1996
DOI: 10.1210/endo.137.7.8770915
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Regulation of preadipocyte factor-1 gene expression during 3T3-L1 cell differentiation.

Abstract: Preadipocyte factor-1 (Pref-1), a novel gene product isolated from murine preadipocyte 3T3-L1 cells, is thought to function as a negative regulator of adipocyte differentiation. We investigated the regulation of Pref-1 expression in 3T3-L1 preadipocytes during proliferation, growth arrest, and early differentiation in the presence and absence of three well described differentiation antagonists: interleukin-11 (IL-11), transforming growth factor-beta, and tumor necrosis factor-alpha. Northern blot analysis was … Show more

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Cited by 36 publications
(29 citation statements)
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“…Tumor necrosis factor α, interferon γ, and interleukins 1 and 11 strongly decrease adipose conversion in cell lines as well as in rat, porcine and human primary cells [22,27,56,91,133,178,240,247]. The mechanism of action of TNFα has been largely investigated.…”
Section: Other Growth Factors and Cytokinesmentioning
confidence: 99%
“…Tumor necrosis factor α, interferon γ, and interleukins 1 and 11 strongly decrease adipose conversion in cell lines as well as in rat, porcine and human primary cells [22,27,56,91,133,178,240,247]. The mechanism of action of TNFα has been largely investigated.…”
Section: Other Growth Factors and Cytokinesmentioning
confidence: 99%
“…The catabolic and antiadipogenic effects of TNFa decrease adipose conversion in various cell lines as well as in rat, porcine, and human primary cells (Grégoire et al 1992, Hotamisligil et al 1994, Vassaux et al 1994, Boney et al 1996, Boone et al 2000. TNFa acts directly on lipid metabolism by decreasing parameters related with fatty acid uptake (decrease in lipoprotein lipase (LPL), fatty acid transport (FAT), and fatty acid transport protein (FATP) expressions) and lipogenesis (decrease in fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC) expression, and glycerol-3-phosphate dehydrogenase (GPDH) activity), and by increasing lipolysis (Dani et al 1989, Sethi & Hotamisligil 1999.…”
Section: Introductionmentioning
confidence: 99%
“…It is well established that IGF-I mitogenic effects are mediated, at least in part, by the members of the mitogen-activated protein kinase family, termed extracellular-signal-regulated kinase 1 and 2 (ERK1 and ERK2), as well as by the activation of phosphoinositide 3-kinase (PI 3-kinase) and Akt. The mechanisms by which IGF-I promotes the differentiation of various mesenchymal cell types, including adipocytes and cardiomyocytes (Boney et al 1996, Milasincic et al 1996, Boney et al 1998, are also under investigation. All of these cell types have in common a requirement that cell-cycle arrest occur prior to progression to differentiation.…”
Section: Introductionmentioning
confidence: 99%