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Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis

ABSTRACT: Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis

PROVIDER: PRJNA1172291 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30972023_1.fastq.gz	Fastqsanger.gz
	SRR30972023_2.fastq.gz	Fastqsanger.gz
	SRR30972024_1.fastq.gz	Fastqsanger.gz
	SRR30972024_2.fastq.gz	Fastqsanger.gz
	SRR30972025_1.fastq.gz	Fastqsanger.gz

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Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [Ribo-seq]

Project description:Increased differentiation or activity of osteoclasts is the key pathogenic factor of postmenopausal osteoporosis (PMOP). N4‐acetylcytidine (ac4C) modification, catalyzed by Nat10, is a novel post-transcriptional mRNA modification related to many diseases. However, its impact on regulating osteoclast activation in PMOP remains uncertain. Here, we initially observed that Nat10-mediated ac4C positively correlates with osteoclast differentiation of monocytes and low bone mass in PMOP. The specific knockout of Nat10 in monocytes and remodelin, a Nat10 inhibitor, alleviates ovariectomized (OVX)-induced bone loss by downregulating osteoclast differentiation. Mechanistically, epitranscriptomic analyses reveal that the nuclear factor of activated T cells cytoplasmic 1 (Nfatc1) is the key downstream target of ac4C modification during osteoclast differentiation. Subsequently, translatomic results demonstrate that Nat10-mediated ac4C enhances the translation efficiency of Nfatc1, thereby inducing Nfatc1 expression and consequent osteoclast maturation. Cumulatively, these findings reveal the promotive role of Nat10 in osteoclast differentiation and PMOP from a novel field of RNA modifications and suggest that Nat10 can be a target of epigenetic therapy for preventing bone loss in PMOP.

2025-03-27 | GSE279363 | GEO

Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [acRIP-seq]

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Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [RNA-seq]

Project description:Increased differentiation or activity of osteoclasts is the key pathogenic factor of postmenopausal osteoporosis (PMOP). N4-acetylcytidine (ac4C) modification, catalyzed by Nat10, is a novel post-transcriptional mRNA modification related to many diseases. However, its impact on regulating osteoclast activation in PMOP remains uncertain. Here, we initially observed that Nat10-mediated ac4C positively correlates with osteoclast differentiation of monocytes and low bone mass in PMOP. The specific knockout of Nat10 in monocytes and remodelin, a Nat10 inhibitor, alleviates ovariectomized (OVX)-induced bone loss by downregulating osteoclast differentiation. Mechanistically, epitranscriptomic analyses reveal that the nuclear factor of activated T cells cytoplasmic 1 (Nfatc1) is the key downstream target of ac4C modification during osteoclast differentiation. Subsequently, translatomic results demonstrate that Nat10-mediated ac4C enhances the translation efficiency of Nfatc1, thereby inducing Nfatc1 expression and consequent osteoclast maturation. Cumulatively, these findings reveal the promotive role of Nat10 in osteoclast differentiation and PMOP from a novel field of RNA modifications and suggest that Nat10 can be a target of epigenetic therapy for preventing bone loss in PMOP.

2025-03-27 | GSE280178 | GEO

Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [Ribo-seq]

Project description:Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [Ribo-seq]

| PRJNA1172296 | ENA

Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [RNA-seq]

Project description:Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [RNA-seq]

| PRJNA1176692 | ENA

Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [acRIP-seq]

Project description:Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [acRIP-seq]

| PRJNA1172295 | ENA

Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis

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

2025-03-27 | GSE279364 | GEO

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

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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