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A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, <t>Cyclin</t> <t>E1,</t> CDK2, p-CDK2); combination treatment increased p27 and decreased <t>Cyclin</t> <t>E1,</t> CDK2, and p-CDK2 (representative of three independent experiments).
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A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, <t>Cyclin</t> <t>E1,</t> CDK2, p-CDK2); combination treatment increased p27 and decreased <t>Cyclin</t> <t>E1,</t> CDK2, and p-CDK2 (representative of three independent experiments).
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To uncover the molecular regulatory network underlying the functions of ZMIZ2 and AR, RNA-seq analysis was meticulously performed to identify the common downstream target genes of these two factors. (a) RNA-seq analysis of differentially expressed genes after ZMIZ2 silencing or AR silencing. (b) Venn diagram analysis of genes commonly upregulated by ZMIZ2 and AR. (c) KEGG analysis of genes commonly upregulated by ZMIZ2 and AR. (d) GO analysis of genes commonly upregulated by ZMIZ2 and AR. (e) Heatmap of the expression levels of cell cycle-related genes after ZMIZ2 silencing or AR silencing. (f–g) A flow cytometry assay was employed to determine the cell cycle distribution. (h) QPCR was utilized to assess the mRNA transcriptional levels of cell cycle-related genes. (i) Western blot analysis was carried out to detect the protein expression levels of CDK1, CCNA2, and <t>CCNE2</t> in each sample group. Significant differences are indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001; ns indicates not significant; n = 3.
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To uncover the molecular regulatory network underlying the functions of ZMIZ2 and AR, RNA-seq analysis was meticulously performed to identify the common downstream target genes of these two factors. (a) RNA-seq analysis of differentially expressed genes after ZMIZ2 silencing or AR silencing. (b) Venn diagram analysis of genes commonly upregulated by ZMIZ2 and AR. (c) KEGG analysis of genes commonly upregulated by ZMIZ2 and AR. (d) GO analysis of genes commonly upregulated by ZMIZ2 and AR. (e) Heatmap of the expression levels of cell cycle-related genes after ZMIZ2 silencing or AR silencing. (f–g) A flow cytometry assay was employed to determine the cell cycle distribution. (h) QPCR was utilized to assess the mRNA transcriptional levels of cell cycle-related genes. (i) Western blot analysis was carried out to detect the protein expression levels of CDK1, CCNA2, and <t>CCNE2</t> in each sample group. Significant differences are indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001; ns indicates not significant; n = 3.
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A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, Cyclin E1, CDK2, p-CDK2); combination treatment increased p27 and decreased Cyclin E1, CDK2, and p-CDK2 (representative of three independent experiments).

Journal: Cell Death & Disease

Article Title: Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma

doi: 10.1038/s41419-026-08593-5

Figure Lengend Snippet: A - C EdU flow plots for Karpas-422, RL, and Sc-1 cells after 24-h treatment (Linperlisib 32 μM; Chiglitazar 16 μM). D – F Quantification of EdU-positive cells showing reduced DNA synthesis with the combination ( n = 3). G – L ( G , H ) for Karpas-422; ( I , J ) for RL; ( K , L ) for Sc-1. Cell-cycle distribution by PI staining, demonstrating G0/G1 accumulation with Linperlisib and further enhancement by the combination (Linperlisib 16 μM; Chiglitazar 8 μM; n = 3). M GSEA indicating negative enrichment of the G1/S transition pathway (NES = − 2.85865, p < 0.00001). N – P Western blots of G1/S checkpoint proteins (p27, Cyclin E1, CDK2, p-CDK2); combination treatment increased p27 and decreased Cyclin E1, CDK2, and p-CDK2 (representative of three independent experiments).

Article Snippet: The primary antibodies used were as follows: PI3K p110δ (A19742; ABclonal), pan-Akt (#4691; CST), phospho-Akt (Ser473, #4060; CST), PPARα (ab227074; Abcam), FoxO1 (#2880; CST), phospho-FoxO1 (Thr24, #9464; CST) and (Ser256, #9461; CST), FoxO3a (#12829; CST), FoxO4 (#9472; CST), Mcl-1 (#16225-1-AP; Proteintech), Bcl-2 (#12789-1-AP; Proteintech), Bim (A19702; ABclonal), Bax (#50599-2-Ig; Proteintech), Cleaved PARP(#5625; CST), P21(#2947; CST), p27 (#3686; CST), Cyclin E1 (#11935-1-AP; Proteintech), CDK2 (#10122-1-AP; Proteintech), phospho-CDK2 (#4539; CST), GLUT1(#73015; CST), PGK1(A12686; ABclonal), β-Tubulin (#10094-1-AP; Proteintech), Lamin B1 (#13435; CST), and β-Actin (#66009-1-Ig; Proteintech).

Techniques: DNA Synthesis, Staining, Western Blot

To uncover the molecular regulatory network underlying the functions of ZMIZ2 and AR, RNA-seq analysis was meticulously performed to identify the common downstream target genes of these two factors. (a) RNA-seq analysis of differentially expressed genes after ZMIZ2 silencing or AR silencing. (b) Venn diagram analysis of genes commonly upregulated by ZMIZ2 and AR. (c) KEGG analysis of genes commonly upregulated by ZMIZ2 and AR. (d) GO analysis of genes commonly upregulated by ZMIZ2 and AR. (e) Heatmap of the expression levels of cell cycle-related genes after ZMIZ2 silencing or AR silencing. (f–g) A flow cytometry assay was employed to determine the cell cycle distribution. (h) QPCR was utilized to assess the mRNA transcriptional levels of cell cycle-related genes. (i) Western blot analysis was carried out to detect the protein expression levels of CDK1, CCNA2, and CCNE2 in each sample group. Significant differences are indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001; ns indicates not significant; n = 3.

Journal: Cancer Biology & Therapy

Article Title: Interaction between ZMIZ2 and AR promotes prostate cancer proliferation in vitro and in vivo

doi: 10.1080/15384047.2025.2604936

Figure Lengend Snippet: To uncover the molecular regulatory network underlying the functions of ZMIZ2 and AR, RNA-seq analysis was meticulously performed to identify the common downstream target genes of these two factors. (a) RNA-seq analysis of differentially expressed genes after ZMIZ2 silencing or AR silencing. (b) Venn diagram analysis of genes commonly upregulated by ZMIZ2 and AR. (c) KEGG analysis of genes commonly upregulated by ZMIZ2 and AR. (d) GO analysis of genes commonly upregulated by ZMIZ2 and AR. (e) Heatmap of the expression levels of cell cycle-related genes after ZMIZ2 silencing or AR silencing. (f–g) A flow cytometry assay was employed to determine the cell cycle distribution. (h) QPCR was utilized to assess the mRNA transcriptional levels of cell cycle-related genes. (i) Western blot analysis was carried out to detect the protein expression levels of CDK1, CCNA2, and CCNE2 in each sample group. Significant differences are indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001; ns indicates not significant; n = 3.

Article Snippet: The ZMIZ2 antibody (Novus Biologicals, LLC, Centennial, CO, USA), AR antibody (Santa Cruz Biotechnology, Dallas, TX, USA), CDK1 antibody (Santa Cruz Biotechnology, Dallas, TX, USA), CCNA2 antibody (Santa Cruz Biotechnology, Dallas, TX, USA), CCNE2 antibody (Santa Cruz Biotechnology, Dallas, TX, USA) were added and incubated overnight at 4 °C and then incubated with HRP-conjugated goat anti-rabbit IgG (Thermo Fisher Scientific, Waltham, MA, USA) at 37 °C for 30 min.

Techniques: RNA Sequencing, Expressing, Flow Cytometry, Western Blot

Depletion of ZMIZ2 expression is associated with reduced AR enrichment on the promoters of downstream target genes, accompanied by a concurrent decrease in H3K27ac levels. (a) Flow chart of the ChIP experiment. (b) The binding sites of AR on the promoters of CDK1, CCNA2, and CCNE2. (c–h) ChIP analysis of AR enrichment on the CDK1, CCNA2, and CCNE2 promoters and H3K27ac levels. Significant differences are indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001; ns indicates not significant; n = 3.

Journal: Cancer Biology & Therapy

Article Title: Interaction between ZMIZ2 and AR promotes prostate cancer proliferation in vitro and in vivo

doi: 10.1080/15384047.2025.2604936

Figure Lengend Snippet: Depletion of ZMIZ2 expression is associated with reduced AR enrichment on the promoters of downstream target genes, accompanied by a concurrent decrease in H3K27ac levels. (a) Flow chart of the ChIP experiment. (b) The binding sites of AR on the promoters of CDK1, CCNA2, and CCNE2. (c–h) ChIP analysis of AR enrichment on the CDK1, CCNA2, and CCNE2 promoters and H3K27ac levels. Significant differences are indicated as follows: * p < 0.05, ** p < 0.01, and *** p < 0.001; ns indicates not significant; n = 3.

Article Snippet: The ZMIZ2 antibody (Novus Biologicals, LLC, Centennial, CO, USA), AR antibody (Santa Cruz Biotechnology, Dallas, TX, USA), CDK1 antibody (Santa Cruz Biotechnology, Dallas, TX, USA), CCNA2 antibody (Santa Cruz Biotechnology, Dallas, TX, USA), CCNE2 antibody (Santa Cruz Biotechnology, Dallas, TX, USA) were added and incubated overnight at 4 °C and then incubated with HRP-conjugated goat anti-rabbit IgG (Thermo Fisher Scientific, Waltham, MA, USA) at 37 °C for 30 min.

Techniques: Expressing, Binding Assay