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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 2554 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/molecules+sb431542/SB+431542/pm42024084-77-12-17
    Average 97 stars, based on 2554 article reviews
    molecule inhibitors sb431542 - by Bioz Stars, 2026-10
    97/100 stars

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    other:

    Article Title: Generation of RRMS and PPMS specific iPSCs as a platform for modeling Multiple Sclerosis.
    Article Snippet: On day 0, medium was switched to N2B27 medium (DMEM/F12 supplemented with N2 (Invitrogen,17502–048, 1:100), B27 without vitamin A (Invitrogen, 12587–010, 1:50), Glutamax (1:100), NEAA (1:100), betamercaptoethanol (1:1000), and 25 μg/ml insulin (Sigma, I9278-5ML)), supplemented with the small molecules SB431542 10 μM (Tocris,1614) and LDN193189 1 μM (MiltenyiBiotec,130–106-540).

    Article Title: SOX10 Single Transcription Factor-Based Fast and Efficient Generation of Oligodendrocytes from Human Pluripotent Stem Cells
    Article Snippet: On day 0, medium was switched to N2B27 medium (DMEM/F12 supplemented with N2 (1:100), B27 (1:50), glutamax (1:100), NEAA (1:100), beta- mercaptoethanol (1:1000), Pen/Strep (1:100), (all from Life Technologies) and 25 μg/ml insulin (Sigma)), supplemented with the small molecules SB431542 10μM (Tocris) and LDN193189 1μM (Miltenyi Biotec) and 100nM retinoic acid (RA; Sigma).

    Article Title: SOX10 Single Transcription Factor-Based Fast and Efficient Generation of Oligodendrocytes from Human Pluripotent Stem Cells
    Article Snippet: hPSCs were maintained in feeder free conditions using mTeSR1 medium (Stemcell Technologies) on hESC-qualified matrigel (Becton Dickinson), splitting twice a week using EDTA (Lonza).

    Article Title: Intervention with metabolites emulating endogenous cell transitions accelerates muscle regeneration in young and aged mice
    Article Snippet: Next day, the medium was switched to N2B27-medium (DMEM/F12, 1X N2, 1X B27, 1X Glutamax, 1X NEAA, β-mercaptoethanol [1:1000], and 25 μg/mL insulin), supplemented with the small molecules SB431542 (Tocris, Cat. 1614) 10μM and LDN193189 (Miltenyl Biotec, Cat. 130-106-540) 1μM.

    Article Title: iPSC-derived cortical neurons to study sporadic Alzheimer disease: A transcriptome comparison with post-mortem brain samples.
    Article Snippet: B27 medium consisted of Neurobasal, B27 without retinoic acid, 1x glutamax, 1 200 mM glutamine and 1x penicillin/streptomycin (all from LifeTechnologies)) supplemented with small molecules SB431542 10 mM (Tocris) and LDN193189 1 m M (Miltenyi Biotec).

    Article Title: Resolving cell state in iPSC-derived human neural samples with multiplexed fluorescence imaging
    Article Snippet: Neural progenitor patterning with the small molecules SB431542 (10 μM; catalog #1614 Tocris), LDN193189 (1 μM; catalog #6053 Tocris) and XAV939 (2 μM; catalog #3748 Tocris) was carried out over the next 4 days, with full medium changes every day.

    Article Title: Self-Organized Nanostructure Modified Microelectrode for Sensitive Electrochemical Glutamate Detection in Stem Cells-Derived Brain Organoids
    Article Snippet: For differentiation to dorsal forebrain neurons, N2B27 defined medium was supplemented with the small molecules SB431542 (10 uM, Tocris, Bristol, UK) and LDN193189 (100 nM, KareBay Biochem, Monmouth Junction, NJ, USA) for 7 days.

    Article Title: Generation of a human induced pluripotent stem cell-based model for tauopathies combining three microtubule-associated protein TAU mutations which displays several phenotypes linked to neurodegeneration.
    Article Snippet: N2B27 medium was supplemented with the small molecules SB431542 10 mM (Tocris) and LDN193189 1 mM (Miltenyi Biotec), and daily medium changes were performed till day 12.



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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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    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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    small molecules sb431542  (STEMCELL Technologies Inc)
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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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    Image Search Results


    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