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N6-methyladenosine modification is not a general trait of viral RNA genomes

ABSTRACT: N6-methyladenosine modification is not a general trait of viral RNA genomes (MinION runs)

PROVIDER: PRJEB61652 | ENA |

REPOSITORIES: ENA

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N6-methyladenosine modification is not a general trait of viral RNA genomes (Plasmid Illumina runs)

Project description:N6-methyladenosine modification is not a general trait of viral RNA genomes (Plasmid Illumina runs)

| PRJEB66350 | ENA

N6-methyladenosine modification is not a general trait of viral RNA genomes.

Project description:N6-methyladenosine modification is not a general trait of viral RNA genomes.

| PRJNA967585 | ENA

N6-methyladenosine modification is not a general trait of viral RNA genomes [Dengue]

Project description:N6-methyladenosine (m6A), the most common internal RNA modification in eukaryotic mRNAs, is described to be abundantly present in the genomes of cytoplasmic-replicating RNA viruses. Yet, how the host nuclear m6A writer has access to the viral RNAs in the cytoplasm and what are the associated biological consequences remain unknown. Here, we comprehensively addressed these questions by combining antibody-dependent (m6A-seq) and antibody-independent (SELECT and nanopore direct RNA sequencing) methods on the cytoplasmic-replicating Chikungunya virus (CHIKV) RNA, and found no evidence of m6A modifications. Moreover, depletion of m6A modification machinery components did not affect CHIKV infection, and CHIKV infection did not alter their cellular localization. Consistent with these observations, no m6A modifications were found in the RNA genome of the dengue virus (DENV), another cytoplasmic-replicating virus. Our results challenge the idea that m6A modification is a general trait of cytoplasmic-replicating RNA viruses and stress the need of confirming antibody-dependent detection of m6A modifications with orthogonal antibody-independent methods.

2024-01-23 | GSE231738 | GEO

N6-methyladenosine modification is not a general trait of viral RNA genomes [CHIKV]

2024-01-23 | GSE231737 | GEO

N6-methyladenosine modification is not a general trait of viral RNA genomes [CHIKV]

Project description:N6-methyladenosine modification is not a general trait of viral RNA genomes [CHIKV]

| PRJNA967595 | ENA

N6-methyladenosine modification is not a general trait of viral RNA genomes [Dengue]

Project description:N6-methyladenosine modification is not a general trait of viral RNA genomes [Dengue]

| PRJNA967597 | ENA

N6-methyladenosine modification is not a general trait of viral RNA genomes.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-01-23 | GSE231739 | GEO

N6-Methyladenosine methylation profile in rat H9C2 cardiomyocytes under the hypoxic stress

Project description:Hypoxia as a crucial pathogenesis factor usually results in huge harmful effects on cardiac injury and dysfunction. In our previous study (PMID: 33294289), We observe a series of differential expressed genes between transcription and translation, which may be attributed to the hypoxia-specific binding affinity of Nuclear cap-binding subunit 3 (NCBP3) at 5’ un-translation region of target genes. But the underlying molecular mechanism of NCBP3 for gene translation modulation remains unclear. Here, we conducted RIP-seq of N6-Methyladenosine methylation in H9C2 cells with the conditions of normoxic, hypoxic and with additional NCBP3 knockdown.

2021-06-30 | E-MTAB-10682 | biostudies-arrayexpress

N6-methyladenosine Modulates Messenger RNA Translation Efficiency

Project description:N6-methyladenosine (m6A) is the most abundant internal messenger (mRNA) modification in mammalian mRNA. This modification is reversible and non-stoichiometric, which potentially adds an additional layer of variety and dynamic control of mRNA metabolism. The m6A-modified mRNA can be selectively recognized by the YTH family “reader” proteins. The preferential binding of m6A-containing mRNA by YTHDF2 is known to reduce the stability of the target transcripts; however, the exact effects of m6A on translation has yet to be elucidated. Here we show that another m6A reader protein, YTHDF1, promotes ribosome loading of its target transcripts. YTHDF1 forms a complex with translation initiation factors to elevate the translation efficiency of its bound mRNA. In a unified mechanism of translation control through m6A, the YTHDF2-mediated decay controls the lifetime of target transcripts; whereas, the YTHDF1-based translation promotion increases the translation efficiency to ensure effective protein production from relatively short-lived transcripts that are marked by m6A. PAR-CLIP and RIP was used to identify YTHDF1 binding sites followed by ribosome profling and RNA seq to assess the consequences of YTHDF1 siRNA knock-down

2015-06-09 | E-GEOD-63591 | biostudies-arrayexpress

YTHDF3 improves translation initiation of mRNAs with N6-methyladenosine methylation at 5’ untranslated region by facilitating eIF2AK2 recruitment in oxaliplatin-resistant colorectal cancer - RIP-seq dataset

Project description:Oxaliplatin as a first-line drug frequently causes the chemo-resistance on colorectal cancer (CRC). N6-methyladenosine (m6A) methylation has been largely acknowledged in multiple biological functions. However, the molecular mechanisms underlying the m6A methylation in modulating anticancer drug resistance in CRC are still obscure. In present study, RIP-seq was conducted to investigate the occupancy of N6-methyladenosine RNA binding protein 3 (YTHDF3) served as “readers” that can recognize m6A modification site in HCT116 cells with oxaliplatin resistance (HCT116R). Then, YTHDF3 was knockdown by siRNA in HCT116 cells with oxaliplatin resistance, and RIP-seq was further conducted to investigate m6A methylation of HCT116, HCT116R and HCT116R cells with YTHDF3 knockdown.

2022-02-04 | E-MTAB-11321 | biostudies-arrayexpress

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