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cyclin-dependent kinase 2 (cdk2) primary antibody  (Thermo Fisher)


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    Thermo Fisher cyclin-dependent kinase 2 (cdk2) primary antibody
    Cyclin Dependent Kinase 2 (Cdk2) Primary Antibody, supplied by Thermo Fisher, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cyclin-dependent kinase 2 (cdk2) primary antibody/product/Thermo Fisher
    Average 90 stars, based on 1 article reviews
    cyclin-dependent kinase 2 (cdk2) primary antibody - by Bioz Stars, 2026-02
    90/100 stars

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    Fucoidan-induced activation of the <t>Akt</t> pathway and Akt inhibitor-mediated reversal of p21WAF1 and CDK expression. (A) HT29 colon cancer cells were treated with fucoidan (100 μg/mL) for various times (0–8 h). The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (B) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 6 h. The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (C and D) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 24 h. Western blot analysis was performed <t>with</t> <t>antibodies</t> specific for p21WAF1, CDK2, and CDK4. The lower panel depicts the mean ± SEM of three independent experiments for each condition, as determined from densitometry relative to β-actin. * p <0.05 and ** p <0.01 vs. control, # p <0.05 and ## p <0.01 vs. fucoidan only group, $ p <0.05 and $ p <0.01 vs. Akt inhibitor only group.
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    https://www.bioz.com/result/primary antibodies against cyclin-dependent kinase 2 (cdk2)/product/Santa Cruz Biotechnology
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    primary antibodies against cyclin-dependent kinase 2 (cdk2) - by Bioz Stars, 2026-02
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    Fucoidan-induced activation of the <t>Akt</t> pathway and Akt inhibitor-mediated reversal of p21WAF1 and CDK expression. (A) HT29 colon cancer cells were treated with fucoidan (100 μg/mL) for various times (0–8 h). The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (B) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 6 h. The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (C and D) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 24 h. Western blot analysis was performed <t>with</t> <t>antibodies</t> specific for p21WAF1, CDK2, and CDK4. The lower panel depicts the mean ± SEM of three independent experiments for each condition, as determined from densitometry relative to β-actin. * p <0.05 and ** p <0.01 vs. control, # p <0.05 and ## p <0.01 vs. fucoidan only group, $ p <0.05 and $ p <0.01 vs. Akt inhibitor only group.
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    Fucoidan-induced activation of the <t>Akt</t> pathway and Akt inhibitor-mediated reversal of p21WAF1 and CDK expression. (A) HT29 colon cancer cells were treated with fucoidan (100 μg/mL) for various times (0–8 h). The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (B) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 6 h. The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (C and D) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 24 h. Western blot analysis was performed <t>with</t> <t>antibodies</t> specific for p21WAF1, CDK2, and CDK4. The lower panel depicts the mean ± SEM of three independent experiments for each condition, as determined from densitometry relative to β-actin. * p <0.05 and ** p <0.01 vs. control, # p <0.05 and ## p <0.01 vs. fucoidan only group, $ p <0.05 and $ p <0.01 vs. Akt inhibitor only group.
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    Fucoidan-induced activation of the Akt pathway and Akt inhibitor-mediated reversal of p21WAF1 and CDK expression. (A) HT29 colon cancer cells were treated with fucoidan (100 μg/mL) for various times (0–8 h). The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (B) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 6 h. The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (C and D) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 24 h. Western blot analysis was performed with antibodies specific for p21WAF1, CDK2, and CDK4. The lower panel depicts the mean ± SEM of three independent experiments for each condition, as determined from densitometry relative to β-actin. * p <0.05 and ** p <0.01 vs. control, # p <0.05 and ## p <0.01 vs. fucoidan only group, $ p <0.05 and $ p <0.01 vs. Akt inhibitor only group.

    Journal: Biomolecules & Therapeutics

    Article Title: Antitumor Effects of Fucoidan on Human Colon Cancer Cells via Activation of Akt Signaling

    doi: 10.4062/biomolther.2014.136

    Figure Lengend Snippet: Fucoidan-induced activation of the Akt pathway and Akt inhibitor-mediated reversal of p21WAF1 and CDK expression. (A) HT29 colon cancer cells were treated with fucoidan (100 μg/mL) for various times (0–8 h). The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (B) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 6 h. The activation of Akt was analyzed by western blot analysis using a phospho-Akt antibody. (C and D) HT29 colon cancer cells were pretreated for 4 h with an Akt inhibitor (10 −6 M) and then incubated with or without fucoidan for 24 h. Western blot analysis was performed with antibodies specific for p21WAF1, CDK2, and CDK4. The lower panel depicts the mean ± SEM of three independent experiments for each condition, as determined from densitometry relative to β-actin. * p <0.05 and ** p <0.01 vs. control, # p <0.05 and ## p <0.01 vs. fucoidan only group, $ p <0.05 and $ p <0.01 vs. Akt inhibitor only group.

    Article Snippet: The membranes were blocked with 5% skim milk and incubated with primary antibodies against vascular endothelial growth factor (VEGF), phospho-AKT, cyclin-dependent kinase 2 (CDK2), CDK4, Cyclin D, Cyclin E, p21, and β-actin (Santa Cruz Biotechnology, Dallas, TX, USA).

    Techniques: Activation Assay, Expressing, Western Blot, Incubation, Control