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aurka inhibitor alisertib  (MedChemExpress)


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    MedChemExpress aurka inhibitor alisertib
    Aurka Inhibitor Alisertib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 86 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/aurka+inhibitor+alisertib/Alisertib/pm41827042-45-4-17
    Average 95 stars, based on 86 article reviews
    aurka inhibitor alisertib - by Bioz Stars, 2026-09
    95/100 stars

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    Recombinant:

    Article Title: SENP5 enhances antiviral innate immunity by promoting AURKA-dependent STAT2 phosphorylation
    Article Snippet: .. Recombinant human interferon α-2a, AURKA inhibitor (Alisertib) and protein phosphatase 2 A (PP2A) inhibitor (Endothall) were purchased from MedChemExpress (New Jersey, USA). .. The proteasome inhibitor MG132 was purchased from Selleck Chemicals (Texas, USA).

    Article Title: SENP5 enhances antiviral innate immunity by promoting AURKA-dependent STAT2 phosphorylation.
    Article Snippet: .. Recombinant human interferon α-2a, AURKA inhibitor (Alisertib) and protein phosphatase 2A (PP2A) inhibitor (Endothall) were purchased from MedChemExpress (New Jersey, USA). .. The proteasome inhibitor MG132 was purchased from Selleck Chemicals (Texas, USA).



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    a, HCT116 cells were synchronised in prometaphase using thymidine-nocodazole treatment, followed by 9 hours of nocodazole incubation. Cells were treated with Palbo or a CDK1-specific inhibitor, RO-3306 (CDK1i, 10 µM), with or without MG132. Samples were collected at 3 and 7 hours after treatment for flow cytometry and immunoblot analysis. Mitotic exit (decrease in pH3-positive cells) induced by Palbo, but not by CDK1i, was effectively blocked by proteasome inhibition. Data are means ± s.d. (N = 3); two-way ANOVA. Western blot analysis shows retention of highly phosphorylated Cdc27 and CycB1 in MG132-treated cells. b, Cells were synchronised in prometaphase as above and treated with Palbo or vehicle control in the presence or absence of the APC/C inhibitor, proTAME (25 µM). Flow cytometry analysis revealed that proTAME blocked mitotic exit induced by CDK4/6 inhibition, as evidenced by retention of pH3-positive cells with high CycB1 levels. c, HCT116 cells were arrested in mitosis using nocodazole and co-treated with MG132 to prevent mitotic exit. BubR1 and centromere marker CENP-C were visualised by immunofluorescence. BubR1 kinetochore localisation decreased over time upon Palbo treatment, while it remained stable in control conditions. <t>Alisertib</t> (1 µM) served as a positive control for SAC inactivation. Scale bar: 10 µm. Pearson correlation coefficients (PCC) quantify BubR1/CENP-C co-localisation; one-way ANOVA. n = 20, 100, 100, 100 (-); 20, 99, 100, 100 (+Palbo); 21, 100, 98, 100 (+Alisertib), at T0, T1, T2, T3 in a single experient. d, CDK4/6 inhibition reduces KNL1 MELT phosphorylation (pMELT) and BubR1 phosphorylation. Left: Immunoblots show decreased pMELT and BubR1 phosphorylation in cells treated with Palbo, Abema (5 µM), or alisertib in the presence of MG132, correlating with SAC inactivation. Right: Immunofluorescence shows partial reduction of kinetochore pMELT signals after Palbo or Abema treatment. Scale bar: 10 µm.
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    a, HCT116 cells were synchronised in prometaphase using thymidine-nocodazole treatment, followed by 9 hours of nocodazole incubation. Cells were treated with Palbo or a CDK1-specific inhibitor, RO-3306 (CDK1i, 10 µM), with or without MG132. Samples were collected at 3 and 7 hours after treatment for flow cytometry and immunoblot analysis. Mitotic exit (decrease in pH3-positive cells) induced by Palbo, but not by CDK1i, was effectively blocked by proteasome inhibition. Data are means ± s.d. (N = 3); two-way ANOVA. Western blot analysis shows retention of highly phosphorylated Cdc27 and CycB1 in MG132-treated cells. b, Cells were synchronised in prometaphase as above and treated with Palbo or vehicle control in the presence or absence of the APC/C inhibitor, proTAME (25 µM). Flow cytometry analysis revealed that proTAME blocked mitotic exit induced by CDK4/6 inhibition, as evidenced by retention of pH3-positive cells with high CycB1 levels. c, HCT116 cells were arrested in mitosis using nocodazole and co-treated with MG132 to prevent mitotic exit. BubR1 and centromere marker CENP-C were visualised by immunofluorescence. BubR1 kinetochore localisation decreased over time upon Palbo treatment, while it remained stable in control conditions. Alisertib (1 µM) served as a positive control for SAC inactivation. Scale bar: 10 µm. Pearson correlation coefficients (PCC) quantify BubR1/CENP-C co-localisation; one-way ANOVA. n = 20, 100, 100, 100 (-); 20, 99, 100, 100 (+Palbo); 21, 100, 98, 100 (+Alisertib), at T0, T1, T2, T3 in a single experient. d, CDK4/6 inhibition reduces KNL1 MELT phosphorylation (pMELT) and BubR1 phosphorylation. Left: Immunoblots show decreased pMELT and BubR1 phosphorylation in cells treated with Palbo, Abema (5 µM), or alisertib in the presence of MG132, correlating with SAC inactivation. Right: Immunofluorescence shows partial reduction of kinetochore pMELT signals after Palbo or Abema treatment. Scale bar: 10 µm.

    Journal: bioRxiv

    Article Title: Mitotic CDK4/6 activity sustains spindle checkpoint signalling to prevent mitotic slippage and genomic instability

    doi: 10.1101/2025.09.13.675969

    Figure Lengend Snippet: a, HCT116 cells were synchronised in prometaphase using thymidine-nocodazole treatment, followed by 9 hours of nocodazole incubation. Cells were treated with Palbo or a CDK1-specific inhibitor, RO-3306 (CDK1i, 10 µM), with or without MG132. Samples were collected at 3 and 7 hours after treatment for flow cytometry and immunoblot analysis. Mitotic exit (decrease in pH3-positive cells) induced by Palbo, but not by CDK1i, was effectively blocked by proteasome inhibition. Data are means ± s.d. (N = 3); two-way ANOVA. Western blot analysis shows retention of highly phosphorylated Cdc27 and CycB1 in MG132-treated cells. b, Cells were synchronised in prometaphase as above and treated with Palbo or vehicle control in the presence or absence of the APC/C inhibitor, proTAME (25 µM). Flow cytometry analysis revealed that proTAME blocked mitotic exit induced by CDK4/6 inhibition, as evidenced by retention of pH3-positive cells with high CycB1 levels. c, HCT116 cells were arrested in mitosis using nocodazole and co-treated with MG132 to prevent mitotic exit. BubR1 and centromere marker CENP-C were visualised by immunofluorescence. BubR1 kinetochore localisation decreased over time upon Palbo treatment, while it remained stable in control conditions. Alisertib (1 µM) served as a positive control for SAC inactivation. Scale bar: 10 µm. Pearson correlation coefficients (PCC) quantify BubR1/CENP-C co-localisation; one-way ANOVA. n = 20, 100, 100, 100 (-); 20, 99, 100, 100 (+Palbo); 21, 100, 98, 100 (+Alisertib), at T0, T1, T2, T3 in a single experient. d, CDK4/6 inhibition reduces KNL1 MELT phosphorylation (pMELT) and BubR1 phosphorylation. Left: Immunoblots show decreased pMELT and BubR1 phosphorylation in cells treated with Palbo, Abema (5 µM), or alisertib in the presence of MG132, correlating with SAC inactivation. Right: Immunofluorescence shows partial reduction of kinetochore pMELT signals after Palbo or Abema treatment. Scale bar: 10 µm.

    Article Snippet: For kinase inhibition, we employed CDK4/6 inhibitors—palbociclib (MCE, HY-50767), abemaciclib (MCE, HY-16297A), and ribociclib (MCE, HY-15777)—as well as the CDK1-specific inhibitor RO3306 (Selleck, 872573-93-8; MCE, HY-12529), the Aurora A kinase inhibitor alisertib (MCE, HY-10971) and the MEK inhibitor PD0325901 (Selleck S1036).).

    Techniques: Incubation, Flow Cytometry, Western Blot, Inhibition, Control, Marker, Immunofluorescence, Positive Control, Phospho-proteomics