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dapt thermo fisher scientific  (Thermo Fisher)


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    Structured Review

    Thermo Fisher dapt thermo fisher scientific
    Dapt Thermo Fisher Scientific, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/dapt thermo fisher scientific/product/Thermo Fisher
    Average 95 stars, based on 1 article reviews
    dapt thermo fisher scientific - by Bioz Stars, 2026-05
    95/100 stars

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    Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and <t>NOTCH</t> <t>inhibitors</t> starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.
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    Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and <t>NOTCH</t> <t>inhibitors</t> starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.
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    dapt  (Tocris)
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    Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and <t>NOTCH</t> <t>inhibitors</t> starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.
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    Thermo Fisher dapt
    Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and <t>NOTCH</t> <t>inhibitors</t> starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.
    Dapt, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and <t>NOTCH</t> <t>inhibitors</t> starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.
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    Tocris notch inhibitor dapt
    (a) αSMA mRNA levels in HCAEC treated with TGFβ1 (10 ng/ml) or exposed to hypoxic conditions (5% O 2 ), in the absence or presence of moderate dose EtOH (25 mM, green bars) or high dose EtOH (100 mM, red bars) +/- the <t>γ-secretase</t> <t>inhibitor</t> <t>DAPT</t> (20 μM). (b) αSMA and fibronectin (FN) mRNA levels in HCAEC treated with TGFβ1 +/- the Notch ligand DLL4 (3 μg/ml) in the absence or presence of DAPT (20 μM). Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.
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    (a) αSMA mRNA levels in HCAEC treated with TGFβ1 (10 ng/ml) or exposed to hypoxic conditions (5% O 2 ), in the absence or presence of moderate dose EtOH (25 mM, green bars) or high dose EtOH (100 mM, red bars) +/- the <t>γ-secretase</t> <t>inhibitor</t> <t>DAPT</t> (20 μM). (b) αSMA and fibronectin (FN) mRNA levels in HCAEC treated with TGFβ1 +/- the Notch ligand DLL4 (3 μg/ml) in the absence or presence of DAPT (20 μM). Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.
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    Tocris dapt treatment
    (a) αSMA mRNA levels in HCAEC treated with TGFβ1 (10 ng/ml) or exposed to hypoxic conditions (5% O 2 ), in the absence or presence of moderate dose EtOH (25 mM, green bars) or high dose EtOH (100 mM, red bars) +/- the <t>γ-secretase</t> <t>inhibitor</t> <t>DAPT</t> (20 μM). (b) αSMA and fibronectin (FN) mRNA levels in HCAEC treated with TGFβ1 +/- the Notch ligand DLL4 (3 μg/ml) in the absence or presence of DAPT (20 μM). Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.
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    Image Search Results


    Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and NOTCH inhibitors starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.

    Journal: Alzheimer's & Dementia

    Article Title: Human iPSC‐derived GABAergic interneuron transplantation restores circuit balance and cognitive function in an Alzheimer's disease model

    doi: 10.1002/alz.71378

    Figure Lengend Snippet: Generation of hiPSC‐derived MGE‐pINs. (A) Schematic illustration of generation of iPSC‐derived MGE‐pINs. (B) Immunocytochemistry of iPSC‐derived MGE progenitor cells after 3 weeks of differentiation (from three independent iPSC lines). Scale bar = 50 µm. (C) Immunocytochemistry of 5‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor starting at 3 weeks of differentiation. Scale bar = 50 µm. (D) Immunocytochemistry of 7‐week‐old pINs derived from iPSCs after 2 weeks of treatment with MEK inhibitor combined with CDK and NOTCH inhibitors starting at 5 weeks of differentiation. Scale bar = 50 µm. (E) Quantitative analysis of 3‐week‐old MGE progenitor cells derived from iPSCs. (F) Quantitative analysis of 5‐week‐old pINs derived from iPSCs. (G) Quantitative analysis of 7‐week‐old pINs derived from iPSCs. Data were presented as mean ± SEM ( n = 3 hiPSC lines). ERBB4, Erb‐B2 receptor tyrosine kinase 4; FOXG1, Forkhead box G1; GABA, gamma‐aminobutyric acid; hiPSC, human induced pluripotent stem cell; KI67, Ki‐67 antigen; LHX6, LIM homeobox 6; LHX8, LIM homeobox 8; MAF, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog; MAFB, v‐maf musculoaponeurotic fibrosarcoma oncogene homolog B; MGE, medial ganglionic eminence; NKX2‐1, NK2 homeobox 1; OCT4, octamer‐binding transcription factor 4; SOX2, SRY‐box transcription factor 2; SOX6, SRY‐box transcription factor 6.

    Article Snippet: From week 5 to week 7, in addition to the continued treatment with the MEK inhibitor, NOTCH inhibitors (DAPT 10 μM; HY‐13027, MCE) and cyclin‐dependent kinase (CDK) inhibitors (PD0332991 2 μM; MCE, HY‐50767) were introduced to induce cell cycle exit in the cells during this stage.

    Techniques: Derivative Assay, Immunocytochemistry, Binding Assay

    (a) αSMA mRNA levels in HCAEC treated with TGFβ1 (10 ng/ml) or exposed to hypoxic conditions (5% O 2 ), in the absence or presence of moderate dose EtOH (25 mM, green bars) or high dose EtOH (100 mM, red bars) +/- the γ-secretase inhibitor DAPT (20 μM). (b) αSMA and fibronectin (FN) mRNA levels in HCAEC treated with TGFβ1 +/- the Notch ligand DLL4 (3 μg/ml) in the absence or presence of DAPT (20 μM). Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.

    Journal: bioRxiv

    Article Title: A Biphasic Effect of Alcohol on Endothelial Plasticity Through Regulation of Endothelial-to-Mesenchymal Transition

    doi: 10.64898/2026.04.14.718463

    Figure Lengend Snippet: (a) αSMA mRNA levels in HCAEC treated with TGFβ1 (10 ng/ml) or exposed to hypoxic conditions (5% O 2 ), in the absence or presence of moderate dose EtOH (25 mM, green bars) or high dose EtOH (100 mM, red bars) +/- the γ-secretase inhibitor DAPT (20 μM). (b) αSMA and fibronectin (FN) mRNA levels in HCAEC treated with TGFβ1 +/- the Notch ligand DLL4 (3 μg/ml) in the absence or presence of DAPT (20 μM). Data are mean±SEM, n=3. *p<0.05 vs control (no treatment), #p<0.05 vs TGFβ1 or hypoxia.

    Article Snippet: Where indicated, cells were treated with Notch inhibitor DAPT (20 μM, Cat. #2634, Tocris,) or Notch ligand DLL4 (2 μg/ml, Cat. # 1506-D4, R&D Systems).

    Techniques: Control

    HCAEC were treated with inflammatory cytokines (IL1β + TGFβ1) in the absence or presence of moderate dose ethanol (25 mM EtOH) or high dose ethanol (100 mM EtOH), with or without the gamma secretase inhibitor DAPT (20 μM), before Cdh5 expression was determined by immunocytochemistry. (a) Representative immunofluorescence images from 2 separate experiments, and (b) cumulative quantitative data of Cdh5 fluorescent staining. Data are mean±SEM, n=6. *p<0.05 vs control (no treatment, grp 1), #p<0.05 vs IL1β + TGFβ1 (grp 2).

    Journal: bioRxiv

    Article Title: A Biphasic Effect of Alcohol on Endothelial Plasticity Through Regulation of Endothelial-to-Mesenchymal Transition

    doi: 10.64898/2026.04.14.718463

    Figure Lengend Snippet: HCAEC were treated with inflammatory cytokines (IL1β + TGFβ1) in the absence or presence of moderate dose ethanol (25 mM EtOH) or high dose ethanol (100 mM EtOH), with or without the gamma secretase inhibitor DAPT (20 μM), before Cdh5 expression was determined by immunocytochemistry. (a) Representative immunofluorescence images from 2 separate experiments, and (b) cumulative quantitative data of Cdh5 fluorescent staining. Data are mean±SEM, n=6. *p<0.05 vs control (no treatment, grp 1), #p<0.05 vs IL1β + TGFβ1 (grp 2).

    Article Snippet: Where indicated, cells were treated with Notch inhibitor DAPT (20 μM, Cat. #2634, Tocris,) or Notch ligand DLL4 (2 μg/ml, Cat. # 1506-D4, R&D Systems).

    Techniques: Expressing, Immunocytochemistry, Immunofluorescence, Staining, Control