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h 1 benzopyran 4 one  (Tocris)


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    Tocris h 1 benzopyran 4 one
    H 1 Benzopyran 4 One, supplied by Tocris, used in various techniques. Bioz Stars score: 95/100, based on 198 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/h+1+benzopyran+4+one/NU+7441/pm41115973-61-10-37
    Average 95 stars, based on 198 article reviews
    h 1 benzopyran 4 one - by Bioz Stars, 2026-11
    95/100 stars

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    Concentration Assay:

    Article Title: CRISPR/Cas9 generated DSB clusters mimic complex lesions induced by high-LET radiation and shift repair from c-NHEJ to mutagenic repair pathways.
    Article Snippet: .. Treatment with DNA repair inhibitors A specific DNA-PKcs inhibitor, 8-(4-Dibenzothienyl)-2-(4-morpholinyl)-4 H-1-benzopyran-4-one (NU7441, DNA-PKcsi) with IC50 for DNA-PKcs of 13 nM was dissolved in DMSO at 10 mM stock concentration and was used at 5 μM final concentration (Tocris Bioscience). .. A specific ATM inhibitor, 2-(4-Morpholinyl)-6(1-thianthrenyl)-4 H-pyran-4-one (KU55933, ATMi) with IC50 for ATM of 2.2 nM, was used at 10 μM final concentration from a DMSO stock solution (10 mM) (Tocris Bioscience).

    Article Title: CRISPR/Cas9 generated DSB clusters mimic complex lesions induced by high-LET radiation and shift repair from c-NHEJ to mutagenic repair pathways
    Article Snippet: .. A specific DNA-PKcs inhibitor, 8-(4-Dibenzothienyl)-2-(4-morpholinyl)-4 H-1-benzopyran-4-one (NU7441, DNA-PKcsi) with IC 50 for DNA-PKcs of 13 nM was dissolved in DMSO at 10 mM stock concentration and was used at 5 μM final concentration (Tocris Bioscience). .. A specific ATM inhibitor, 2-(4-Morpholinyl)-6-(1-thianthrenyl)-4 H-pyran-4-one (KU55933, ATMi) with IC 50 for ATM of 2.2 nM, was used at 10 μM final concentration from a DMSO stock solution (10 mM) (Tocris Bioscience).



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    Figure 2. Activation of the <t>PI3K/Akt</t> pathway after treatment with Wnt3a, IGF1, or Wnt3a and IGF1 in CRC cells. Western blotting of pAkt, total Akt, pGSK, total GSK3β, and total IGFR in CRC cell lines HT-29 (a) and HCT-116 (b). The graphs are presented as a densitometric analysis of the ratio between the phosphorylated protein and its total protein expression. Data are presented as the mean ± SEM of three independent experiments. Significance was determined using ANOVA followed by Bonferroni’s post-hoc test (*p < .05, **p < .01 and ***p < .001).
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    Figure 2. Activation of the <t>PI3K/Akt</t> pathway after treatment with Wnt3a, IGF1, or Wnt3a and IGF1 in CRC cells. Western blotting of pAkt, total Akt, pGSK, total GSK3β, and total IGFR in CRC cell lines HT-29 (a) and HCT-116 (b). The graphs are presented as a densitometric analysis of the ratio between the phosphorylated protein and its total protein expression. Data are presented as the mean ± SEM of three independent experiments. Significance was determined using ANOVA followed by Bonferroni’s post-hoc test (*p < .05, **p < .01 and ***p < .001).
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    Figure 2. Activation of the <t>PI3K/Akt</t> pathway after treatment with Wnt3a, IGF1, or Wnt3a and IGF1 in CRC cells. Western blotting of pAkt, total Akt, pGSK, total GSK3β, and total IGFR in CRC cell lines HT-29 (a) and HCT-116 (b). The graphs are presented as a densitometric analysis of the ratio between the phosphorylated protein and its total protein expression. Data are presented as the mean ± SEM of three independent experiments. Significance was determined using ANOVA followed by Bonferroni’s post-hoc test (*p < .05, **p < .01 and ***p < .001).
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    Journal: iScience

    Article Title: Acetyl-NPKY of integrin-β1 binds KINDLIN2 to control endothelial cell proliferation and junctional integrity

    doi: 10.1016/j.isci.2024.110129

    Figure Lengend Snippet:

    Article Snippet: LY294002 (IUPAC Name: 2-(4-Morpholinyl)-8-phenyl-4 H -1-benzopyran-4-one hydrochloride) , Sigma-Aldrich , Cat# 19-142.

    Techniques: Virus, Recombinant, Synthesized, Real-time Polymerase Chain Reaction, Plasmid Preparation, Software

    Figure 2. Activation of the PI3K/Akt pathway after treatment with Wnt3a, IGF1, or Wnt3a and IGF1 in CRC cells. Western blotting of pAkt, total Akt, pGSK, total GSK3β, and total IGFR in CRC cell lines HT-29 (a) and HCT-116 (b). The graphs are presented as a densitometric analysis of the ratio between the phosphorylated protein and its total protein expression. Data are presented as the mean ± SEM of three independent experiments. Significance was determined using ANOVA followed by Bonferroni’s post-hoc test (*p < .05, **p < .01 and ***p < .001).

    Journal: Cancer biology & therapy

    Article Title: Crosstalk between PI3K/Akt and Wnt/β-catenin pathways promote colorectal cancer progression regardless of mutational status.

    doi: 10.1080/15384047.2022.2108690

    Figure Lengend Snippet: Figure 2. Activation of the PI3K/Akt pathway after treatment with Wnt3a, IGF1, or Wnt3a and IGF1 in CRC cells. Western blotting of pAkt, total Akt, pGSK, total GSK3β, and total IGFR in CRC cell lines HT-29 (a) and HCT-116 (b). The graphs are presented as a densitometric analysis of the ratio between the phosphorylated protein and its total protein expression. Data are presented as the mean ± SEM of three independent experiments. Significance was determined using ANOVA followed by Bonferroni’s post-hoc test (*p < .05, **p < .01 and ***p < .001).

    Article Snippet: The 2-(4-morpholinyl)8-phenyl-1(4 H)-benzopyran-4-one LY294002 (PI3K inhibitor) was obtained from Cell Signaling and diluted in dimethyl sulfoxide (DMSO) to obtain a stock concentration of 3 mg/mL.

    Techniques: Activation Assay, Western Blot, Expressing

    Figure 6. Pharmacological inhibition of PI3K/Akt pathway using LY294002. (a) Western Blotting of pAkt, total Akt, pGSK3β and total GSK3β in HCT-116 cells after respective treatments. (b) The graphs are presented as a densitometric analysis of the ratio between the phosphorylated protein and its total protein expression. (c) Transcriptional activity of β-catenin using a Luciferase assay. Data are presented as the mean ± SEM of three independent experiments. Significance was determined using ANOVA followed by Bonferroni’s post-hoc test (*p < .05, **p < .01 and ***p < .001).

    Journal: Cancer biology & therapy

    Article Title: Crosstalk between PI3K/Akt and Wnt/β-catenin pathways promote colorectal cancer progression regardless of mutational status.

    doi: 10.1080/15384047.2022.2108690

    Figure Lengend Snippet: Figure 6. Pharmacological inhibition of PI3K/Akt pathway using LY294002. (a) Western Blotting of pAkt, total Akt, pGSK3β and total GSK3β in HCT-116 cells after respective treatments. (b) The graphs are presented as a densitometric analysis of the ratio between the phosphorylated protein and its total protein expression. (c) Transcriptional activity of β-catenin using a Luciferase assay. Data are presented as the mean ± SEM of three independent experiments. Significance was determined using ANOVA followed by Bonferroni’s post-hoc test (*p < .05, **p < .01 and ***p < .001).

    Article Snippet: The 2-(4-morpholinyl)8-phenyl-1(4 H)-benzopyran-4-one LY294002 (PI3K inhibitor) was obtained from Cell Signaling and diluted in dimethyl sulfoxide (DMSO) to obtain a stock concentration of 3 mg/mL.

    Techniques: Inhibition, Western Blot, Expressing, Activity Assay, Luciferase

    Figure 7. Schematic diagram of PI3K and WNT crosstalk in colorectal cancer. Wnt3a activating its receptor leads to GSK3β phosphorylation, hindering the formation of the destructive complex, and promoting increased β-catenin avail ability in the cytoplasm (blue pathway). IGF1 interacts with its receptor with subsequent PI3K and AKT activation (green pathway). In the article we show that both pathways promote cellular proliferation and migration, and crosstalk through PI3K activation (exemplified with LY294002 inhibition results/red arrows indicate activation of alternate pathways upon inhibition of PI3K in the combined treatment).

    Journal: Cancer biology & therapy

    Article Title: Crosstalk between PI3K/Akt and Wnt/β-catenin pathways promote colorectal cancer progression regardless of mutational status.

    doi: 10.1080/15384047.2022.2108690

    Figure Lengend Snippet: Figure 7. Schematic diagram of PI3K and WNT crosstalk in colorectal cancer. Wnt3a activating its receptor leads to GSK3β phosphorylation, hindering the formation of the destructive complex, and promoting increased β-catenin avail ability in the cytoplasm (blue pathway). IGF1 interacts with its receptor with subsequent PI3K and AKT activation (green pathway). In the article we show that both pathways promote cellular proliferation and migration, and crosstalk through PI3K activation (exemplified with LY294002 inhibition results/red arrows indicate activation of alternate pathways upon inhibition of PI3K in the combined treatment).

    Article Snippet: The 2-(4-morpholinyl)8-phenyl-1(4 H)-benzopyran-4-one LY294002 (PI3K inhibitor) was obtained from Cell Signaling and diluted in dimethyl sulfoxide (DMSO) to obtain a stock concentration of 3 mg/mL.

    Techniques: Phospho-proteomics, Activation Assay, Migration, Inhibition