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human ythdf2 expression vector pcdna3 flag ythdf2  (Addgene inc)


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    Addgene inc human ythdf2 expression vector pcdna3 flag ythdf2
    The expression of <t>YTHDF2</t> in ovarian cancer tissues. a Relative expression of YTHDF2 in ovarian cancer tissues and normal ovarian tissues. b The relationship between the expression level of YTHDF2 and clinical stage. c The relationship between the expression level of YTHDF2 and pathological grade. d The relationship between the expression level of YTHDF2 and metastasis. All experiments were carried out in triplicate and the results were presented as means ± SE. * P < 0.05, ** P < 0.001, t-test. N normal ovarian tissue, C ovarian cancer tissues
    Human Ythdf2 Expression Vector Pcdna3 Flag Ythdf2, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ythdf2/pmc07501604-44-1-9?v=Addgene+inc
    Average 92 stars, based on 8 article reviews
    human ythdf2 expression vector pcdna3 flag ythdf2 - by Bioz Stars, 2026-08
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    Images

    1) Product Images from "YTHDF2, a protein repressed by miR-145, regulates proliferation, apoptosis, and migration in ovarian cancer cells"

    Article Title: YTHDF2, a protein repressed by miR-145, regulates proliferation, apoptosis, and migration in ovarian cancer cells

    Journal: Journal of Ovarian Research

    doi: 10.1186/s13048-020-00717-5

    The expression of YTHDF2 in ovarian cancer tissues. a Relative expression of YTHDF2 in ovarian cancer tissues and normal ovarian tissues. b The relationship between the expression level of YTHDF2 and clinical stage. c The relationship between the expression level of YTHDF2 and pathological grade. d The relationship between the expression level of YTHDF2 and metastasis. All experiments were carried out in triplicate and the results were presented as means ± SE. * P < 0.05, ** P < 0.001, t-test. N normal ovarian tissue, C ovarian cancer tissues
    Figure Legend Snippet: The expression of YTHDF2 in ovarian cancer tissues. a Relative expression of YTHDF2 in ovarian cancer tissues and normal ovarian tissues. b The relationship between the expression level of YTHDF2 and clinical stage. c The relationship between the expression level of YTHDF2 and pathological grade. d The relationship between the expression level of YTHDF2 and metastasis. All experiments were carried out in triplicate and the results were presented as means ± SE. * P < 0.05, ** P < 0.001, t-test. N normal ovarian tissue, C ovarian cancer tissues

    Techniques Used: Expressing

    YTHDF2 significantly downregulates global mRNA m6A levels to promotes EOC cell proliferation and migration. a The mRNA and protein level of YTHDF2 was downregulated after transfection of YTHDF2 siRNA. b Knocking down YTHDF2 increased global mRNA m6A level. (C)CCK8 assay result showed knock-down of YTHDF2 decreased proliferation of ovarian cancer cells. d Knock-down of YTHDF2 promoted apoptosis of ovarian cancer cells. e Knock-down of YTHDF2 inhibited migration of ovarian cancer cells. f The mRNA and protein level of YTHDF2 was upregulated after overexpression of YTHDF2. g overexpression of YTHDF2 decreased global mRNA m6A level. (H)CCK8 assay result showed upregulated of YTHDF2 increased proliferation of ovarian cancer cells. (I) overexpression of YTHDF2 inhibited apoptosis of ovarian cancer cells. j overexpression of YTHDF2 promoted migration of ovarian cancer cells. All experiments were carried out in triplicate and the results were presented as means ± SE. * P < 0.05, ** P < 0.001, t-test
    Figure Legend Snippet: YTHDF2 significantly downregulates global mRNA m6A levels to promotes EOC cell proliferation and migration. a The mRNA and protein level of YTHDF2 was downregulated after transfection of YTHDF2 siRNA. b Knocking down YTHDF2 increased global mRNA m6A level. (C)CCK8 assay result showed knock-down of YTHDF2 decreased proliferation of ovarian cancer cells. d Knock-down of YTHDF2 promoted apoptosis of ovarian cancer cells. e Knock-down of YTHDF2 inhibited migration of ovarian cancer cells. f The mRNA and protein level of YTHDF2 was upregulated after overexpression of YTHDF2. g overexpression of YTHDF2 decreased global mRNA m6A level. (H)CCK8 assay result showed upregulated of YTHDF2 increased proliferation of ovarian cancer cells. (I) overexpression of YTHDF2 inhibited apoptosis of ovarian cancer cells. j overexpression of YTHDF2 promoted migration of ovarian cancer cells. All experiments were carried out in triplicate and the results were presented as means ± SE. * P < 0.05, ** P < 0.001, t-test

    Techniques Used: Migration, Transfection, CCK-8 Assay, Over Expression

    YTHDF2 is the direct target gene of miR-145. a Scatter diagram showing. YTHDF2 expression and miR-145 expression by qRT-PCR and their correlations (R 2 = 0.914, P = 0.000) in 31 EOC tissue samples. b qRT-PCR results showed a negative correlation between YTHDF2 and miR-145 in both SKOV3 and 3AO cells. c qRT-PCR showed that transfection of miR-145 mimic rescued miR-145 level in SKOV3 and 3AO cells. d The mRNA and protein levels of YTHDF2 decreased after overexpression of miR-145. e The expression level of miR-145 increased after overexpression of YTHDF2. f Luciferase reporter assays showed that miR-145 targeted YTHDF2 directly. All experiments were carried out in triplicate and the results were presented as means ± SE. *P < 0.05, **P < 0.001, t-test
    Figure Legend Snippet: YTHDF2 is the direct target gene of miR-145. a Scatter diagram showing. YTHDF2 expression and miR-145 expression by qRT-PCR and their correlations (R 2 = 0.914, P = 0.000) in 31 EOC tissue samples. b qRT-PCR results showed a negative correlation between YTHDF2 and miR-145 in both SKOV3 and 3AO cells. c qRT-PCR showed that transfection of miR-145 mimic rescued miR-145 level in SKOV3 and 3AO cells. d The mRNA and protein levels of YTHDF2 decreased after overexpression of miR-145. e The expression level of miR-145 increased after overexpression of YTHDF2. f Luciferase reporter assays showed that miR-145 targeted YTHDF2 directly. All experiments were carried out in triplicate and the results were presented as means ± SE. *P < 0.05, **P < 0.001, t-test

    Techniques Used: Expressing, Quantitative RT-PCR, Transfection, Over Expression, Luciferase

    Overexpression of YTHDF2 rescues miR-145-induced reduction of proliferation and migration in EOC. a overexpression of YTHDF2 reversed the proliferation repressed by overexpression of miR-145. b miR-145 promoted apoptosis of ovarian cancer cells, which was counteracted by overexpression of YTHDF2. c overexpression of YTHDF2 reversed the migration repressed by overexpression of miR-145. d The effect of overexpression of miR-145 on the global mRNA m6A levels was offset by overexpression of YTHDF2. e The expression of YTDHF2 at mRNA levels after overexpression of miR-145 and YTHDF2. f The expression of YTDHF2 at protein levels after overexpression of miR-145 and YTHDF2. All experiments were carried out in triplicate and the results were presented as means ± SE. * P < 0.05, ** P < 0.001, t-test
    Figure Legend Snippet: Overexpression of YTHDF2 rescues miR-145-induced reduction of proliferation and migration in EOC. a overexpression of YTHDF2 reversed the proliferation repressed by overexpression of miR-145. b miR-145 promoted apoptosis of ovarian cancer cells, which was counteracted by overexpression of YTHDF2. c overexpression of YTHDF2 reversed the migration repressed by overexpression of miR-145. d The effect of overexpression of miR-145 on the global mRNA m6A levels was offset by overexpression of YTHDF2. e The expression of YTDHF2 at mRNA levels after overexpression of miR-145 and YTHDF2. f The expression of YTDHF2 at protein levels after overexpression of miR-145 and YTHDF2. All experiments were carried out in triplicate and the results were presented as means ± SE. * P < 0.05, ** P < 0.001, t-test

    Techniques Used: Over Expression, Migration, Expressing



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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