FTO influences adipogenesis by regulating mitotic clonal expansion
نویسندگان
چکیده
منابع مشابه
FTO influences adipogenesis by regulating mitotic clonal expansion
The fat mass and obesity-associated (FTO) gene plays a pivotal role in regulating body weight and fat mass; however, the underlying mechanisms are poorly understood. Here we show that primary adipocytes and mouse embryonic fibroblasts (MEFs) derived from FTO overexpression (FTO-4) mice exhibit increased potential for adipogenic differentiation, while MEFs derived from FTO knockout (FTO-KO) mice...
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When induced to differentiate, growth-arrested 3T3-L1 preadipocytes synchronously reenter the cell cycle and undergo mitotic clonal expansion (MCE) followed by expression of genes that produce the adipocyte phenotype. The preadipocytes traverse the G(1)S checkpoint synchronously as evidenced by the expressionactivation of cdk2-cyclin-EA, turnover of p27kip1, hyperphosphorylation of Rb, transloc...
متن کاملCCAAT/enhancer-binding protein beta is required for mitotic clonal expansion during adipogenesis.
Hormonal induction of growth-arrested 3T3-L1 preadipocytes triggers a signaling cascade that culminates in adipogenesis. CCAATenhancer-binding protein (CEBP)beta is expressed immediately but gains DNA-binding activity only after a long lag as the cells synchronously begin mitotic clonal expansion (MCE). After MCE, a process required for adipogenesis, CEBPbeta activates expression of CEBPalpha a...
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متن کاملG9a is transactivated by C/EBPβ to facilitate mitotic clonal expansion during 3T3-L1 preadipocyte differentiation.
In 3T3-L1 preadipocyte differentiation, the CCAAT/enhancer-binding protein-β (C/EBPβ) is an important early transcription factor that activates cell cycle genes during mitotic clonal expansion (MCE), sequentially activating peroxisome proliferator-activated receptor-γ (PPARγ) and C/EBPα during terminal differentiation. Although C/EBPβ acquires its DNA binding activity via dual phosphorylation a...
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ژورنال
عنوان ژورنال: Nature Communications
سال: 2015
ISSN: 2041-1723
DOI: 10.1038/ncomms7792