N6-methyladenosine modification enables viral RNA to escape recognition by RNA sensor RIG-I is a research paper published in Nature Microbiology (2020). On theSindex it has a DataRank of 0.848. It has been cited 285 times.
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Base Score Contribution
0.848
From this paper's citation signal
Citation Network Contribution
0
Citation network not refreshed for this result
This paper's DataRank is currently driven only by its base citation score. Citation network data was not refreshed for this result.
Learn more about DataRank methodology →U.S. Department of Health & Human Services | National Institutes of Health
Grant: AI112524
U.S. Department of Health & Human Services | National Institutes of Health
Grant: HG008688
U.S. Department of Health & Human Services | National Institutes of Health
Grant: HG008935
U.S. Department of Health & Human Services | NIH | National Institute of Allergy and Infectious Diseases
Grant: AI090060
NIAID NIH HHS
Grant: P01 AI112524
NHGRI NIH HHS
Grant: RM1 HG008935
NHGRI NIH HHS
Grant: R01 HG008688
NIAID NIH HHS
Grant: R01 AI090060
National Institutes of Health
Grant: 1R01HG008688-01
Base-resolution sequencing of m6A in RNA
National Institutes of Health
Grant: 5R01AI090060-02
Messenger RNA Capping and Methylation in Pneumoviruses
National Institutes of Health
Grant: 5P01AI112524-02
Live Attenuated RSV Vaccine with Optimized Safety and Immunogenicity
National Institutes of Health
Grant: 3RM1HG008935-05S1
Center for dynamic RNA epitranscriptomes - Covid 19 Supplement Version 2
Howard Hughes Medical Institute
Howard Hughes Medical Institute
FWCI
13.18
Citation Percentile
1.0%
Citation Trend
Fields of Study
MeSH Terms
Keywords
Sustainable Development Goals
Additional file 3 of The m6A demethylase ALKBH5 promotes tumor progression by inhibiting RIG-I expression and interferon alpha production through the IKKε/TBK1/IRF3 pathway in head and neck squamous cell carcinoma
Additional file 3 of The m6A demethylase ALKBH5 promotes tumor progression by inhibiting RIG-I expression and interferon alpha production through the IKKε/TBK1/IRF3 pathway in head and neck squamous cell carcinoma
Additional file 1 of Attenuation of IFN signaling due to m6A modification of the host epitranscriptome promotes EBV lytic reactivation
Additional file 1 of Attenuation of IFN signaling due to m6A modification of the host epitranscriptome promotes EBV lytic reactivation
Additional file 2 of Attenuation of IFN signaling due to m6A modification of the host epitranscriptome promotes EBV lytic reactivation
Additional file 2 of Attenuation of IFN signaling due to m6A modification of the host epitranscriptome promotes EBV lytic reactivation
Additional file 2 of N6-methyladenosine modification positively regulate Japanese encephalitis virus replication
Additional file 2 of N6-methyladenosine modification positively regulate Japanese encephalitis virus replication
Additional file 1 of A bibliometric analysis of m6A methylation in viral infection from 2000 to 2022
Additional file 1 of A bibliometric analysis of m6A methylation in viral infection from 2000 to 2022
Additional file 2 of A bibliometric analysis of m6A methylation in viral infection from 2000 to 2022
Additional file 2 of A bibliometric analysis of m6A methylation in viral infection from 2000 to 2022
Additional file 3 of A bibliometric analysis of m6A methylation in viral infection from 2000 to 2022
Additional file 3 of A bibliometric analysis of m6A methylation in viral infection from 2000 to 2022
Additional file 9 of N6-methyladenosine modification positively regulate Japanese encephalitis virus replication
Additional file 7 of N6-methyladenosine modification positively regulate Japanese encephalitis virus replication
Additional file 8 of N6-methyladenosine modification positively regulate Japanese encephalitis virus replication
Additional file 8 of N6-methyladenosine modification positively regulate Japanese encephalitis virus replication
Additional file 9 of N6-methyladenosine modification positively regulate Japanese encephalitis virus replication
Additional file 6 of N6-methyladenosine modification positively regulate Japanese encephalitis virus replication