We are analyzing https://link.springer.com/article/10.1007/s11010-019-03641-5.

Title:
The m6A methyltransferase METTL3 cooperates with demethylase ALKBH5 to regulate osteogenic differentiation through NF-κB signaling | Molecular and Cellular Biochemistry
Description:
As a m6A methylation modifier, METTL3 is functionally involved in various biological processes. Nevertheless, the role of METTL3 in osteogenesis is not determined up to date. In the current study, METTL3 is identified as a crucial regulator in the progression of osteogenic differentiation. Loss of METTL3 significantly augments calcium deposition and enhances alkaline phosphatase activity of mesenchymal stem cells, uncovering an inhibitory role of METTL3 in osteogenesis. More importantly, the underlying molecular basis by which METTL3 regulates osteogenesis is illustrated. We find that METTL3 positively regulates expression of MYD88, a critical upstream regulator of NF-κB signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-κB which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. Moreover, the METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5. In summary, this study highlights the functional importance of METTL3 in osteogenic differentiation and METTL3 may serve as a promising molecular target in regenerative medicine, as well as in the field of bone tissue engineering.
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Keywords {🔍}

pubmed, article, google, scholar, stem, cell, cas, mettl, cells, zhang, central, methylation, liu, mesenchymal, xinxiang, alkbh, differentiation, lin, osteogenesis, osteogenic, bone, nmethyladenosine, chen, rna, medical, university, data, methyltransferase, zhu, regulates, access, zhou, httpsdoiorgs, wang, huang, china, henan, privacy, cookies, content, research, demethylase, nfκb, signaling, shen, regeneration, mrna, information, publish, search,

Topics {✒️}

aff4/nf-kappab/myc signaling network nf-κb signaling published rna n6-methyladenosine methylation mettl3-mediated m6a methylation enhanced nf-kappab activity inactivating nf-kappab signalling month download article/chapter collagen-induced arthritic mice nf-κb signaling mettl3-/mettl14-mediated mrna hypoxia/reoxygenation-treated cardiomyocytes m6a methylation modifier rna methyltransferase complex activate rna methylation n6-methyladenosine modification full article pdf mettl3 regulates osteogenesis xinxing zhu peripheral blood rna mesenchymal stem cells human cancer cells n6-methyladenosine menscs regulate osteogenic differentiation nf-κb mettl3-mediated mrna privacy choices/manage cookies related subjects suppressing osteogenic progression lujun shen modulates haematopoietic stem stem cell therapy alkbh5 oppositely regulate maoping chu tnf-alpha stem cell medicine article yu article molecular cell-based strategy progenitor cell specification demethylase alkbh5 juntang lin bone tissue engineering underlying molecular basis promising molecular target mol cell biol check access instant access european economic area cellular biochemistry aims targeting beta-catenin

Schema {🗺️}

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         headline:The m6A methyltransferase METTL3 cooperates with demethylase ALKBH5 to regulate osteogenic differentiation through NF-κB signaling
         description:As a m6A methylation modifier, METTL3 is functionally involved in various biological processes. Nevertheless, the role of METTL3 in osteogenesis is not determined up to date. In the current study, METTL3 is identified as a crucial regulator in the progression of osteogenic differentiation. Loss of METTL3 significantly augments calcium deposition and enhances alkaline phosphatase activity of mesenchymal stem cells, uncovering an inhibitory role of METTL3 in osteogenesis. More importantly, the underlying molecular basis by which METTL3 regulates osteogenesis is illustrated. We find that METTL3 positively regulates expression of MYD88, a critical upstream regulator of NF-κB signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-κB which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. Moreover, the METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5. In summary, this study highlights the functional importance of METTL3 in osteogenic differentiation and METTL3 may serve as a promising molecular target in regenerative medicine, as well as in the field of bone tissue engineering.
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            M6A methylation
            Osteogenesis
            NF-κB signaling
            ALKBH5
            Biochemistry
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            Cardiology
            Cancer Research
            Medical Biochemistry
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      headline:The m6A methyltransferase METTL3 cooperates with demethylase ALKBH5 to regulate osteogenic differentiation through NF-κB signaling
      description:As a m6A methylation modifier, METTL3 is functionally involved in various biological processes. Nevertheless, the role of METTL3 in osteogenesis is not determined up to date. In the current study, METTL3 is identified as a crucial regulator in the progression of osteogenic differentiation. Loss of METTL3 significantly augments calcium deposition and enhances alkaline phosphatase activity of mesenchymal stem cells, uncovering an inhibitory role of METTL3 in osteogenesis. More importantly, the underlying molecular basis by which METTL3 regulates osteogenesis is illustrated. We find that METTL3 positively regulates expression of MYD88, a critical upstream regulator of NF-κB signaling, by facilitating m6A methylation modification to MYD88-RNA, subsequently inducing the activation of NF-κB which is widely regarded as a repressor of osteogenesis and therefore suppressing osteogenic progression. Moreover, the METTL3-mediated m6A methylation is found to be dynamically reversed by the demethylase ALKBH5. In summary, this study highlights the functional importance of METTL3 in osteogenic differentiation and METTL3 may serve as a promising molecular target in regenerative medicine, as well as in the field of bone tissue engineering.
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         M6A methylation
         Osteogenesis
         NF-κB signaling
         ALKBH5
         Biochemistry
         general
         Cardiology
         Cancer Research
         Medical Biochemistry
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