Adipocyte P2 gene: developmental expression and homology of 5'-flanking sequences among fat cell-specific genes.

Hunt, Clayton R.; Ro, Hyo‐Sung; Dobson, Deborah E.; Min, Hye Yeong; Spiegelman, Bruce M.

doi:10.1073/pnas.83.11.3786

Cited by 318 publications

(175 citation statements)

References 28 publications

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“…The UCP-1 probe was obtained by PCR from position 261 to 1086 of the coding phase, 23 using sense 5 0 -AGACATCAT-CACCTTCCC-3 0 and antisense 5 0 -CAGCTGTTCAAAGCA-CAC-3 0 primers; the aP2 probe was a 525 bp PstI digest of the mouse aP2 cDNA, 24 and the 36B4 probe was a 750 bp PstI digest of the mouse 36B4 cDNA. 25 …”

Section: Probesmentioning

confidence: 99%

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

et al. 2001

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BACKGROUND: Several indirect arguments agree with the existence of a brown preadipocyte distinct from a white one. Nevertheless, to date, no molecular marker has been available to directly in vivo demonstrate this hypothesis. OBJECTIVE: The aim of this study was to find a gene expressed in brown preadipocyte but not in white and to use it as a molecular marker to analyse brown preadipocyte recruitment in different physiological and physiopathological situations. METHOD: Differential display was performed on stromal-vascular and adipocyte fractions of white and brown adipose tissues in rat. RESULTS: We identified a new gene, BUG, preferentially expressed in the stromal-vascular fraction of brown fat vs other adipose tissues fractions in adult rat. This RNA is also highly expressed in heart and, to a lesser extent, in other tissues such as kidney and brain. The BUG transcript is detected by in situ hybridization in putative preadipocytes within brown adipose tissue. Its level is transiently and specifically up-regulated during early stages of brown preadipocyte differentiation in a primary culture system, before the acquisition of late brown adipocyte phenotype. During development, BUG can be detected before the emergence of UCP-1 expression. In adult rats, BUG expression is inversely associated to brown adipose tissue (BAT) activation during cold exposure as well as in obese animals. CONCLUSIONS: The pattern of BUG expression agrees with an early divergence between brown and white adipocyte lineages. It also reveals the existence of a pool of committed brown preadipocytes within BAT that are recruited during cold exposure. BUG expression is increased in obese animals, suggesting that an early defect in brown preadipocyte differentiation could account for impaired BAT function in genetically obese rats.

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Section: Probesmentioning

confidence: 99%

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

et al. 2001

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“…PPAR␥ forms stable heterodimers with retinoid X receptors (RXR), and this complex binds to a specific DNA sequence, designated peroxisome proliferator-activated receptor response element (PPRE), in the promoter of the target genes (13). PPRE has been identified in the promoters of several genes whose protein products are indispensable for the adipocyte characteristics, such as fatty acid transport protein 1 (FATP1) (14), lipoprotein lipase (15), acyl-CoA synthase (16), and adipocyte lipid-binding protein (17).…”

mentioning

confidence: 99%

Enhancement of the Aquaporin Adipose Gene Expression by a Peroxisome Proliferator-activated Receptor γ

Kishida

Shimomura

Nishizawa

et al. 2001

Journal of Biological Chemistry

112

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The current study demonstrates that aquaporin adipose (AQPap), an adipose-specific glycerol channel (Kishida, K., Kuriyama, H., Funahashi, T., Shimomura, I., Kihara, S., Ouchi, N., Nishida, M., Nishizawa, H., Matsuda, M., Takahashi, M., Hotta, K., Nakamura, T. ؉/؊ heterozygous knockout mice. In 3T3-L1 adipocytes, PGZ augmented the AQPap mRNA expression and its promoter activity. Serial deletion of the promoter revealed the putative peroxisome proliferator-activated receptor response element (PPRE) at ؊93/؊77. In 3T3-L1 preadipocytes, the expression of PPAR␥ by transfection and PGZ activated the luciferase activity of the promoter containing the PPRE, whereas the PPRE-deleted mutant was not affected. The gel mobility shift assay showed the direct binding of PPAR␥-retinoid X receptor ␣ complex to the PPRE. ⌬PPAR␥, which we generated as the dominant negative PPAR␥ lacking the activation function-2 domain, suppressed the promoter activity in 3T3-L1 cells, dose-dependently. We conclude that AQPap is a novel adipose-specific target gene of PPAR␥ through the binding of PPAR␥-retinoid X receptor complex to the PPRE region in its promoter.

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“…The 422(aP2) and SCDl genes have been cloned and their 5'-flanking sequences characterized (Hunt et al 1986;Phillips et al 1986;Cook et al 1988;Ntambi et al 1988). Transfection experiments with chimeric 422(aP2) promoter-CAT constructs show that the gene is activated by glucocorticoid and cAMP (Cook et al 1988;Yang et al 1989), two agents used to induce differentiation of 3T3-L1 preadipocytes.…”

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confidence: 99%

Differentiation-induced gene expression in 3T3-L1 preadipocytes: CCAAT/enhancer binding protein interacts with and activates the promoters of two adipocyte-specific genes.

et al. 1989

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Previous studies have shown that differentiation of 3T3-L1 preadipocytes leads to the transcriptional activation of a group of adipose-specific genes. As an approach to defining the mechanism responsible for activating the expression of these genes, we investigated the binding of nuclear factors to the promoters of two differentiation-induced genes, the 422(aP2) and stearoyl-CoA desaturase 1 (SCDl) genes. DNase I footprinting and gel retardation analysis identified two binding regions within the promoters of each gene that interact with nuclear factors present in differentiated 3T3-L1 adipocytes. One differentiation-induced nuclear factor interacts specifically with a single binding site in the promoter of each gene. Competition experiments showed that the interaction of this nuclear factor with the SCDl promoter was prevented specifically by a synthetic oligonucleotide corresponding to the site footprinted in the 422(aP2) promoter. Several lines of evidence indicate that the differentiation-induced nuclear factor is CCAAT/enhancer binding protein (C/EBP), a DNA-binding protein first isolated from rat liver. Bacterially expressed recombinant C/EBP binds to the same site at which the differentiation-specific nuclear factor interacts within the promoter of each gene. Northern analysis with RNA from 3T3-L1 cells shows that C/EBP mRNA abundance increases markedly during differentiation. Transient cotransfection studies using a C/EBP expression vector demonstrate that C/EBP can function as a trans-activator of both the 422(aP2) and SCDl gene promoters.

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Adipocyte P2 gene: developmental expression and homology of 5'-flanking sequences among fat cell-specific genes.

Cited by 318 publications

References 28 publications

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

Cloning of BUG demonstrates the existence of a brown preadipocyte distinct from a white one

Enhancement of the Aquaporin Adipose Gene Expression by a Peroxisome Proliferator-activated Receptor γ

Differentiation-induced gene expression in 3T3-L1 preadipocytes: CCAAT/enhancer binding protein interacts with and activates the promoters of two adipocyte-specific genes.

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