Enhancer ID: | E_01_0391 |
Species: | human |
Position : | chr16:53698968-53700968 |
Biosample name: | |
Experiment class : | High+Lowthroughput |
Enhancer type: | Enhancer |
Disease: | Diabetes mellitus, obesity |
Pubmed ID: | 29934339 |
Enhancer experiment: | transfection,RNA expression studies, RNA-Seq,m6A-RIP,6mA DNA Immunoprecipitation,Lipid Staining,Quantitative real time PCR,ChIP,Western blot, |
Enhancer experiment description: | We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebp?-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebp?-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. |
Target gene : | FTO |
Strong evidence: | qRT-PCR,qPCR,ChIP,3C |
Less strong evidence: | RNA-Seq |
Target gene experiment description: | We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebp?-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebp?-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. ;We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebp?-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebp?-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. |
TF name : | CEBPB(C/EBP-beta,IL6DBP,NF-IL6,TCF5) |
TF experiment: | transfection,RNA expression studies, RNA-Seq,m6A-RIP,6mA DNA Immunoprecipitation,Lipid Staining,Quantitative real time PCR,ChIP,Western blot, |
TF experiment description: | We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebp?-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebp?-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. ;We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebp?-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebp?-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. |
Enhancer function : | We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebp?-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebp?-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. |
Enhancer function experiment: | Immunohistochemical staining |
Enhancer function experiment description: |
We employed in vitro adipogenesis models to investigate molecular mechanisms by which Fto affects adipocyte development and function. Fto expression is upregulated during adipogenesis, and is required for the maintenance of CEBPB and Cebpd/CEBPD expression in murine and human adipocytes in vitro. Fto knockdown decreases both the number of 3T3-L1 cells that differentiate into adipocytes as well as the amount of lipid per mature adipocyte. This effect on adipocyte programming is conveyed, in part, by modulation of C/ebp?-regulated transcription. We find that Fto also affects Cebpd transcription by demethylating DNA N6-methyldeoxyadenosine in the Cebpd promoter. Fto is permissive for adipogenesis and promotes maintenance of lipid content in mature adipocytes by enabling C/ebp?-driven transcription and expression of Cebpd. These findings are consistent with the loss of fat mass in mice segregating for a dominant-negative Fto allele. |