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hes1  (Cell Signaling Technology Inc)


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    Structured Review

    Cell Signaling Technology Inc hes1
    Hes1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/hes1/us12599634-167-37-39
    Average 86 stars, based on 1 article reviews
    hes1 - by Bioz Stars, 2026-09
    86/100 stars

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    Related Articles

    Activation Assay:

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. Notch pathway activation was confirmed by Western blot for activated Notch1 (CST, Catalog No. 3608) and Hes1 (CST, Catalog No. 11988) with β-actin (Sigma-Aldrich, Catalog No. A5441) as loading control., , Murine fibroblasts derived from skin of Notch1 F/F ( Fsp1.Cre –/– ; Notch1 LoxP/LoxP+/+ ), Notch1 −/− ( Fsp1.Cre ± ; Notch1 LoxP/LoxP+/+ ), N1 IC F/F ( Fsp1.Cre -/ - ; ROSA LSL-N1IC+/+ ), and N1 IC +/+ ( Fsp1.Cre ± ; ROSA LSL-N1IC+/+ ) mice were similarly transduced by GFP-lentivirus. ..

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. Notch pathway activation was confirmed by Western blot for activated Notch1 (CST, Cat# 3608) and Hes1 (CST, Cat# 11988) with β-actin (Sigma-Aldrich, Cat# A5441) as loading control.14,15,17 Murine fibroblasts derived from skin of Notch1F/F (Fsp1.Cre-/-;Notch1LoxP/LoxP+/+), Notch1−/− (Fsp1.Cre+/-;Notch1LoxP/LoxP+/+), N1IC F/F (Fsp1.Cre-/-;ROSALSL-N1IC+/+ ), and N1IC +/+ (Fsp1.Cre+/;ROSALSL-N1IC+/+) mice 17 were similarly transduced by GFP/lentivirus.14 ..

    Western Blot:

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. Notch pathway activation was confirmed by Western blot for activated Notch1 (CST, Catalog No. 3608) and Hes1 (CST, Catalog No. 11988) with β-actin (Sigma-Aldrich, Catalog No. A5441) as loading control., , Murine fibroblasts derived from skin of Notch1 F/F ( Fsp1.Cre –/– ; Notch1 LoxP/LoxP+/+ ), Notch1 −/− ( Fsp1.Cre ± ; Notch1 LoxP/LoxP+/+ ), N1 IC F/F ( Fsp1.Cre -/ - ; ROSA LSL-N1IC+/+ ), and N1 IC +/+ ( Fsp1.Cre ± ; ROSA LSL-N1IC+/+ ) mice were similarly transduced by GFP-lentivirus. ..

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. For Western blotting, protein lysates (30 μg) were separated on 10% SDS-PAGE, transferred to PVDF membranes, and probed with antibodies against aNotch1 (CST, Cat# 3608), Hes1 (CST, Cat# 11988), and β-actin (Sigma, Cat# A5441). ..

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. For Western blotting, protein lysates (30 μg) were separated on 10% sodium dodecyl sulfate–polyacrylamide gel electrophoresis, transferred to polyvinylidene difluoride membranes, and probed with antibodies against aNotch1 (CST, Catalog No. 3608), Hes1 (CST, Catalog No. 11988), and β-actin (Sigma, Catalog No. A5441). ..

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. Notch pathway activation was confirmed by Western blot for activated Notch1 (CST, Cat# 3608) and Hes1 (CST, Cat# 11988) with β-actin (Sigma-Aldrich, Cat# A5441) as loading control.14,15,17 Murine fibroblasts derived from skin of Notch1F/F (Fsp1.Cre-/-;Notch1LoxP/LoxP+/+), Notch1−/− (Fsp1.Cre+/-;Notch1LoxP/LoxP+/+), N1IC F/F (Fsp1.Cre-/-;ROSALSL-N1IC+/+ ), and N1IC +/+ (Fsp1.Cre+/;ROSALSL-N1IC+/+) mice 17 were similarly transduced by GFP/lentivirus.14 ..

    Control:

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. Notch pathway activation was confirmed by Western blot for activated Notch1 (CST, Catalog No. 3608) and Hes1 (CST, Catalog No. 11988) with β-actin (Sigma-Aldrich, Catalog No. A5441) as loading control., , Murine fibroblasts derived from skin of Notch1 F/F ( Fsp1.Cre –/– ; Notch1 LoxP/LoxP+/+ ), Notch1 −/− ( Fsp1.Cre ± ; Notch1 LoxP/LoxP+/+ ), N1 IC F/F ( Fsp1.Cre -/ - ; ROSA LSL-N1IC+/+ ), and N1 IC +/+ ( Fsp1.Cre ± ; ROSA LSL-N1IC+/+ ) mice were similarly transduced by GFP-lentivirus. ..

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. Notch pathway activation was confirmed by Western blot for activated Notch1 (CST, Cat# 3608) and Hes1 (CST, Cat# 11988) with β-actin (Sigma-Aldrich, Cat# A5441) as loading control.14,15,17 Murine fibroblasts derived from skin of Notch1F/F (Fsp1.Cre-/-;Notch1LoxP/LoxP+/+), Notch1−/− (Fsp1.Cre+/-;Notch1LoxP/LoxP+/+), N1IC F/F (Fsp1.Cre-/-;ROSALSL-N1IC+/+ ), and N1IC +/+ (Fsp1.Cre+/;ROSALSL-N1IC+/+) mice 17 were similarly transduced by GFP/lentivirus.14 ..

    Derivative Assay:

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. Notch pathway activation was confirmed by Western blot for activated Notch1 (CST, Catalog No. 3608) and Hes1 (CST, Catalog No. 11988) with β-actin (Sigma-Aldrich, Catalog No. A5441) as loading control., , Murine fibroblasts derived from skin of Notch1 F/F ( Fsp1.Cre –/– ; Notch1 LoxP/LoxP+/+ ), Notch1 −/− ( Fsp1.Cre ± ; Notch1 LoxP/LoxP+/+ ), N1 IC F/F ( Fsp1.Cre -/ - ; ROSA LSL-N1IC+/+ ), and N1 IC +/+ ( Fsp1.Cre ± ; ROSA LSL-N1IC+/+ ) mice were similarly transduced by GFP-lentivirus. ..

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. Notch pathway activation was confirmed by Western blot for activated Notch1 (CST, Cat# 3608) and Hes1 (CST, Cat# 11988) with β-actin (Sigma-Aldrich, Cat# A5441) as loading control.14,15,17 Murine fibroblasts derived from skin of Notch1F/F (Fsp1.Cre-/-;Notch1LoxP/LoxP+/+), Notch1−/− (Fsp1.Cre+/-;Notch1LoxP/LoxP+/+), N1IC F/F (Fsp1.Cre-/-;ROSALSL-N1IC+/+ ), and N1IC +/+ (Fsp1.Cre+/;ROSALSL-N1IC+/+) mice 17 were similarly transduced by GFP/lentivirus.14 ..

    Nucleic Acid Electrophoresis:

    Article Title: Targeting Melanoma-Associated Fibroblasts to Overcome Cancer Stem Cell-Driven Drug Resistance
    Article Snippet: .. For Western blotting, protein lysates (30 μg) were separated on 10% sodium dodecyl sulfate–polyacrylamide gel electrophoresis, transferred to polyvinylidene difluoride membranes, and probed with antibodies against aNotch1 (CST, Catalog No. 3608), Hes1 (CST, Catalog No. 11988), and β-actin (Sigma, Catalog No. A5441). ..

    Blocking Assay:

    Article Title: Anlotinib + Toripalimab maintenance in Extensive-Stage small cell lung Cancer: Clinical efficacy and preclinical mechanism of anlotinib-induced neuroendocrine differentiation Suppression via Notch1.
    Article Snippet: Purpose: To evaluate the efficacy, safety and underlying mechanisms of toripalimab combined with anlotinib as maintenance therapy in patients with extensive-stage small cell lung cancer (ES-SCLC) who achieved disease control after first-line platinum-etoposide chemotherapy.. Experimental: Design: A multi-center, single-arm, open-label phase II trial (NCT04363255) enrolled 20 patients with ES-SCLC.. Participants received maintenance therapy with toripalimab (240mgevery3weeks) plus anlotinib (12mgorallyondays1–14ofeach21–daycycle) until disease progression or unacceptable toxicity.

    Incubation:

    Article Title: Anlotinib + Toripalimab maintenance in Extensive-Stage small cell lung Cancer: Clinical efficacy and preclinical mechanism of anlotinib-induced neuroendocrine differentiation Suppression via Notch1.
    Article Snippet: Purpose: To evaluate the efficacy, safety and underlying mechanisms of toripalimab combined with anlotinib as maintenance therapy in patients with extensive-stage small cell lung cancer (ES-SCLC) who achieved disease control after first-line platinum-etoposide chemotherapy.. Experimental: Design: A multi-center, single-arm, open-label phase II trial (NCT04363255) enrolled 20 patients with ES-SCLC.. Participants received maintenance therapy with toripalimab (240mgevery3weeks) plus anlotinib (12mgorallyondays1–14ofeach21–daycycle) until disease progression or unacceptable toxicity.

    other:

    Article Title: Nerve guidance conduit comprising neural crest stem-like cells and/or Schwann cell precursor-like cells and methods of making and using the same
    Article Snippet: Western Blot Cells cultured in the 3D-collagen gel were recovered following enzymatic dissociation with collagenase 1 (2 mg/mL) and whole cell lysates were prepared by incubation with radioimmunoprecipitation (RIPA) assay buffer (Santa Cruz) supplemented with a cocktail of protease inhibitors (Santa Cruz) and the total protein concentrations were determined using bicinchoninic acid (BCA) method (BioVision).



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    Image Search Results


    Notch signaling is impaired in the eIF5A ΔPANC mutant pancreas. Representative images of E11.5 (A) Ptf1a-cre and (B) eIF5A ΔPANC pancreata stained for E-cadherin (green), Hes1 (red) and nuclei (DAPI, blue). These tissue sections also show expression of the tdTomato reporter, which is visualized in the green channel. (C) Quantification of the Hes1-expressing cells within the pancreas showed no significant difference between Ptf1a-cre controls and eIF5A ΔPANC mutants. Representative images of E14.5 (D) Ptf1a-cre and (E) eIF5A ΔPANC pancreata stained for E-cadherin (green), Hes1 (red) and nuclei (DAPI, blue). (F) Quantification of the Hes1-expressing cells within the pancreas showed a significant decrease in eIF5A ΔPANC mutants. Gene expression analysis of (G) Hes1 , (H) Notch1 , (I) Ngn3 , and (J) Eif5a in E14.5 pancreata from Ptf1a-cre controls and eIF5A ΔPANC mutants. Data are presented as mean +/− SEM; n = 4–5/group; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001.

    Journal: Molecular Metabolism

    Article Title: Translating the blueprint of cell fate: eIF5A-mediated translation regulates cellular identity in the pancreas

    doi: 10.1016/j.molmet.2026.102362

    Figure Lengend Snippet: Notch signaling is impaired in the eIF5A ΔPANC mutant pancreas. Representative images of E11.5 (A) Ptf1a-cre and (B) eIF5A ΔPANC pancreata stained for E-cadherin (green), Hes1 (red) and nuclei (DAPI, blue). These tissue sections also show expression of the tdTomato reporter, which is visualized in the green channel. (C) Quantification of the Hes1-expressing cells within the pancreas showed no significant difference between Ptf1a-cre controls and eIF5A ΔPANC mutants. Representative images of E14.5 (D) Ptf1a-cre and (E) eIF5A ΔPANC pancreata stained for E-cadherin (green), Hes1 (red) and nuclei (DAPI, blue). (F) Quantification of the Hes1-expressing cells within the pancreas showed a significant decrease in eIF5A ΔPANC mutants. Gene expression analysis of (G) Hes1 , (H) Notch1 , (I) Ngn3 , and (J) Eif5a in E14.5 pancreata from Ptf1a-cre controls and eIF5A ΔPANC mutants. Data are presented as mean +/− SEM; n = 4–5/group; ∗, p < 0.05; ∗∗, p < 0.01; ∗∗∗, p < 0.001.

    Article Snippet: Real-time PCR was performed using TaqMan Gene Expression Master Mix (Applied Biosystems) and TaqMan probes for Notch1 (catalog #: Mm00627185_m1), Hes1 (catalog #: Mm00468601_m1), Ngn3 (catalog #: Mm00437606_s1), Eif5a (catalog #: Mm00839121_gH), Ins1 (catalog # Mm01259683_g1), Gcg (catalog # Mm00801714_m1), Sst (catalog # Mm00436671_m1), and Luciferase (catalog #: Mr03987587_mr).

    Techniques: Mutagenesis, Staining, Expressing, Gene Expression