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anti ythdf2 nbp2 31785  (Novus Biologicals)


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    Novus Biologicals anti ythdf2 nbp2 31785
    Anti Ythdf2 Nbp2 31785, supplied by Novus Biologicals, used in various techniques. Bioz Stars score: 90/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ythdf2/YTHDF2+Antibody/pmc06056540-157-31-33
    Average 90 stars, based on 2 article reviews
    anti ythdf2 nbp2 31785 - by Bioz Stars, 2026-09
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    Western Blot:

    Article Title: METTL3 regulates WTAP protein homeostasis
    Article Snippet: .. Immunoblots were incubated with antibodies Anti-FLAG M2 F3165 (Sigma-Aldrich), Anti-WTAP 60188-1-Ig (Proteintech), Anti-METTL3 [EPR18810] (Abcam), Anti-METTL14 antibody HPA038002 (Sigma Aldrich), anti-Actinin H-300 sc-15335 (Santa Cruz Biotechnology), anti-GAPDH sc-25778 (Santa Cruz Biotechnology), anti-YTHDF2 NBP2-31785 (Novus Biological) and anti-eIF3A ab86146 (Abcam). ..

    Incubation:

    Article Title: METTL3 regulates WTAP protein homeostasis
    Article Snippet: .. Immunoblots were incubated with antibodies Anti-FLAG M2 F3165 (Sigma-Aldrich), Anti-WTAP 60188-1-Ig (Proteintech), Anti-METTL3 [EPR18810] (Abcam), Anti-METTL14 antibody HPA038002 (Sigma Aldrich), anti-Actinin H-300 sc-15335 (Santa Cruz Biotechnology), anti-GAPDH sc-25778 (Santa Cruz Biotechnology), anti-YTHDF2 NBP2-31785 (Novus Biological) and anti-eIF3A ab86146 (Abcam). ..



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    Role of m 6 A in adipogenesis. Insufficient adipogenesis in adipose tissue leads to persistent, chronic inflammation. m 6 A modification plays a crucial role in all stages of adipogenesis, from commitment to terminal differentiation. During commitment, METTL3 promotes lipogenic differentiation in BMSCs by regulating the m 6 A levels of PTH1R and JAK1, whereas silencing METTL14 reduces the expression of SMAD1, inhibiting BMSC proliferation. During terminal differentiation, m 6 A regulates MCE and the transition to mature adipocytes. FTO influences key genes such as ATG5, ATG7 and JAK2, affecting autophagy, STAT3 phosphorylation and adipogenesis. FTO knockout increases the m 6 A levels of CCND1 and CDK2, blocking MCE. m 6 A, N6-methyladenine; METTL, methyltransferase-like; PTH1R, parathyroid hormone 1 receptor; JAK, Janus kinase; BMSC, bone marrow mesenchymal stem cell; MCE, mitotic clone amplification; FTO, Fat mass and obesity-associated protein; ATG, autophagy-related; STAT3, signal transducer and activator of transcription 3; CCND1, cyclin D1; CDK2, cyclin-dependent kinase 2; IGF2BP1, insulin-like growth factor 2 mRNA-binding protein 1; YTHDF2, YTH domain family 2.

    Journal: International Journal of Molecular Medicine

    Article Title: m 6 A in adipose tissue inflammation: A novel regulator of obesity and metabolic diseases (Review)

    doi: 10.3892/ijmm.2026.5795

    Figure Lengend Snippet: Role of m 6 A in adipogenesis. Insufficient adipogenesis in adipose tissue leads to persistent, chronic inflammation. m 6 A modification plays a crucial role in all stages of adipogenesis, from commitment to terminal differentiation. During commitment, METTL3 promotes lipogenic differentiation in BMSCs by regulating the m 6 A levels of PTH1R and JAK1, whereas silencing METTL14 reduces the expression of SMAD1, inhibiting BMSC proliferation. During terminal differentiation, m 6 A regulates MCE and the transition to mature adipocytes. FTO influences key genes such as ATG5, ATG7 and JAK2, affecting autophagy, STAT3 phosphorylation and adipogenesis. FTO knockout increases the m 6 A levels of CCND1 and CDK2, blocking MCE. m 6 A, N6-methyladenine; METTL, methyltransferase-like; PTH1R, parathyroid hormone 1 receptor; JAK, Janus kinase; BMSC, bone marrow mesenchymal stem cell; MCE, mitotic clone amplification; FTO, Fat mass and obesity-associated protein; ATG, autophagy-related; STAT3, signal transducer and activator of transcription 3; CCND1, cyclin D1; CDK2, cyclin-dependent kinase 2; IGF2BP1, insulin-like growth factor 2 mRNA-binding protein 1; YTHDF2, YTH domain family 2.

    Article Snippet: In addition, for mitotic clone amplification (MCE) in the early stage of terminal differentiation, the inhibition of FTO expression in 3T3-L1 cells leads to increased m 6 A methylation levels of cyclin D1 (CCND1) and cyclin-dependent kinase 2, the protein expression of which is reduced after recognition by YTHDF2, resulting in blockade of the MCE process and in turn the inhibition of lipogenesis ( ) ( ).

    Techniques: Modification, Expressing, Phospho-proteomics, Knock-Out, Blocking Assay, Amplification, Binding Assay