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List of antibodies used for this study
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The differentiated expression of YTHDF1 and <t>YTHDF2</t> 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.
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The differentiated expression of YTHDF1 and <t>YTHDF2</t> 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.
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The differentiated expression of YTHDF1 and <t>YTHDF2</t> 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.
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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; <t>YTHDF2,</t> YTH domain family 2.
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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; <t>YTHDF2,</t> YTH domain family 2.
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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; <t>YTHDF2,</t> YTH domain family 2.
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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; <t>YTHDF2,</t> YTH domain family 2.
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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