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molecule inhibitors sb431542  (Tocris)


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    Tocris molecule inhibitors sb431542
    Molecule Inhibitors Sb431542, supplied by Tocris, used in various techniques. Bioz Stars score: 97/100, based on 2545 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/molecule+inhibitors+sb431542/SB+431542/pm42024084-77-12-17
    Average 97 stars, based on 2545 article reviews
    molecule inhibitors sb431542 - by Bioz Stars, 2026-09
    97/100 stars

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    Article Title: Transcriptome-based identification and experimental validation of a key gene in Alzheimer's disease using dermal fibroblasts.
    Article Snippet: Background: Alzheimer’s disease (AD) is a neurodegenerative disorder primarily characterized by progressive cognitive impairment and neuronal damage.. The pathogenesis of AD is complex and involves multiple pathological processes.. Currently, effective methods for early diagnosis and treatment are lacking.



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    LBH is transcriptionally upregulated by TGF-β in liver cancer cells. (A) Heatmap displaying the common 474 DEGs whose expressions were altered upon treatment with 100 pM of TGF-β1 for 4 h in three different HCC cell lines, i.e. MHCC97H, MHCC97L and HCCLM3. (B) Heatmap classification displaying some typical upregulated genes in response to TGF-β1 administration in HCC cell lines. (C-H) After being treated with 100 pM of TGF-β1 (C-E) or 10 µM of <t>SB431542</t> (F-H) for the indicated periods, HCCLM3, HLE and SMMC-7721 cells were harvested for RNA purification and gene expression analyses through qPCR. (I-J) HCCLM3, HLE cells transfected with a control siRNA (NS) or those targeting Smad2/3 were treated with 100 pM of TGF-β1 for 6 h. Then the expression levels of Smad2, Smad3 and LBH were analyzed by qPCR. (K) Gene track view of Smad2/3, H3K4me3, and H3K27ac at the LBH promoter from the Cistrome Data database (top), and schematic diagram of ChIP primers designed within and near the LBH promoter region (bottom). HCCLM3 cells were treated with 2.5 ng/ml TGF-β for 24 h. ChIP assays were then performed to examine the binding of Smad2/3 to the LBH promoter region, and the enriched DNA fragments were quantitatively analyzed by qPCR. qPCR experiments described above were analyzed by one-way ANOVA followed by Tukey’s or Dunnett’s post hoc test. Statistical significance: * p < 0.05, ** p < 0.01 and *** p < 0.001; ns, no significance. Data were shown as mean ± SD
    Molecule Inhibitor Sb431542, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    LBH is transcriptionally upregulated by TGF-β in liver cancer cells. (A) Heatmap displaying the common 474 DEGs whose expressions were altered upon treatment with 100 pM of TGF-β1 for 4 h in three different HCC cell lines, i.e. MHCC97H, MHCC97L and HCCLM3. (B) Heatmap classification displaying some typical upregulated genes in response to TGF-β1 administration in HCC cell lines. (C-H) After being treated with 100 pM of TGF-β1 (C-E) or 10 µM of <t>SB431542</t> (F-H) for the indicated periods, HCCLM3, HLE and SMMC-7721 cells were harvested for RNA purification and gene expression analyses through qPCR. (I-J) HCCLM3, HLE cells transfected with a control siRNA (NS) or those targeting Smad2/3 were treated with 100 pM of TGF-β1 for 6 h. Then the expression levels of Smad2, Smad3 and LBH were analyzed by qPCR. (K) Gene track view of Smad2/3, H3K4me3, and H3K27ac at the LBH promoter from the Cistrome Data database (top), and schematic diagram of ChIP primers designed within and near the LBH promoter region (bottom). HCCLM3 cells were treated with 2.5 ng/ml TGF-β for 24 h. ChIP assays were then performed to examine the binding of Smad2/3 to the LBH promoter region, and the enriched DNA fragments were quantitatively analyzed by qPCR. qPCR experiments described above were analyzed by one-way ANOVA followed by Tukey’s or Dunnett’s post hoc test. Statistical significance: * p < 0.05, ** p < 0.01 and *** p < 0.001; ns, no significance. Data were shown as mean ± SD
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    LBH is transcriptionally upregulated by TGF-β in liver cancer cells. (A) Heatmap displaying the common 474 DEGs whose expressions were altered upon treatment with 100 pM of TGF-β1 for 4 h in three different HCC cell lines, i.e. MHCC97H, MHCC97L and HCCLM3. (B) Heatmap classification displaying some typical upregulated genes in response to TGF-β1 administration in HCC cell lines. (C-H) After being treated with 100 pM of TGF-β1 (C-E) or 10 µM of <t>SB431542</t> (F-H) for the indicated periods, HCCLM3, HLE and SMMC-7721 cells were harvested for RNA purification and gene expression analyses through qPCR. (I-J) HCCLM3, HLE cells transfected with a control siRNA (NS) or those targeting Smad2/3 were treated with 100 pM of TGF-β1 for 6 h. Then the expression levels of Smad2, Smad3 and LBH were analyzed by qPCR. (K) Gene track view of Smad2/3, H3K4me3, and H3K27ac at the LBH promoter from the Cistrome Data database (top), and schematic diagram of ChIP primers designed within and near the LBH promoter region (bottom). HCCLM3 cells were treated with 2.5 ng/ml TGF-β for 24 h. ChIP assays were then performed to examine the binding of Smad2/3 to the LBH promoter region, and the enriched DNA fragments were quantitatively analyzed by qPCR. qPCR experiments described above were analyzed by one-way ANOVA followed by Tukey’s or Dunnett’s post hoc test. Statistical significance: * p < 0.05, ** p < 0.01 and *** p < 0.001; ns, no significance. Data were shown as mean ± SD
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    LBH is transcriptionally upregulated by TGF-β in liver cancer cells. (A) Heatmap displaying the common 474 DEGs whose expressions were altered upon treatment with 100 pM of TGF-β1 for 4 h in three different HCC cell lines, i.e. MHCC97H, MHCC97L and HCCLM3. (B) Heatmap classification displaying some typical upregulated genes in response to TGF-β1 administration in HCC cell lines. (C-H) After being treated with 100 pM of TGF-β1 (C-E) or 10 µM of <t>SB431542</t> (F-H) for the indicated periods, HCCLM3, HLE and SMMC-7721 cells were harvested for RNA purification and gene expression analyses through qPCR. (I-J) HCCLM3, HLE cells transfected with a control siRNA (NS) or those targeting Smad2/3 were treated with 100 pM of TGF-β1 for 6 h. Then the expression levels of Smad2, Smad3 and LBH were analyzed by qPCR. (K) Gene track view of Smad2/3, H3K4me3, and H3K27ac at the LBH promoter from the Cistrome Data database (top), and schematic diagram of ChIP primers designed within and near the LBH promoter region (bottom). HCCLM3 cells were treated with 2.5 ng/ml TGF-β for 24 h. ChIP assays were then performed to examine the binding of Smad2/3 to the LBH promoter region, and the enriched DNA fragments were quantitatively analyzed by qPCR. qPCR experiments described above were analyzed by one-way ANOVA followed by Tukey’s or Dunnett’s post hoc test. Statistical significance: * p < 0.05, ** p < 0.01 and *** p < 0.001; ns, no significance. Data were shown as mean ± SD
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    LBH is transcriptionally upregulated by TGF-β in liver cancer cells. (A) Heatmap displaying the common 474 DEGs whose expressions were altered upon treatment with 100 pM of TGF-β1 for 4 h in three different HCC cell lines, i.e. MHCC97H, MHCC97L and HCCLM3. (B) Heatmap classification displaying some typical upregulated genes in response to TGF-β1 administration in HCC cell lines. (C-H) After being treated with 100 pM of TGF-β1 (C-E) or 10 µM of <t>SB431542</t> (F-H) for the indicated periods, HCCLM3, HLE and SMMC-7721 cells were harvested for RNA purification and gene expression analyses through qPCR. (I-J) HCCLM3, HLE cells transfected with a control siRNA (NS) or those targeting Smad2/3 were treated with 100 pM of TGF-β1 for 6 h. Then the expression levels of Smad2, Smad3 and LBH were analyzed by qPCR. (K) Gene track view of Smad2/3, H3K4me3, and H3K27ac at the LBH promoter from the Cistrome Data database (top), and schematic diagram of ChIP primers designed within and near the LBH promoter region (bottom). HCCLM3 cells were treated with 2.5 ng/ml TGF-β for 24 h. ChIP assays were then performed to examine the binding of Smad2/3 to the LBH promoter region, and the enriched DNA fragments were quantitatively analyzed by qPCR. qPCR experiments described above were analyzed by one-way ANOVA followed by Tukey’s or Dunnett’s post hoc test. Statistical significance: * p < 0.05, ** p < 0.01 and *** p < 0.001; ns, no significance. Data were shown as mean ± SD
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    dual smad small molecule inhibitors sb431542  (Tocris)
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    LBH is transcriptionally upregulated by TGF-β in liver cancer cells. (A) Heatmap displaying the common 474 DEGs whose expressions were altered upon treatment with 100 pM of TGF-β1 for 4 h in three different HCC cell lines, i.e. MHCC97H, MHCC97L and HCCLM3. (B) Heatmap classification displaying some typical upregulated genes in response to TGF-β1 administration in HCC cell lines. (C-H) After being treated with 100 pM of TGF-β1 (C-E) or 10 µM of <t>SB431542</t> (F-H) for the indicated periods, HCCLM3, HLE and SMMC-7721 cells were harvested for RNA purification and gene expression analyses through qPCR. (I-J) HCCLM3, HLE cells transfected with a control siRNA (NS) or those targeting Smad2/3 were treated with 100 pM of TGF-β1 for 6 h. Then the expression levels of Smad2, Smad3 and LBH were analyzed by qPCR. (K) Gene track view of Smad2/3, H3K4me3, and H3K27ac at the LBH promoter from the Cistrome Data database (top), and schematic diagram of ChIP primers designed within and near the LBH promoter region (bottom). HCCLM3 cells were treated with 2.5 ng/ml TGF-β for 24 h. ChIP assays were then performed to examine the binding of Smad2/3 to the LBH promoter region, and the enriched DNA fragments were quantitatively analyzed by qPCR. qPCR experiments described above were analyzed by one-way ANOVA followed by Tukey’s or Dunnett’s post hoc test. Statistical significance: * p < 0.05, ** p < 0.01 and *** p < 0.001; ns, no significance. Data were shown as mean ± SD
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    LBH is transcriptionally upregulated by TGF-β in liver cancer cells. (A) Heatmap displaying the common 474 DEGs whose expressions were altered upon treatment with 100 pM of TGF-β1 for 4 h in three different HCC cell lines, i.e. MHCC97H, MHCC97L and HCCLM3. (B) Heatmap classification displaying some typical upregulated genes in response to TGF-β1 administration in HCC cell lines. (C-H) After being treated with 100 pM of TGF-β1 (C-E) or 10 µM of SB431542 (F-H) for the indicated periods, HCCLM3, HLE and SMMC-7721 cells were harvested for RNA purification and gene expression analyses through qPCR. (I-J) HCCLM3, HLE cells transfected with a control siRNA (NS) or those targeting Smad2/3 were treated with 100 pM of TGF-β1 for 6 h. Then the expression levels of Smad2, Smad3 and LBH were analyzed by qPCR. (K) Gene track view of Smad2/3, H3K4me3, and H3K27ac at the LBH promoter from the Cistrome Data database (top), and schematic diagram of ChIP primers designed within and near the LBH promoter region (bottom). HCCLM3 cells were treated with 2.5 ng/ml TGF-β for 24 h. ChIP assays were then performed to examine the binding of Smad2/3 to the LBH promoter region, and the enriched DNA fragments were quantitatively analyzed by qPCR. qPCR experiments described above were analyzed by one-way ANOVA followed by Tukey’s or Dunnett’s post hoc test. Statistical significance: * p < 0.05, ** p < 0.01 and *** p < 0.001; ns, no significance. Data were shown as mean ± SD

    Journal: Cellular Oncology

    Article Title: Upregulation of limb-bud and heart (LBH) drives liver cancer progression by interacting with the oncoprotein Mortalin

    doi: 10.1007/s13402-026-01228-z

    Figure Lengend Snippet: LBH is transcriptionally upregulated by TGF-β in liver cancer cells. (A) Heatmap displaying the common 474 DEGs whose expressions were altered upon treatment with 100 pM of TGF-β1 for 4 h in three different HCC cell lines, i.e. MHCC97H, MHCC97L and HCCLM3. (B) Heatmap classification displaying some typical upregulated genes in response to TGF-β1 administration in HCC cell lines. (C-H) After being treated with 100 pM of TGF-β1 (C-E) or 10 µM of SB431542 (F-H) for the indicated periods, HCCLM3, HLE and SMMC-7721 cells were harvested for RNA purification and gene expression analyses through qPCR. (I-J) HCCLM3, HLE cells transfected with a control siRNA (NS) or those targeting Smad2/3 were treated with 100 pM of TGF-β1 for 6 h. Then the expression levels of Smad2, Smad3 and LBH were analyzed by qPCR. (K) Gene track view of Smad2/3, H3K4me3, and H3K27ac at the LBH promoter from the Cistrome Data database (top), and schematic diagram of ChIP primers designed within and near the LBH promoter region (bottom). HCCLM3 cells were treated with 2.5 ng/ml TGF-β for 24 h. ChIP assays were then performed to examine the binding of Smad2/3 to the LBH promoter region, and the enriched DNA fragments were quantitatively analyzed by qPCR. qPCR experiments described above were analyzed by one-way ANOVA followed by Tukey’s or Dunnett’s post hoc test. Statistical significance: * p < 0.05, ** p < 0.01 and *** p < 0.001; ns, no significance. Data were shown as mean ± SD

    Article Snippet: Recombinant human TGF-β1 protein was obtained from R&D Systems Inc., and the small molecule inhibitor SB431542 was purchased from MedChemExpress (MCE, USA).

    Techniques: Purification, Gene Expression, Transfection, Control, Expressing, Binding Assay