General Information of the m6A Target Gene (ID: M6ATAR00173)
Target Name Protein argonaute-1 (AGO1)
Synonyms
Argonaute1; hAgo1; Argonaute RISC catalytic component 1; Eukaryotic translation initiation factor 2C 1; eIF-2C 1; eIF2C 1; Putative RNA-binding protein Q99; EIF2C1
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Gene Name AGO1
Chromosomal Location 1p34.3
Family argonaute family; Ago subfamily
Function
Required for RNA-mediated gene silencing (RNAi). Binds to short RNAs such as microRNAs (miRNAs) or short interfering RNAs (siRNAs), and represses the translation of mRNAs which are complementary to them. Lacks endonuclease activity and does not appear to cleave target mRNAs. Also required for transcriptional gene silencing (TGS) of promoter regions which are complementary to bound short antigene RNAs (agRNAs).
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Gene ID 26523
Uniprot ID
AGO1_HUMAN
HGNC ID
HGNC:3262
Ensembl Gene ID
ENSG00000092847
KEGG ID
hsa:26523
Full List of m6A Methylation Regulator of This Target Gene and Corresponding Disease/Drug Response(s)
AGO1 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).
Browse Regulator
Browse Disease
Fat mass and obesity-associated protein (FTO) [ERASER]
In total 1 item(s) under this regulator
Experiment 1 Reporting the m6A Methylation Regulator of This Target Gene [1]
Response Summary loss of m6A RNA methylation and increased translation in human glioblastoma cells as well as a role for miRNAs in the modulation of m6A RNA demethylation in genes that are most efficiently translated during glioma stem cells differentiation. Ectopic expression of the RRACH-binding miR-145 induces loss of m6A, formation of FTO/Protein argonaute-1 (AGO1)/ILF3/miR-145 complexes on a clinically relevant tumor suppressor gene (CLIP3) and significant increase in its nascent translation.
Target Regulation Up regulation
Responsed Disease Glioblastoma ICD-11: 2A00.00
In-vitro Model GBM1 Glioblastoma Homo sapiens CVCL_DG57
GBM2 Glioblastoma Homo sapiens CVCL_DG58
GBM3 Glioblastoma Homo sapiens CVCL_DG59
Brain cancer [ICD-11: 2A00]
In total 1 item(s) under this disease
Experiment 1 Reporting the m6A-centered Disease Response [1]
Response Summary loss of m6A RNA methylation and increased translation in human glioblastoma cells as well as a role for miRNAs in the modulation of m6A RNA demethylation in genes that are most efficiently translated during glioma stem cells differentiation. Ectopic expression of the RRACH-binding miR-145 induces loss of m6A, formation of FTO/Protein argonaute-1 (AGO1)/ILF3/miR-145 complexes on a clinically relevant tumor suppressor gene (CLIP3) and significant increase in its nascent translation.
Responsed Disease Glioblastoma [ICD-11: 2A00.00]
Target Regulator Fat mass and obesity-associated protein (FTO) ERASER
Target Regulation Up regulation
In-vitro Model GBM1 Glioblastoma Homo sapiens CVCL_DG57
GBM2 Glioblastoma Homo sapiens CVCL_DG58
GBM3 Glioblastoma Homo sapiens CVCL_DG59
References
Ref 1 miRNA-mediated loss of m6A increases nascent translation in glioblastoma. PLoS Genet. 2021 Mar 8;17(3):e1009086. doi: 10.1371/journal.pgen.1009086. eCollection 2021 Mar.