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act  (Worthington Biochemical)


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    Worthington Biochemical act
    Act, supplied by Worthington Biochemical, used in various techniques. Bioz Stars score: 99/100, based on 490 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/act/act/custom%40act%4042421033
    Average 99 stars, based on 490 article reviews
    act - by Bioz Stars, 2026-09
    99/100 stars

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    Recombinant:

    Article Title: Evaluation of the effects of A-PRF and oral dexamethasone use on postoperative complications in third molar extraction: a split-mouth randomized-controlled trial.
    Article Snippet: tegrity and act as ‘guarantors.’ All authors read and approved the final manuscript. Acknowledgements: Not applicable. REFERENCES AR TIC LE IN PR ES S ARTICLE IN PRESS 1. Bailey E, Kashbour W, Shah N, Worthington H V, Renton TF, Coulthard P. Surgical techniques for the removal of mandibular wisdom teeth. Cochrane Database of Systematic Reviews. 2020 Jul 26;2020(7). doi:10.1002/14651858.CD004345.pub

    Staining:

    Article Title: Evaluation of the effects of A-PRF and oral dexamethasone use on postoperative complications in third molar extraction: a split-mouth randomized-controlled trial.
    Article Snippet: tegrity and act as ‘guarantors.’ All authors read and approved the final manuscript. Acknowledgements: Not applicable. REFERENCES AR TIC LE IN PR ES S ARTICLE IN PRESS 1. Bailey E, Kashbour W, Shah N, Worthington H V, Renton TF, Coulthard P. Surgical techniques for the removal of mandibular wisdom teeth. Cochrane Database of Systematic Reviews. 2020 Jul 26;2020(7). doi:10.1002/14651858.CD004345.pub

    Plasmid Preparation:

    Article Title: Evaluation of the effects of A-PRF and oral dexamethasone use on postoperative complications in third molar extraction: a split-mouth randomized-controlled trial.
    Article Snippet: tegrity and act as ‘guarantors.’ All authors read and approved the final manuscript. Acknowledgements: Not applicable. REFERENCES AR TIC LE IN PR ES S ARTICLE IN PRESS 1. Bailey E, Kashbour W, Shah N, Worthington H V, Renton TF, Coulthard P. Surgical techniques for the removal of mandibular wisdom teeth. Cochrane Database of Systematic Reviews. 2020 Jul 26;2020(7). doi:10.1002/14651858.CD004345.pub



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    Analysis of ligands and receptors in senescent and receiving cells. (A) Schematic depicting BulkSignalR pipeline which uses known ligand‐receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). (B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown (Figure ) to be capable of receiving senescence signals and becoming SA β‐gal positive: <t>CXCR7,</t> KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) (Figure , Figure ). (C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (gray) and BrdU (red) treated cell lines ( n = 3 replicates). (D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO‐1 is a <t>MIF</t> <t>antagonist,</t> <t>ACT‐1004‐1239</t> is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data were analyzed by two‐way ANOVA with Tukey's multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, ** p < 0.01, *** p < 0.001).
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    Analysis of ligands and receptors in senescent and receiving cells. (A) Schematic depicting BulkSignalR pipeline which uses known ligand‐receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). (B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown (Figure ) to be capable of receiving senescence signals and becoming SA β‐gal positive: <t>CXCR7,</t> KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) (Figure , Figure ). (C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (gray) and BrdU (red) treated cell lines ( n = 3 replicates). (D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO‐1 is a <t>MIF</t> <t>antagonist,</t> <t>ACT‐1004‐1239</t> is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data were analyzed by two‐way ANOVA with Tukey's multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, ** p < 0.01, *** p < 0.001).
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    Image Search Results


    Analysis of ligands and receptors in senescent and receiving cells. (A) Schematic depicting BulkSignalR pipeline which uses known ligand‐receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). (B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown (Figure ) to be capable of receiving senescence signals and becoming SA β‐gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) (Figure , Figure ). (C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (gray) and BrdU (red) treated cell lines ( n = 3 replicates). (D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO‐1 is a MIF antagonist, ACT‐1004‐1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data were analyzed by two‐way ANOVA with Tukey's multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, ** p < 0.01, *** p < 0.001).

    Journal: Aging Cell

    Article Title: Characterizing the SASP ‐Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

    doi: 10.1111/acel.70673

    Figure Lengend Snippet: Analysis of ligands and receptors in senescent and receiving cells. (A) Schematic depicting BulkSignalR pipeline which uses known ligand‐receptor interactions and affected downstream pathways to analyze their activation based on our bulk RNAseq data from DMSO and BrdU treated human cell lines (created with BioRender). (B) Venn diagram showing the number of receptors inferred from BulkSignalR to be activated across each of the five human cell types. Three receptors were identified in common between astrocytes (purple), endothelial cells (pink), and microglia (yellow) which were the cell types shown (Figure ) to be capable of receiving senescence signals and becoming SA β‐gal positive: CXCR7, KREMEN2, and GIPR. Only CXCR7 was expressed in the cell types capable of entering secondary senescence (astrocytes, endothelial cells, microglia) (Figure , Figure ). (C) TPM expression values of CXCR7 , its ligand CXCL12 , and DPP4 which cleaves and inactivates CXCL12 in DMSO (gray) and BrdU (red) treated cell lines ( n = 3 replicates). (D) Schematic of the four selected SASP inhibitors mechanisms of action: Bindarit is a CCL2 synthesis inhibitor which prevents p65 activation of the CCL2 gene at the promoter region, ISO‐1 is a MIF antagonist, ACT‐1004‐1239 is a CXCR7 antagonist, and Sitagliptin inhibits DPP4 preventing its action of cleaving and inactivating CXCL12 (created with BioRender). Data were analyzed by two‐way ANOVA with Tukey's multiple comparisons test (C). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, ** p < 0.01, *** p < 0.001).

    Article Snippet: Treatment with CXCR7 antagonist ACT‐1004‐1239 (MedChemExpress, Catalog No. HY‐142617) was utilized to prevent CXCR7‐associated communication between senescence inducers and receiving cells.

    Techniques: Activation Assay, RNA sequencing, Expressing, Standard Deviation

    Targeting SASP ligands and receptors to prevent the spreading of senescence. (A) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with 100 μM BrdU (red) along with 200 μM Bindarit (pink), 50 μM ISO‐1 (blue), 200 μM ACT‐1004‐1239 (orange), or 2 μM Sitagliptin (green) ( n = 6 replicates). (B) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with 100 μM BrdU (red) along with 200 μM Bindarit (pink), 50 μM ISO‐1 (blue), 200 μM ACT‐1004‐1239 (orange), or 2 μM Sitagliptin (green) ( n = 6 replicates). (C) Timeline showing treatment with DMSO + Bindarit CM or BrdU + Bindarit CM for 7 days. Timeline showing treatment with DMSO or 100 μM BrdU along with SASP inhibitors (ISO‐1, ACT‐1004‐1239, or Sitagliptin) for 7 days. Features of senescence were analyzed 8 days after the initial plating of cells (created with BioRender). (D) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO + Bindarit CM from astrocytes (gray), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (gray), or BrdU CM from astrocytes + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from astrocytes + Bindarit (gray) or BrdU CM from astrocytes + Bindarit (red) ( n = 4 replicates). (E) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO + Bindarit CM from microglia (gray), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (gray), or BrdU CM from microglia + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from microglia + Bindarit (gray) or BrdU CM from microglia + Bindarit (red) ( n = 4 replicates). (F) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with DMSO + Bindarit CM from microglia (gray), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (gray), or BrdU CM from microglia + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from microglia + Bindarit (gray) or BrdU CM from microglia + Bindarit (red) ( n = 4 replicates). (G) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with DMSO + Bindarit CM from astrocytes (gray), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (gray), or BrdU CM from astrocytes + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from astrocytes + Bindarit (gray) or BrdU CM from astrocytes + Bindarit (red) ( n = 4 replicates). Data analyzed by unpaired t ‐test (A, B) and two‐way ANOVA with Tukey's or Šídák's multiple comparisons test (D–G). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001).

    Journal: Aging Cell

    Article Title: Characterizing the SASP ‐Dependent Paracrine Spreading of Senescence Between Human Brain Cell Types

    doi: 10.1111/acel.70673

    Figure Lengend Snippet: Targeting SASP ligands and receptors to prevent the spreading of senescence. (A) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with 100 μM BrdU (red) along with 200 μM Bindarit (pink), 50 μM ISO‐1 (blue), 200 μM ACT‐1004‐1239 (orange), or 2 μM Sitagliptin (green) ( n = 6 replicates). (B) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with 100 μM BrdU (red) along with 200 μM Bindarit (pink), 50 μM ISO‐1 (blue), 200 μM ACT‐1004‐1239 (orange), or 2 μM Sitagliptin (green) ( n = 6 replicates). (C) Timeline showing treatment with DMSO + Bindarit CM or BrdU + Bindarit CM for 7 days. Timeline showing treatment with DMSO or 100 μM BrdU along with SASP inhibitors (ISO‐1, ACT‐1004‐1239, or Sitagliptin) for 7 days. Features of senescence were analyzed 8 days after the initial plating of cells (created with BioRender). (D) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO + Bindarit CM from astrocytes (gray), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (gray), or BrdU CM from astrocytes + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from astrocytes + Bindarit (gray) or BrdU CM from astrocytes + Bindarit (red) ( n = 4 replicates). (E) Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO + Bindarit CM from microglia (gray), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (gray), or BrdU CM from microglia + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from microglia + Bindarit (gray) or BrdU CM from microglia + Bindarit (red) ( n = 4 replicates). (F) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with DMSO + Bindarit CM from microglia (gray), BrdU + Bindarit CM from microglia (red), DMSO CM from microglia + SASP inhibitor (gray), or BrdU CM from microglia + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from microglia + Bindarit (gray) or BrdU CM from microglia + Bindarit (red) ( n = 4 replicates). (G) Quantification of percentage of SA β‐gal positive microglia following 7‐day treatment with DMSO + Bindarit CM from astrocytes (gray), BrdU + Bindarit CM from astrocytes (red), DMSO CM from astrocytes + SASP inhibitor (gray), or BrdU CM from astrocytes + SASP inhibitor (red) ( n = 4 replicates). Quantification of percentage of SA β‐gal positive astrocytes following 7‐day treatment with DMSO CM from astrocytes + Bindarit (gray) or BrdU CM from astrocytes + Bindarit (red) ( n = 4 replicates). Data analyzed by unpaired t ‐test (A, B) and two‐way ANOVA with Tukey's or Šídák's multiple comparisons test (D–G). All graphs show mean with error bars depicting standard deviation (ns, p > 0.05, * p < 0.05, ** p < 0.01, *** p < 0.001).

    Article Snippet: Treatment with CXCR7 antagonist ACT‐1004‐1239 (MedChemExpress, Catalog No. HY‐142617) was utilized to prevent CXCR7‐associated communication between senescence inducers and receiving cells.

    Techniques: Standard Deviation