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

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

PROVIDER: PRJNA1172295 | ENA |

REPOSITORIES: ENA

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Nat10-mediated N4-acetylcytidine modification enhances Nfact1 translation to exacerbate osteoclastogenesis in postmenopausal osteoporosis [acRIP-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 | GSE279361 | GEO

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

2025-03-27 | GSE279363 | GEO

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

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

| PRJNA1172291 | ENA

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

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

2025-03-27 | GSE279364 | GEO

The acRIP-seq of SiHa and KONAT10SiHa cells

Project description:We investigate genes that the different degrees of N4-acetylcytidine in the SiHa and Knockout NAT10 SiHa.

2023-10-09 | GSE216812 | GEO

ac4C RIP-seq analysis of AGS cells upon NAT10 knockout.

Project description:N4-acetylcytidine (ac4C), a conserved chemical modification in eukaryotic prokaryotes that is catalyzed by the N-acetyltransferase 10 (NAT10) enzyme, plays a crucial role in promoting mRNA stability and translation. However, the biological function and mechanisms of NAT10-mediated ac4C in human cancer were poorly defined. In order to investigate the regulatory mechanism of NAT10 in gastric cancer, we performed ac4C RIP-seq(acRIP-seq) analysis in AGS cells with NAT10 knockout compared with control in two repeats.

2024-07-07 | GSE180494 | GEO

Transcriptome and N4-acetylcytidine RNA acetylation analyses in human multiple myeloma cells

Project description:To identify the ac4C acetylation in the human multiple meloma cells .acRIP-seq and RNA-seq experiments of human multiple myeloma cells including NAT10 overexpression and controls were conducted.

2021-11-30 | GSE155417 | GEO

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