m6A-centered Disease Response Information

General Information of the Disease (ID: M6ADIS0178)
Name
Acute viral hepatitis
ICD
ICD-11: 1E50
Full List of Target Gene(s) of This m6A-centered Disease Response
RIG-I-like receptor 1 (RIG-I)
 Target Info 
In total 4 item(s) under this target gene
Experiment 1 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary METTL3 and METTL14 leads to an increase in viral RNA recognition by RIG-I-like receptor 1 (RIG-I), thereby stimulating type I interferon production. The obvious advantage is that m6A deficiency in HBV and HCV induces a higher IFN synthesis and in turn enhance adaptive immunity.
Responsed Disease Acute hepatitis B [ICD-11: 1E50.1]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Down regulation
Pathway Response RIG-I-like receptor signaling pathway hsa04622
In-vitro Model Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
Experiment 2 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary METTL3 and METTL14 leads to an increase in viral RNA recognition by RIG-I-like receptor 1 (RIG-I), thereby stimulating type I interferon production. The obvious advantage is that m6A deficiency in HBV and HCV induces a higher IFN synthesis and in turn enhance adaptive immunity.
Responsed Disease Acute hepatitis B [ICD-11: 1E50.1]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
 Regulator Info 
Target Regulation Down regulation
Pathway Response RIG-I-like receptor signaling pathway hsa04622
In-vitro Model Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
Experiment 3 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary METTL3 and METTL14 leads to an increase in viral RNA recognition by RIG-I-like receptor 1 (RIG-I), thereby stimulating type I interferon production. The obvious advantage is that m6A deficiency in HBV and HCV induces a higher IFN synthesis and in turn enhance adaptive immunity.
Responsed Disease Acute hepatitis C [ICD-11: 1E50.2]
Target Regulator Methyltransferase-like 3 (METTL3) WRITER
 Regulator Info 
Target Regulation Down regulation
Pathway Response RIG-I-like receptor signaling pathway hsa04622
In-vitro Model Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
Experiment 4 Reporting the m6A-centered Disease Response by This Target Gene [1]
Response Summary METTL3 and METTL14 leads to an increase in viral RNA recognition by RIG-I-like receptor 1 (RIG-I), thereby stimulating type I interferon production. The obvious advantage is that m6A deficiency in HBV and HCV induces a higher IFN synthesis and in turn enhance adaptive immunity.
Responsed Disease Acute hepatitis C [ICD-11: 1E50.2]
Target Regulator Methyltransferase-like 14 (METTL14) WRITER
 Regulator Info 
Target Regulation Down regulation
Pathway Response RIG-I-like receptor signaling pathway hsa04622
In-vitro Model Huh-7 Adult hepatocellular carcinoma Homo sapiens CVCL_0336
Hep-G2 Hepatoblastoma Homo sapiens CVCL_0027
References
Ref 1 N (6)-Methyladenosine modification of hepatitis B and C viral RNAs attenuates host innate immunity via RIG-I signaling. J Biol Chem. 2020 Sep 11;295(37):13123-13133. doi: 10.1074/jbc.RA120.014260. Epub 2020 Jul 27.