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N4-acetylcytidine of Nop2 mRNA is Required to the Transition of Morula-to-Blastocyst

ABSTRACT: N4-acetylcytidine of Nop2 mRNA is Required to the Transition of Morula-to-Blastocyst

PROVIDER: PRJNA993164 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25221738_1.fastq.gz	Fastqsanger.gz
	SRR25221738_2.fastq.gz	Fastqsanger.gz
	SRR25221739_1.fastq.gz	Fastqsanger.gz
	SRR25221739_2.fastq.gz	Fastqsanger.gz

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N4-acetylcytidine of Nop2 mRNA is Required to the Transition of Morula-to-Blastocyst

Project description:N-acetyltransferase 10 (NAT10)-mediated N4-acetylcytidine (ac4C) modification is crucial for mRNA stability and translation efficiency, yet the underlying function in mammalian preimplantation embryos remains unclear.

2023-07-17 | GSE236943 | GEO

Antibody-free fluorine assisted metabolic sequencing of RNA N4-acetylcytidine

Project description:More researches have revealed that N4-acetylcytidine (ac4C) affected a variety of cellular and biological processes. In order to better understand the ac4C roles in biology and disease, we present an antibody-free, fluorine assisted metabolic sequencing method to detect RNA N4-acetylcytidine, called ‘FAM-seq’. We have successfully applied FAM-seq to profile ac4C landscapes in humans. By comparing with the classic ac4C antibody sequencing method, we demonstrated that FAM-seq is a convenient and specific method for transcriptome-wide detection of ac4C. This method holds promise to detect nascent RNA ac4C modifications.

2023-10-02 | GSE234988 | GEO

C12orf43-NAT10 Enhance breast cancer proliferation and chemotherapy resistance via BMI1-P53 signaling axis in a N4-acetylcytidine-dependent manner

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Project description:N4-acetylcytidine modifies primary microRNAs for processing in cancer cells

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Chromatin remodeler INO80 mediates trophectoderm permeability barrier to modulate morula-to-blastocyst transition

Project description:Chromatin remodeler INO80 mediates trophectoderm permeability barrier to modulate morula-to-blastocyst transition

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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.

2024-08-09 | GSE237840 | GEO

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

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N4-acetylcytidine modifies primary microRNAs for processing in cancer cells

Project description:N4 acetylcytidine (ac4C) modification mainly occurs on tRNA, rRNA, and mRNA, playing an important role in the expression of genetic information. However, it is still unclear whether microRNAs have undergone ac4C modification and their potential physiological and pathological functions. In this study, we identified that NAT10/THUMPD1 acetylates primary microRNAs (pri-miRNAs) with ac4C modification. Knockdown of NAT10 suppresses and augments the expression levels of mature miRNAs and pri-miRNAs, respectively. Molecular mechanism studies found that pri-miRNA ac4C promotes the processing of pri-miRNA into precursor miRNA (pre-miRNA) by enhancing the interaction of pri-miRNA and DGCR8, thereby increasing the biogenesis of mature miRNA. Knockdown of NAT10 attenuates the oncogenic characters of lung cancer cells by regulating miRNA production in cancers. Moreover, NAT10 is highly expressed in various clinical cancers and negatively correlated with poor prognosis. Thus, our results reveal that NAT10 plays a crucial role in cancer initiation and progression by modulating pri-miRNA ac4C to affect miRNA production, which would provide an attractive therapeutic strategy for cancers.

2024-01-01 | GSE223148 | GEO

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