintains preadipocytes in an undifferentiated state through inhibition of the adipogenic transcription
factors and stimulators. Developing SHP agonist may promise a future treatment for obesity. (IJCEP810002).
Key Words: nuclear receptor, SHP, adipocyte differentiation
Full text PDF , Supplemental figure 1 and figure 2, Supplemental table 1 and table 2-9
Address all correspondence to: Li Wang, PhD, Departments of Medicine and Oncological Sciences, Huntsman Cancer Institute, University of
Utah School of Medicine, Salt Lake City, UT 84112Tel: 801-587-4616; Fax: 801-587-9415; E-mail: l.wang@hsc.utah.edu
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