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Identification of NAT10 targets in CRC by RNA immunoprecipitation and acethyl-RNA immunoprecipitation

ABSTRACT: Identification of NAT10 targets in CRC by RNA immunoprecipitation and acethyl-RNA immunoprecipitation

PROVIDER: PRJNA865552 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20781979_1.fastq.gz	Fastqsanger.gz
	SRR20781979_2.fastq.gz	Fastqsanger.gz
	SRR20781980_1.fastq.gz	Fastqsanger.gz
	SRR20781980_2.fastq.gz	Fastqsanger.gz
	SRR20781981_1.fastq.gz	Fastqsanger.gz

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Identification of NAT10 targets in CRC by RNA immunoprecipitation and acethyl-RNA immunoprecipitation

Project description:To identify potential mRNAs that are acetylated by NAT10, RIP with a NAT10 antibody and acRIP with a ac4C antibody were conducted in DLD-1 and SW480 cells

2022-12-27 | GSE210385 | GEO

acRIP-seq to identify NAT10 mediates mRNA ac4C modification in colorectal cancer

Project description:We performedacRIP-seq between control CRC cells and CRC cells with NAT10 knockdown to identify NAT10 mediates mRNA ac4C modification

2022-08-19 | GSE202826 | GEO

Transcriptomic ac4C profiling in NAT10 knockdown acute myeloid leukemia cells

Project description:RNA modification represents an important post-transcriptional regulatory mechanism in acute myeloid leukemia (AML), however the function and mechanism of RNA acetylation ac4C in AML remains elusive. Here, we report that NAT10, as the ac4C writing enzyme, plays a critical oncogenic function in AML and represents a promising therapeutic target for AML. To understand the mechanisms underlying the function of NAT10 as an RNA ac4C writer in AML, we profiled ac4C modification in the transcriptome of MOLM13 cells using a refined ac4C RNA immunoprecipitation and high throughput sequencing (RacRIP-seq) protocol, and performed systematic calibration with a modification-free control library generated from the in vitro- transcribed MOLM13 transcriptome (referred to as IVT control) to eliminate most of the false- positive signals. We also applied the RacRIP-seq in NAT10 knockdown and control MOLM13 cells to characterize NAT10 targets.

2024-08-26 | GSE246505 | GEO

NAT10 modulates fatty acid metabolism of palmitate driven MCF7 in ac4C dependent manner

Project description:We show that non-toxic exogenous palmitate uptake in MCF7 cells promotes NAT10 expression and NAT10-dependent ac4C RNA modification. It was previously reported that NAT10 modulates the addition of ac4C on RNA transcripts in normal and cancer conditions. However, no study report the impact of NAT10 in palmitate driven cells. Here we performed RNA immunoprecipitation sequencing (RIP-seq) in palmitate loaded MCF7 knockdown with NAT10 siRNA. Based on the pathways and enrichment landscape identified. We found that ac4C peaks of fatty acid metabolic genes including ELOVL6, ACSL1, ACSL3, ACSL4, ACADSB and ACAT1 were significantly decreased upon knockdown with NAT10 siRNA. Overall, our results revealed the impact of NAT10 as a regulator of fatty acid metabolism in ac4C-dependent manner

2022-08-03 | GSE210017 | GEO

RNA-seq analysis of mRNA expression profiles upon NAT10 depletion

Project description:NAT10 (N-acetyltransferase-like protein) regulates N4-acetylcytidine formation in RNA. However, the biological function and mechanisms of NAT10 were poorly defined. To understand the molecular mechanism by which NAT10 affect GC progression, we performed RNA sequencing (RNA-seq) in AGS cells with NAT10 knockout and in BGC823 cells with shNAT10, with independent biological replicates.

2024-06-30 | GSE180422 | GEO

The underlying mechanism by which NAT10 exerted carcinogenesis and its potential targets in MM

Project description:An acRIP experiment was performed in KMS28-PE WT and KMS28-PE NAT10-OE cells. We compared the peak summit of KMS28-PE WT and KMS28-PE NAT10 OE cells to find the differences between KMS28-PE WT and KMS28-PE NAT10 OE cells.

2024-06-01 | GSE199524 | GEO

Identification of ALKBH5 targets in osteosarcoma by methyl RNA immunoprecipitation [MeRIP-seq]

Project description:Identification of ALKBH5 targets in osteosarcoma by methyl RNA immunoprecipitation [MeRIP-seq]

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Function and Mechanism of NAT10-mediated N4-acetylcytidine modification in osteosarcoma [RIP-seq]

Project description:Despite the advance in diagnosis and treatment, the prognosis of osteosarcoma patients remains unsatisfied. Therefore, it is imperative to identify novel therapeutic targets for osteosarcoma. Through RNA sequencing (RNA-seq) combined with functional screening, N4-acetylcytidine (ac4C) acetyltransferase 10 (NAT10) was identified as a candidate therapeutic target in osteosarcoma. Upregulated NAT10 correlated with poor prognosis in osteosarcoma patients and NAT10 knockout drastically inhibited cell proliferation and metastasis in vitro and in vivo. NAT10 enhanced mRNA stability and translation efficiency of activating transcription factor 4 (ATF4) through ac4C modification. ATF4 induced transcription of asparagine synthetase (ASNS), which catalyzes asparagine (Asn) biosynthesis. Asn promote protein and nucleotide synthesis, facilitating osteosarcoma progression. Overexpression of ATF4, ASNS or supplementation of asparagine rescue the tumor inhibitory effect of NAT10 knockout.

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Acetylation of cytidines by NAT10 enhances HIV-1 replication through stabilization of viral RNA

Project description:As obligate parasites, viruses need to navigate a variety of cellular regulatory systems while infecting and replicating in the host cell. Post-transcriptional modifications have recently emerged as an important layer of regulation of viral RNA function. For example, our lab and others have shown that the RNA modification N6-methyladenosine (m6A) can enhance the replication of multiple viruses in cis, including Human Immunodeficiency virus 1 (HIV-1), Influenza A virus, SV40 and Kaposi's sarcoma-associated herpesvirus (KSHV). Recent reports have revealed the presence of another RNA modification, N4-acetylcytidine (ac4C) on cellular mRNAs and have shown that ac4C can enhance mRNA stability and translation. Here, we demonstrate that ac4C is present at multiple sites on HIV-1 mRNAs and on the viral genomic RNA. Through ac4C RNA immunoprecipitation (RNA-IP) and RNA-seq, we found ac4C on HIV-1 mRNAs as well as the virion genomic RNA, with ac4C sites in the coding regions of the pol, env, nef genes, and the trans-activation response (TAR) hairpin. Phenotypically, we observe that increasing the expression level of the ac4C acetyltransferase NAT10 leads to an increase in viral replication that is dependent on the RNA binding and enzymatic domains of NAT10. Moreover, both CRISPR-depletion of NAT10 (ΔNAT10) and treatment with the small molecule NAT10 inhibitor Remodelin, diminishes HIV-1 replication in T cells. Lastly, silent mutations introduced to prevent ac4C deposition on the viral genome indeed diminished HIV-1 replication. Our data suggest that HIV-1 has evolved to incorporate ac4C in essential viral gene coding regions and regulatory RNA structures, and that NAT10-dependent ac4C addition enhances HIV-1 replication.

2020-06-11 | GSE142490 | GEO

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