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cdk2 polyclonal antibody  (Bioss)


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    Bioss cdk2 polyclonal antibody
    Cdk2 Polyclonal Antibody, supplied by Bioss, used in various techniques. Bioz Stars score: 94/100, based on 8 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/cdk2+polyclonal+antibody/CDK2+Polyclonal+Antibody/custom%40bs-10726r%4042030802
    Average 94 stars, based on 8 article reviews
    cdk2 polyclonal antibody - by Bioz Stars, 2026-11
    94/100 stars

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    cdk2 polyclonal antibody  (Bioss)
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    PKF inhibits CRC cell growth by inducing apoptosis and cell cycle arrest. (A, B) Cell viability of HCT15 and HCT116 cells treated with PKF for 24 h. (C) Cell migration of HCT15 and HCT116 cells after PKF treatment for 24. (D) Colony formation of HCT15 and HCT116 cells following PKF treatment for 24 h. (E) Cell apoptosis analysis of HCT15 and HCT116 cells after 24 h of PKF treatment. (F, G) Cell cycle analysis in HCT15 and HCT116 cells following PKF treatment for 24 h. (H) Protein expression levels of cell cycle‐related proteins (Cyclin D1, Cyclin A2, CDK1, <t>CDK2,</t> CDK7) and apoptosis markers (c‐Caspase‐3, c‐Caspase‐8) in HCT15 and HCT116 cells treated with PKF for 24 h. (I, J) Cell viability of HCT15 and HCT116 cells treated with PKF alone or in combination with Z‐VAD‐FMK (Z‐VAD). *** p < 0.001, **** p < 0.0001; ns, not significant.
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    PKF inhibits CRC cell growth by inducing apoptosis and cell cycle arrest. (A, B) Cell viability of HCT15 and HCT116 cells treated with PKF for 24 h. (C) Cell migration of HCT15 and HCT116 cells after PKF treatment for 24. (D) Colony formation of HCT15 and HCT116 cells following PKF treatment for 24 h. (E) Cell apoptosis analysis of HCT15 and HCT116 cells after 24 h of PKF treatment. (F, G) Cell cycle analysis in HCT15 and HCT116 cells following PKF treatment for 24 h. (H) Protein expression levels of cell cycle‐related proteins (Cyclin D1, Cyclin A2, CDK1, <t>CDK2,</t> CDK7) and apoptosis markers (c‐Caspase‐3, c‐Caspase‐8) in HCT15 and HCT116 cells treated with PKF for 24 h. (I, J) Cell viability of HCT15 and HCT116 cells treated with PKF alone or in combination with Z‐VAD‐FMK (Z‐VAD). *** p < 0.001, **** p < 0.0001; ns, not significant.
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    PKF inhibits CRC cell growth by inducing apoptosis and cell cycle arrest. (A, B) Cell viability of HCT15 and HCT116 cells treated with PKF for 24 h. (C) Cell migration of HCT15 and HCT116 cells after PKF treatment for 24. (D) Colony formation of HCT15 and HCT116 cells following PKF treatment for 24 h. (E) Cell apoptosis analysis of HCT15 and HCT116 cells after 24 h of PKF treatment. (F, G) Cell cycle analysis in HCT15 and HCT116 cells following PKF treatment for 24 h. (H) Protein expression levels of cell cycle‐related proteins (Cyclin D1, Cyclin A2, CDK1, <t>CDK2,</t> CDK7) and apoptosis markers (c‐Caspase‐3, c‐Caspase‐8) in HCT15 and HCT116 cells treated with PKF for 24 h. (I, J) Cell viability of HCT15 and HCT116 cells treated with PKF alone or in combination with Z‐VAD‐FMK (Z‐VAD). *** p < 0.001, **** p < 0.0001; ns, not significant.
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    PKF inhibits CRC cell growth by inducing apoptosis and cell cycle arrest. (A, B) Cell viability of HCT15 and HCT116 cells treated with PKF for 24 h. (C) Cell migration of HCT15 and HCT116 cells after PKF treatment for 24. (D) Colony formation of HCT15 and HCT116 cells following PKF treatment for 24 h. (E) Cell apoptosis analysis of HCT15 and HCT116 cells after 24 h of PKF treatment. (F, G) Cell cycle analysis in HCT15 and HCT116 cells following PKF treatment for 24 h. (H) Protein expression levels of cell cycle‐related proteins (Cyclin D1, Cyclin A2, CDK1, <t>CDK2,</t> CDK7) and apoptosis markers (c‐Caspase‐3, c‐Caspase‐8) in HCT15 and HCT116 cells treated with PKF for 24 h. (I, J) Cell viability of HCT15 and HCT116 cells treated with PKF alone or in combination with Z‐VAD‐FMK (Z‐VAD). *** p < 0.001, **** p < 0.0001; ns, not significant.
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    phospho cdk2 thr14  (Bioss)
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    PKF inhibits CRC cell growth by inducing apoptosis and cell cycle arrest. (A, B) Cell viability of HCT15 and HCT116 cells treated with PKF for 24 h. (C) Cell migration of HCT15 and HCT116 cells after PKF treatment for 24. (D) Colony formation of HCT15 and HCT116 cells following PKF treatment for 24 h. (E) Cell apoptosis analysis of HCT15 and HCT116 cells after 24 h of PKF treatment. (F, G) Cell cycle analysis in HCT15 and HCT116 cells following PKF treatment for 24 h. (H) Protein expression levels of cell cycle‐related proteins (Cyclin D1, Cyclin A2, CDK1, <t>CDK2,</t> CDK7) and apoptosis markers (c‐Caspase‐3, c‐Caspase‐8) in HCT15 and HCT116 cells treated with PKF for 24 h. (I, J) Cell viability of HCT15 and HCT116 cells treated with PKF alone or in combination with Z‐VAD‐FMK (Z‐VAD). *** p < 0.001, **** p < 0.0001; ns, not significant.
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    Image Search Results


    PKF inhibits CRC cell growth by inducing apoptosis and cell cycle arrest. (A, B) Cell viability of HCT15 and HCT116 cells treated with PKF for 24 h. (C) Cell migration of HCT15 and HCT116 cells after PKF treatment for 24. (D) Colony formation of HCT15 and HCT116 cells following PKF treatment for 24 h. (E) Cell apoptosis analysis of HCT15 and HCT116 cells after 24 h of PKF treatment. (F, G) Cell cycle analysis in HCT15 and HCT116 cells following PKF treatment for 24 h. (H) Protein expression levels of cell cycle‐related proteins (Cyclin D1, Cyclin A2, CDK1, CDK2, CDK7) and apoptosis markers (c‐Caspase‐3, c‐Caspase‐8) in HCT15 and HCT116 cells treated with PKF for 24 h. (I, J) Cell viability of HCT15 and HCT116 cells treated with PKF alone or in combination with Z‐VAD‐FMK (Z‐VAD). *** p < 0.001, **** p < 0.0001; ns, not significant.

    Journal: Advanced Science

    Article Title: Homoisoflavanone Delays Colorectal Cancer Progression via DNA Damage‐Induced Mitochondrial Apoptosis and Parthanatos‐Like Cell Death

    doi: 10.1002/advs.202511406

    Figure Lengend Snippet: PKF inhibits CRC cell growth by inducing apoptosis and cell cycle arrest. (A, B) Cell viability of HCT15 and HCT116 cells treated with PKF for 24 h. (C) Cell migration of HCT15 and HCT116 cells after PKF treatment for 24. (D) Colony formation of HCT15 and HCT116 cells following PKF treatment for 24 h. (E) Cell apoptosis analysis of HCT15 and HCT116 cells after 24 h of PKF treatment. (F, G) Cell cycle analysis in HCT15 and HCT116 cells following PKF treatment for 24 h. (H) Protein expression levels of cell cycle‐related proteins (Cyclin D1, Cyclin A2, CDK1, CDK2, CDK7) and apoptosis markers (c‐Caspase‐3, c‐Caspase‐8) in HCT15 and HCT116 cells treated with PKF for 24 h. (I, J) Cell viability of HCT15 and HCT116 cells treated with PKF alone or in combination with Z‐VAD‐FMK (Z‐VAD). *** p < 0.001, **** p < 0.0001; ns, not significant.

    Article Snippet: The membranes were then blocked with a 5% non‐fat milk TBST (TBS containing 0.1% Tween‐20) for 1 h at room temperature and incubated at 4°C for overnight with primary antibodies against the following proteins: cleaved Caspase 3 (25128‐1‐AP, Proteintech), cleaved Caspase 8 (9496, CST), PARP (9542, CST), cleaved PARP (9541, CST), P21 (2947, CST), P53 (2527, CST), Cyclin A2 (91500, CST), Cyclin D1 (2978, CST), CDK1 (bs‐1341R, Bioss), CDK2 (bs‐10726R, Bioss), CDK7 (bs‐0569R, Bioss), AKT (4691, CST), p‐AKT (4060, CST), ERK (9102, CST), p‐ERK (9101, CST), MEK (9126, CST), p‐MEK (9154, CST), ATR (13934, CST), p‐ATR (2853, CST), Chk1 (2360, CST), p‐Chk1 (2348, CST), RAD51 (14961‐1‐AP, Proteintech), ATM (27156‐1‐AP, Proteintech), p‐ATM (5883, CST), γ‐H2AX (9718, CST), AIF (5318, CST), MIF (75038, CST), Cyt c (10993‐1‐AP, Proteintech), Lamin B (66095‐1‐Ig, Proteintech), VDAC1 (81538‐1‐RR, Proteintech) and GAPDH (60004‐1‐Ig, Proteintech).

    Techniques: Migration, Cell Cycle Assay, Expressing

    HIF inhibits CRC cells growth. (A, B) Cell viability of HCT15 and HCT116 cells treated with trans‐coumaroyltyramine (trans‐Coum), N‐feruloyloctopamine (Feru), N‐trans‐feruloyltyramine (trans‐Feru), disporopsin (Disp), or HIF for 24 h. (C) IC50 values of HIF in HCT15 and HCT116 cells. (D) Cell migration analysis of HCT15 and HCT116 cells following HIF treatment. (E) Colony formation assessment of HCT15 and HCT116 cells after HIF treatment for 24 h. (F) Apoptosis analysis of HCT15 and HCT116 cells after 24 h of HIF treatment. (G, H) Cell cycle distribution analysis of HCT15 and HCT116 cells following HIF treatment for 24 h. (I) Expression levels of cell cycle proteins (Cyclin D1, Cyclin A2, CDK1, CDK2, CDK7) and apoptosis markers (c‐Caspase3, c‐Caspase8). (J, K) The impact of Z‐VAD‐FMK (Z‐VAD) co‐treatment on HIF‐induced cell death in HCT15 and HCT116 cells. ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.

    Journal: Advanced Science

    Article Title: Homoisoflavanone Delays Colorectal Cancer Progression via DNA Damage‐Induced Mitochondrial Apoptosis and Parthanatos‐Like Cell Death

    doi: 10.1002/advs.202511406

    Figure Lengend Snippet: HIF inhibits CRC cells growth. (A, B) Cell viability of HCT15 and HCT116 cells treated with trans‐coumaroyltyramine (trans‐Coum), N‐feruloyloctopamine (Feru), N‐trans‐feruloyltyramine (trans‐Feru), disporopsin (Disp), or HIF for 24 h. (C) IC50 values of HIF in HCT15 and HCT116 cells. (D) Cell migration analysis of HCT15 and HCT116 cells following HIF treatment. (E) Colony formation assessment of HCT15 and HCT116 cells after HIF treatment for 24 h. (F) Apoptosis analysis of HCT15 and HCT116 cells after 24 h of HIF treatment. (G, H) Cell cycle distribution analysis of HCT15 and HCT116 cells following HIF treatment for 24 h. (I) Expression levels of cell cycle proteins (Cyclin D1, Cyclin A2, CDK1, CDK2, CDK7) and apoptosis markers (c‐Caspase3, c‐Caspase8). (J, K) The impact of Z‐VAD‐FMK (Z‐VAD) co‐treatment on HIF‐induced cell death in HCT15 and HCT116 cells. ** p < 0.01, *** p < 0.001, **** p < 0.0001; ns, not significant.

    Article Snippet: The membranes were then blocked with a 5% non‐fat milk TBST (TBS containing 0.1% Tween‐20) for 1 h at room temperature and incubated at 4°C for overnight with primary antibodies against the following proteins: cleaved Caspase 3 (25128‐1‐AP, Proteintech), cleaved Caspase 8 (9496, CST), PARP (9542, CST), cleaved PARP (9541, CST), P21 (2947, CST), P53 (2527, CST), Cyclin A2 (91500, CST), Cyclin D1 (2978, CST), CDK1 (bs‐1341R, Bioss), CDK2 (bs‐10726R, Bioss), CDK7 (bs‐0569R, Bioss), AKT (4691, CST), p‐AKT (4060, CST), ERK (9102, CST), p‐ERK (9101, CST), MEK (9126, CST), p‐MEK (9154, CST), ATR (13934, CST), p‐ATR (2853, CST), Chk1 (2360, CST), p‐Chk1 (2348, CST), RAD51 (14961‐1‐AP, Proteintech), ATM (27156‐1‐AP, Proteintech), p‐ATM (5883, CST), γ‐H2AX (9718, CST), AIF (5318, CST), MIF (75038, CST), Cyt c (10993‐1‐AP, Proteintech), Lamin B (66095‐1‐Ig, Proteintech), VDAC1 (81538‐1‐RR, Proteintech) and GAPDH (60004‐1‐Ig, Proteintech).

    Techniques: Migration, Expressing