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Reporter Vector Pcpgfree Promoter Lucia, supplied by InvivoGen, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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dual luciferase reporter assay kit  (Vazyme Biotech Co)
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. <t>(L)</t> <t>Dual-luciferase</t> reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.
Dual Luciferase Reporter Assay Kit, supplied by Vazyme Biotech Co, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. <t>(L)</t> <t>Dual-luciferase</t> reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.
Miseq Reporter, supplied by Illumina Inc, used in various techniques. Bioz Stars score: 99/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. <t>(L)</t> <t>Dual-luciferase</t> reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.
Nf κb Luciferase Reporter Lentivirus, supplied by BPS Bioscience, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. <t>(L)</t> <t>Dual-luciferase</t> reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.
Transdetect Double Luciferase Reporter Assay Kit, supplied by TransGen biotech co, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. <t>(L)</t> <t>Dual-luciferase</t> reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.
Codex Reporter Plate Brand Tech, supplied by BrandTech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. <t>(L)</t> <t>Dual-luciferase</t> reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.
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tlr7 8 9 inhibition reporter assays hek bluetm  (InvivoGen)
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. <t>(L)</t> <t>Dual-luciferase</t> reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.
Tlr7 8 9 Inhibition Reporter Assays Hek Bluetm, supplied by InvivoGen, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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black reporter plate  (BrandTech)
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. <t>(L)</t> <t>Dual-luciferase</t> reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.
Black Reporter Plate, supplied by BrandTech, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. (L) Dual-luciferase reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.

Journal: Translational Oncology

Article Title: REST-driven upregulation of SFXN3 promotes AML progression via Wnt/β-catenin activation and confers decitabine resistance

doi: 10.1016/j.tranon.2026.102705

Figure Lengend Snippet: REST Regulates SFXN3 Expression by Directly Binding to Its Promoter Region. (A) Identification of transcription factors potentially regulating SFXN3 expression by integrating data from the JASPAR, GTEx, ChIP Atlas, and ENCODE databases. A Venn diagram highlights TFAP2C and REST as common candidates, suggesting them as potential upstream regulators. (B) Quantitative mRNA analysis reveals that REST is significantly upregulated in AML tissues compared to adjacent non-tumor tissues. (C) Spearman correlation analysis shows a strong positive correlation between REST and SFXN3 expression. (D) RT-PCR analysis confirms the knockdown efficiency of two shRNA constructs targeting REST (sh-REST#1 and sh-REST#2), and evaluates their impact on SFXN3 mRNA levels. (E) Western blot analysis validates the protein-level knockdown efficiency of sh-REST#1 and sh-REST#2, along with their effects on SFXN3 protein expression. (F) Quantification of REST and SFXN3 protein expression levels. (G) Prediction of REST binding sites in the SFXN3 promoter using JASPAR and ENCODE databases, with the highest affinity region localized between positions −415 and −395. (H) Binding motif analysis from the JASPAR database confirms a predicted REST binding site within the SFXN3 promoter. A mutant version of this binding site was designed for subsequent experiments. (I) ChIP-seq data demonstrates a prominent REST binding peak at the −415 to −395 region of the SFXN3 promoter. (J) Molecular docking simulation reveals that the DNA-binding domain of REST forms a stable complex with the specific binding site in the SFXN3 promoter. (K) ChIP-qPCR analysis confirms significant enrichment of REST at the SFXN3 promoter, which is markedly reduced following REST knockdown. (L) Dual-luciferase reporter assays show that REST significantly enhances the activity of the wild-type SFXN3 promoter, while mutation of the binding site substantially diminishes this effect.

Article Snippet: Subsequently, luciferase activity was measured using a Dual-Luciferase Reporter Assay Kit (#DL101, Vazyme, Nanjing, China).

Techniques: Expressing, Binding Assay, Reverse Transcription Polymerase Chain Reaction, Knockdown, shRNA, Construct, Western Blot, Mutagenesis, ChIP-sequencing, ChIP-qPCR, Luciferase, Activity Assay