| http://purl.uniprot.org/citations/35543357 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/35543357 | http://www.w3.org/2000/01/rdf-schema#comment | "To explore the METTL14-dependent m6A modification mechanism involved in the development of atherosclerosis. Oxidized low-density lipoprotein (ox-LDL) and the HUVEC cell line were used to establish an atherosclerosis cell model in vitro, and APOE-/- mice fed a high-fat diet were used as the animal model. Cell viability and apoptosis were assessed using MTT assays and flow cytometry. The status of m6A in HUVECs was examined using MeRIP-qPCR. Oil Red O staining was used to evaluate the lesions or plaques on aortas separated from the target mice. METTL14 and METTL3 were upregulated in HUVECs after ox-LDL treatment. After transfection with si-METTL14, the bcl-2 expression level and the viability of ox-LDL-incubated cells increased, whereas the apoptosis rate and the expressions of Bax and cleaved caspase-3 decreased. However, the effect of METTL14 knockdown was reversed by p65 overexpression. After METTL14 knockdown, there was a decrease in the total m6A content in HUVECs, m6A modification, and p65 expression. The plaques and lesion areas on the high-fat diet APOE-/- mouse aortas were smaller after METTL14 silencing. METTL14 reduced cell viability and promoted apoptosis of HUVECs, which were both induced by ox-LDL via m6A modification of p65. Knocking down METTL14 could inhibit the development of atherosclerosis in high-fat diet-treated APOE-/- mice."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.org/dc/terms/identifier | "doi:10.1080/21655979.2022.2031409"xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/author | "Liu Y."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/author | "Liu D."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/author | "Luo G."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/author | "Ma J."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/author | "Song Y."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/author | "Wang H."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/author | "Tang Q."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/date | "2022"xsd:gYear |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/name | "Bioengineered"xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/pages | "11832-11843"xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/title | "Methyltransferase-like 14 silencing relieves the development of atherosclerosis via m6A modification of p65 mRNA."xsd:string |
| http://purl.uniprot.org/citations/35543357 | http://purl.uniprot.org/core/volume | "13"xsd:string |
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