Reference Report
| Reference | |||
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| Citation | Okamura, T., Shimizu, H., Nagao, T., Ueda, R., Ishii, S. (2007). ATF-2 regulates fat metabolism in Drosophila. Mol. Biol. Cell 18(4): 1519--1529. (Export to RIS) | ||
| FlyBase ID | FBrf0201502 | ||
| Publication Type | Research paper | ||
| PubMed ID | 17314398 | ||
| PubMed Abstract | ATF-2 is a member of the ATF/CREB family of transcription factors that is activated by stress-activated protein kinases such as p38. To analyze the physiological role of Drosophila ATF-2 (dATF-2), we generated dATF-2 knockdown flies using RNA interference. Reduced dATF-2 in the fat body, the fly equivalent of the mammalian liver and adipose tissue, decreased survival under starvation conditions. This was due to smaller triglyceride reserves of dATF-2 knockdown flies than control flies. Among multiple genes that control triglyceride levels, expression of the Drosophila PEPCK (dPEPCK) gene was strikingly reduced in dATF-2 knockdown flies. PEPCK is a key enzyme for both gluconeogenesis and glyceroneogenesis, which is a pathway required for triglyceride synthesis via glycerol-3-phosphate. Although the blood sugar level in dATF-2 knockdown flies was almost same as that in control flies, the activity of glyceroneogenesis was reduced in the fat bodies of dATF-2 knockdown flies. Thus, reduced glyceroneogenesis may at least partly contribute to decreased triglyceride stores in the dATF-2 knockdown flies. Furthermore we showed that dATF-2 positively regulated dPEPCK gene transcription via several CRE half-sites in the PEPCK promoter. Thus, dATF-2 is critical for regulation of fat metabolism. | ||
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| Secondary IDs | FBrf0195111 | ||
| Language of Publication | English | ||
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Parent Publication
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| Publication Type | Journal | ||
| Abbreviation | Mol. Biol. Cell | ||
| Title | Molecular Biology of the Cell | ||
| Publication Year | 1992- | ||
| ISBN/ISSN | 1059-1524 | ||
Data from Reference
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Alleles (7)
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Constructs (5)
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Genes (9)
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Insertions (1)
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Natural transposons (1)
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