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Proteintech c ebpβ
<t>C/EBPβ</t> <t>promoted</t> DNMT3B expression through transcriptional activation. (A) The results of PROMO database prediction. (B, C) Effects of maternal fructose intake during pregnancy on the C/EBPβ expression in the liver of offspring at 0 days and 4 weeks. Actin was used as a loading control ( n = 4 offspring samples per group). (D) Knockdown of C/EBPβ inhibited DNMT3B expression at the protein level in AML12 cells. Actin was used as a loading control ( n = 3 samples per group). (E) Dual‐Luciferase Assay revealed that C/EBPβ trans‐activates the Dnmt3b promoter ( n = 6 samples per group). (F) CHIP‐PCR results showed that C/EBPβ bound to the Dnmt3b promoter. All data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, and **** p < 0.0001.
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Image Search Results


C/EBPβ promoted DNMT3B expression through transcriptional activation. (A) The results of PROMO database prediction. (B, C) Effects of maternal fructose intake during pregnancy on the C/EBPβ expression in the liver of offspring at 0 days and 4 weeks. Actin was used as a loading control ( n = 4 offspring samples per group). (D) Knockdown of C/EBPβ inhibited DNMT3B expression at the protein level in AML12 cells. Actin was used as a loading control ( n = 3 samples per group). (E) Dual‐Luciferase Assay revealed that C/EBPβ trans‐activates the Dnmt3b promoter ( n = 6 samples per group). (F) CHIP‐PCR results showed that C/EBPβ bound to the Dnmt3b promoter. All data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, and **** p < 0.0001.

Journal: The FASEB Journal

Article Title: Maternal Fructose Intake During Pregnancy Induced the Hepatic Glucose Homeostasis Imbalance in the Offspring by Inhibiting Glucokinase

doi: 10.1096/fj.202503081R

Figure Lengend Snippet: C/EBPβ promoted DNMT3B expression through transcriptional activation. (A) The results of PROMO database prediction. (B, C) Effects of maternal fructose intake during pregnancy on the C/EBPβ expression in the liver of offspring at 0 days and 4 weeks. Actin was used as a loading control ( n = 4 offspring samples per group). (D) Knockdown of C/EBPβ inhibited DNMT3B expression at the protein level in AML12 cells. Actin was used as a loading control ( n = 3 samples per group). (E) Dual‐Luciferase Assay revealed that C/EBPβ trans‐activates the Dnmt3b promoter ( n = 6 samples per group). (F) CHIP‐PCR results showed that C/EBPβ bound to the Dnmt3b promoter. All data were presented as mean ± SEM. * p < 0.05, ** p < 0.01, and **** p < 0.0001.

Article Snippet: The primary antibodies used were as follows: GK (Abclonal, A15059, 1:1000), DNMT3B (Abclonal, A22658, 1:5000), HK2 (Proteintech, 22029‐1‐AP, 1:1500), GLUT2 (Proteintech, 20436‐1‐AP, 1:1500), KHK (Proteintech, 15681‐1‐AP, 1:1000), ALDOB (Proteintech, 18065‐1‐AP, 1:5000), ACLY (Proteintech, 15421‐1‐AP, 1:1000), Actin (Bioworld, BS6007M, 1:5000), and C/EBPβ (Proteintech, 23 431‐1‐AP, 1:15,000).

Techniques: Expressing, Activation Assay, Control, Knockdown, Luciferase

Schematic diagram of the core mechanisms. The study demonstrated that maternal fructose intake during pregnancy led to glucose intolerance and insulin resistance in offspring. The abnormal hepatic glucose metabolism in offspring was associated with decreased GK expression, which was inhibited by DNMT3B. Besides, the expression of DNMT3B was regulated by C/EBPβ at the transcriptional level. This condition was improved by the administration of dorzagliatin.

Journal: The FASEB Journal

Article Title: Maternal Fructose Intake During Pregnancy Induced the Hepatic Glucose Homeostasis Imbalance in the Offspring by Inhibiting Glucokinase

doi: 10.1096/fj.202503081R

Figure Lengend Snippet: Schematic diagram of the core mechanisms. The study demonstrated that maternal fructose intake during pregnancy led to glucose intolerance and insulin resistance in offspring. The abnormal hepatic glucose metabolism in offspring was associated with decreased GK expression, which was inhibited by DNMT3B. Besides, the expression of DNMT3B was regulated by C/EBPβ at the transcriptional level. This condition was improved by the administration of dorzagliatin.

Article Snippet: The primary antibodies used were as follows: GK (Abclonal, A15059, 1:1000), DNMT3B (Abclonal, A22658, 1:5000), HK2 (Proteintech, 22029‐1‐AP, 1:1500), GLUT2 (Proteintech, 20436‐1‐AP, 1:1500), KHK (Proteintech, 15681‐1‐AP, 1:1000), ALDOB (Proteintech, 18065‐1‐AP, 1:5000), ACLY (Proteintech, 15421‐1‐AP, 1:1000), Actin (Bioworld, BS6007M, 1:5000), and C/EBPβ (Proteintech, 23 431‐1‐AP, 1:15,000).

Techniques: Expressing