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ythdf2  (MedChemExpress)


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    Structured Review

    MedChemExpress ythdf2
    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; <t>YTHDF2,</t> YTH domain family 2.
    Ythdf2, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ythdf2/YTHDF2%2C+Human/pmc13007997-102-48-54
    Average 91 stars, based on 1 article reviews
    ythdf2 - by Bioz Stars, 2026-10
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    Images

    1) Product Images from "m 6 A in adipose tissue inflammation: A novel regulator of obesity and metabolic diseases (Review)"

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

    Journal: International Journal of Molecular Medicine

    doi: 10.3892/ijmm.2026.5795

    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.
    Figure Legend 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.

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

    Related Articles

    Mutagenesis:

    Article Title: O-GlcNAcylation of YTHDF2 promotes HBV-related hepatocellular carcinoma progression in an N 6 -methyladenosine-dependent manner
    Article Snippet: .. For stability detection of endogenous YTHDF2 protein, HepAD38 cells were treated with 100 μM cycloheximide (CHX, MCE, Monmouth Junction, NJ, USA) and collected at 0, 12, 24 and 36 h. For protein stability detection of exogenous YTHDF2 (WT and S263A mutant), HepG2-shYTHDF2 cells were re-expressed with Flag-WT or Flag-S263A mutant, respectively. ..

    Article Title: O-GlcNAcylation of YTHDF2 promotes HBV-related hepatocellular carcinoma progression in an N 6 -methyladenosine-dependent manner.
    Article Snippet: .. YTHDF2 protein stability assay For stability detection of endogenous YTHDF2 protein, HepAD38 cells were treated with 100 μM cycloheximide (CHX, MCE, Monmouth Junction, NJ, USA) and collected at 0, 12, 24 and 36 h. For protein stability detection of exogenous YTHDF2 (WT and S263A mutant), HepG2-shYTHDF2 cells were re-expressed with Flag-WT or Flag-S263A mutant, respectively. ..

    Knockdown:

    Article Title: YTHDF2 alleviates the radioresistance of rectal cancer cells by targeting methylated MYC
    Article Snippet: .. Cells were seeded in six-well plates, and YTHDF2 knockdown or overexpression was achieved by lentivirus infection for over 48 h. The cells were treated with 5 μg/ml Actinomycin D (MedChemExpress) for 0, 1, 2 and 4 h, respectively. ..

    Article Title: YTHDF2 alleviates the radioresistance of rectal cancer cells by targeting methylated MYC.
    Article Snippet: .. RNA stability measure Cells were seeded in six-well plates, and YTHDF2 knockdown or overexpression was achieved by lentivirus infection for over 48 h. The cells were treated with 5 μg/ml Actinomycin D (MedChemExpress) for 0, 1, 2 and 4 h, respectively. ..

    Over Expression:

    Article Title: YTHDF2 alleviates the radioresistance of rectal cancer cells by targeting methylated MYC
    Article Snippet: .. Cells were seeded in six-well plates, and YTHDF2 knockdown or overexpression was achieved by lentivirus infection for over 48 h. The cells were treated with 5 μg/ml Actinomycin D (MedChemExpress) for 0, 1, 2 and 4 h, respectively. ..

    Article Title: YTHDF2 alleviates the radioresistance of rectal cancer cells by targeting methylated MYC.
    Article Snippet: .. RNA stability measure Cells were seeded in six-well plates, and YTHDF2 knockdown or overexpression was achieved by lentivirus infection for over 48 h. The cells were treated with 5 μg/ml Actinomycin D (MedChemExpress) for 0, 1, 2 and 4 h, respectively. ..

    Infection:

    Article Title: YTHDF2 alleviates the radioresistance of rectal cancer cells by targeting methylated MYC
    Article Snippet: .. Cells were seeded in six-well plates, and YTHDF2 knockdown or overexpression was achieved by lentivirus infection for over 48 h. The cells were treated with 5 μg/ml Actinomycin D (MedChemExpress) for 0, 1, 2 and 4 h, respectively. ..

    Article Title: YTHDF2 alleviates the radioresistance of rectal cancer cells by targeting methylated MYC.
    Article Snippet: .. RNA stability measure Cells were seeded in six-well plates, and YTHDF2 knockdown or overexpression was achieved by lentivirus infection for over 48 h. The cells were treated with 5 μg/ml Actinomycin D (MedChemExpress) for 0, 1, 2 and 4 h, respectively. ..

    Amplification:

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

    Inhibition:

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

    Expressing:

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

    Methylation:

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

    Stability Assay:

    Article Title: O-GlcNAcylation of YTHDF2 promotes HBV-related hepatocellular carcinoma progression in an N 6 -methyladenosine-dependent manner.
    Article Snippet: .. YTHDF2 protein stability assay For stability detection of endogenous YTHDF2 protein, HepAD38 cells were treated with 100 μM cycloheximide (CHX, MCE, Monmouth Junction, NJ, USA) and collected at 0, 12, 24 and 36 h. For protein stability detection of exogenous YTHDF2 (WT and S263A mutant), HepG2-shYTHDF2 cells were re-expressed with Flag-WT or Flag-S263A mutant, respectively. ..



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    Image Search Results


    List of antibodies used for this study

    Journal: Experimental Hematology & Oncology

    Article Title: Tumor-intrinsic NSUN2 orchestrates immunosuppression in lung adenocarcinoma via the m 5 C-HDAC8-CCL5 axis

    doi: 10.1186/s40164-026-00826-9

    Figure Lengend Snippet: List of antibodies used for this study

    Article Snippet: A25318 , Anti-YTHDF2 , ABclonal.

    Techniques: Control

    The differentiated expression of YTHDF1 and YTHDF2 in tumor tissues and normal tissues. (A) YTHDF1 expression in non-paired lung cancer tissues and normal tissues according to the TCGA dataset. (B) YTHDF1 expression in paired lung cancer tissues and normal tissues in the TCGA database. (C) YTHDF2 expression in non-paired lung cancer tissues and normal tissues according to the TCGA dataset. (D) YTHDF2 expression in paired lung cancer tissues and normal tissues in the TCGA database. ns, not significant; *, P<0.05; ***, P<0.001. TCGA, The Cancer Genome Atlas.

    Journal: Journal of Thoracic Disease

    Article Title: Expression of YTHDF1 and YTHDF2 in lung squamous cell carcinoma and their correlation with PD-L1

    doi: 10.21037/jtd-2026-1-0312

    Figure Lengend Snippet: The differentiated expression of YTHDF1 and YTHDF2 in tumor tissues and normal tissues. (A) YTHDF1 expression in non-paired lung cancer tissues and normal tissues according to the TCGA dataset. (B) YTHDF1 expression in paired lung cancer tissues and normal tissues in the TCGA database. (C) YTHDF2 expression in non-paired lung cancer tissues and normal tissues according to the TCGA dataset. (D) YTHDF2 expression in paired lung cancer tissues and normal tissues in the TCGA database. ns, not significant; *, P<0.05; ***, P<0.001. TCGA, The Cancer Genome Atlas.

    Article Snippet: YTHDF2 antibodies were purchased from ABclonal Biotechnology Co., Ltd. (Wuhan, China), and Ethylene Glycol-bis (2-aminoethyl Ether)-N,N,N',N'-tetraacetic Acid (EGTA) antigen retrieval buffer (pH 9.0), antibody diluent, polylysine, phosphate buffered saline (PBS), super-sensitive 3,3'-diaminobenzidine (DAB) substrate, instant immunohistochemistry MaxVision TM kit, and neutral balsam were purchased from Fuzhou Maxim Biotechnology Co., Ltd. (Fuzhou, China).

    Techniques: Expressing

    Relationship between YTHDF1/YTHDF2 expression and prognosis of LUSC patients. (A,C) Association between YTHDF1, YTHDF2 expression and DSS of LUSC patients. (B,D) Association between YTHDF1, YTHDF2 expression and OS of LUSC patients. DSS, disease-specific survival; LUSC, lung squamous cell carcinoma; OS, overall survival.

    Journal: Journal of Thoracic Disease

    Article Title: Expression of YTHDF1 and YTHDF2 in lung squamous cell carcinoma and their correlation with PD-L1

    doi: 10.21037/jtd-2026-1-0312

    Figure Lengend Snippet: Relationship between YTHDF1/YTHDF2 expression and prognosis of LUSC patients. (A,C) Association between YTHDF1, YTHDF2 expression and DSS of LUSC patients. (B,D) Association between YTHDF1, YTHDF2 expression and OS of LUSC patients. DSS, disease-specific survival; LUSC, lung squamous cell carcinoma; OS, overall survival.

    Article Snippet: YTHDF2 antibodies were purchased from ABclonal Biotechnology Co., Ltd. (Wuhan, China), and Ethylene Glycol-bis (2-aminoethyl Ether)-N,N,N',N'-tetraacetic Acid (EGTA) antigen retrieval buffer (pH 9.0), antibody diluent, polylysine, phosphate buffered saline (PBS), super-sensitive 3,3'-diaminobenzidine (DAB) substrate, instant immunohistochemistry MaxVision TM kit, and neutral balsam were purchased from Fuzhou Maxim Biotechnology Co., Ltd. (Fuzhou, China).

    Techniques: Expressing

    Potential molecular mechanisms of YTHDF1 and YTHDF2 in LUSC progression. (A,C) Gene set enrichment analysis showed that YTHDF1 (A) and YTHDF2 (C) high expression subgroups of LUSC patients were significantly associated with E2F targets, G2M checkpoint, mitotic spindle, pancreas beta cells, spermatogenesis and other pathways. (B,D) Gene set enrichment analysis showed that YTHDF1 (B) and YTHDF2 (D) low expression subgroups of LUSC patients were significantly associated with allograft rejection, coagulation, inflammatory response, interferon gamma response and other pathways. LUSC, lung squamous cell carcinoma.

    Journal: Journal of Thoracic Disease

    Article Title: Expression of YTHDF1 and YTHDF2 in lung squamous cell carcinoma and their correlation with PD-L1

    doi: 10.21037/jtd-2026-1-0312

    Figure Lengend Snippet: Potential molecular mechanisms of YTHDF1 and YTHDF2 in LUSC progression. (A,C) Gene set enrichment analysis showed that YTHDF1 (A) and YTHDF2 (C) high expression subgroups of LUSC patients were significantly associated with E2F targets, G2M checkpoint, mitotic spindle, pancreas beta cells, spermatogenesis and other pathways. (B,D) Gene set enrichment analysis showed that YTHDF1 (B) and YTHDF2 (D) low expression subgroups of LUSC patients were significantly associated with allograft rejection, coagulation, inflammatory response, interferon gamma response and other pathways. LUSC, lung squamous cell carcinoma.

    Article Snippet: YTHDF2 antibodies were purchased from ABclonal Biotechnology Co., Ltd. (Wuhan, China), and Ethylene Glycol-bis (2-aminoethyl Ether)-N,N,N',N'-tetraacetic Acid (EGTA) antigen retrieval buffer (pH 9.0), antibody diluent, polylysine, phosphate buffered saline (PBS), super-sensitive 3,3'-diaminobenzidine (DAB) substrate, instant immunohistochemistry MaxVision TM kit, and neutral balsam were purchased from Fuzhou Maxim Biotechnology Co., Ltd. (Fuzhou, China).

    Techniques: Expressing, Coagulation

    Correlation of YTHDF2 expression levels with LUSC immune cell infiltration. (A) Resting memory CD4+T cells. (B) Memory B cells. (C) Plasma cells. (D) Activated memory CD4+T cells. LUSC, lung squamous cell carcinoma.

    Journal: Journal of Thoracic Disease

    Article Title: Expression of YTHDF1 and YTHDF2 in lung squamous cell carcinoma and their correlation with PD-L1

    doi: 10.21037/jtd-2026-1-0312

    Figure Lengend Snippet: Correlation of YTHDF2 expression levels with LUSC immune cell infiltration. (A) Resting memory CD4+T cells. (B) Memory B cells. (C) Plasma cells. (D) Activated memory CD4+T cells. LUSC, lung squamous cell carcinoma.

    Article Snippet: YTHDF2 antibodies were purchased from ABclonal Biotechnology Co., Ltd. (Wuhan, China), and Ethylene Glycol-bis (2-aminoethyl Ether)-N,N,N',N'-tetraacetic Acid (EGTA) antigen retrieval buffer (pH 9.0), antibody diluent, polylysine, phosphate buffered saline (PBS), super-sensitive 3,3'-diaminobenzidine (DAB) substrate, instant immunohistochemistry MaxVision TM kit, and neutral balsam were purchased from Fuzhou Maxim Biotechnology Co., Ltd. (Fuzhou, China).

    Techniques: Expressing, Clinical Proteomics

    Comparison of YTHDF1 (A) and YTHDF2 (B) expression levels in tumor tissues and adjacent tissues. IOD, integrated optical density.

    Journal: Journal of Thoracic Disease

    Article Title: Expression of YTHDF1 and YTHDF2 in lung squamous cell carcinoma and their correlation with PD-L1

    doi: 10.21037/jtd-2026-1-0312

    Figure Lengend Snippet: Comparison of YTHDF1 (A) and YTHDF2 (B) expression levels in tumor tissues and adjacent tissues. IOD, integrated optical density.

    Article Snippet: YTHDF2 antibodies were purchased from ABclonal Biotechnology Co., Ltd. (Wuhan, China), and Ethylene Glycol-bis (2-aminoethyl Ether)-N,N,N',N'-tetraacetic Acid (EGTA) antigen retrieval buffer (pH 9.0), antibody diluent, polylysine, phosphate buffered saline (PBS), super-sensitive 3,3'-diaminobenzidine (DAB) substrate, instant immunohistochemistry MaxVision TM kit, and neutral balsam were purchased from Fuzhou Maxim Biotechnology Co., Ltd. (Fuzhou, China).

    Techniques: Comparison, Expressing

    Comparison of YTHDF1 positive (A), YTHDF1 negative (B), YTHDF2 positive (C) and YTHDF2 negative (D) expression.

    Journal: Journal of Thoracic Disease

    Article Title: Expression of YTHDF1 and YTHDF2 in lung squamous cell carcinoma and their correlation with PD-L1

    doi: 10.21037/jtd-2026-1-0312

    Figure Lengend Snippet: Comparison of YTHDF1 positive (A), YTHDF1 negative (B), YTHDF2 positive (C) and YTHDF2 negative (D) expression.

    Article Snippet: YTHDF2 antibodies were purchased from ABclonal Biotechnology Co., Ltd. (Wuhan, China), and Ethylene Glycol-bis (2-aminoethyl Ether)-N,N,N',N'-tetraacetic Acid (EGTA) antigen retrieval buffer (pH 9.0), antibody diluent, polylysine, phosphate buffered saline (PBS), super-sensitive 3,3'-diaminobenzidine (DAB) substrate, instant immunohistochemistry MaxVision TM kit, and neutral balsam were purchased from Fuzhou Maxim Biotechnology Co., Ltd. (Fuzhou, China).

    Techniques: Comparison, Expressing

    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