m6A Target Gene Information
General Information of the m6A Target Gene (ID: M6ATAR00236)
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
EHHADH
can be regulated by the following regulator(s), and cause disease/drug response(s). You can browse detail information of regulator(s) or disease/drug response(s).
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Methyltransferase-like 3 (METTL3) [WRITER]
Representative RNA-seq result indicating the expression of this target gene regulated by METTL3 | ||
Cell Line | Caco-2 cell line | Homo sapiens |
Treatment: shMETTL3 Caco-2 cells
Control: shNTC Caco-2 cells
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GSE167075 | |
Regulation |
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logFC: -7.43E-01 p-value: 3.92E-35 |
More Results | Click to View More RNA-seq Results | |
Representative RIP-seq result supporting the interaction between EHHADH and the regulator | ||
Cell Line | MDA-MB-231 | Homo sapiens |
Regulation | logFC: 7.66E+00 | GSE60213 |
In total 1 item(s) under this regulator | ||||
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene | [1] | |||
Response Summary | Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acc1, Acly, Dgat2, Peroxisomal bifunctional enzyme (EHHADH), Fasn, Foxo, Pgc1a and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice. | |||
Target Regulation | Up regulation | |||
Responsed Disease | Type 2 diabetes mellitus | ICD-11: 5A11 | ||
Pathway Response | Insulin resistance | hsa04931 | ||
Cell Process | Lipid metabolism | |||
In-vitro Model | Hep-G2 | Hepatoblastoma | Homo sapiens | CVCL_0027 |
In-vivo Model | Hepatocyte-specific METTL3 knockout mice (TBG-Cre, METTL3 fl/fl) were generated by crossing mice with TBG-Cre Tg mice. METTL3 flox (METTL3 fl/fl) and hepatocyte-specific METTL3 knockout mice (TBG-Cre, METTL3 fl/fl) were used for experiments. | |||
Type 2 diabetes mellitus [ICD-11: 5A11]
In total 1 item(s) under this disease | ||||
Experiment 1 Reporting the m6A-centered Disease Response | [1] | |||
Response Summary | Type 2 diabetes (T2D) is characterized by lack of insulin, insulin resistance and high blood sugar. METTL3 silence decreased the m6A methylated and total mRNA level of Fatty acid synthase (Fasn), subsequently inhibited fatty acid metabolism. The expression of Acc1, Acly, Dgat2, Peroxisomal bifunctional enzyme (EHHADH), Fasn, Foxo, Pgc1a and Sirt1, which are critical to the regulation of fatty acid synthesis and oxidation were dramatically decreased in livers of hepatocyte-specific METTL3 knockout mice. | |||
Responsed Disease | Type 2 diabetes mellitus [ICD-11: 5A11] | |||
Target Regulator | Methyltransferase-like 3 (METTL3) | WRITER | ||
Target Regulation | Up regulation | |||
Pathway Response | Insulin resistance | hsa04931 | ||
Cell Process | Lipid metabolism | |||
In-vitro Model | Hep-G2 | Hepatoblastoma | Homo sapiens | CVCL_0027 |
In-vivo Model | Hepatocyte-specific METTL3 knockout mice (TBG-Cre, METTL3 fl/fl) were generated by crossing mice with TBG-Cre Tg mice. METTL3 flox (METTL3 fl/fl) and hepatocyte-specific METTL3 knockout mice (TBG-Cre, METTL3 fl/fl) were used for experiments. | |||