Review

cyclin e1 (Proteintech)

Proteintech is a verified supplier

About

News

Press Release

Team

Advisors

Partners

Contact

Bioz Stars

Bioz vStars

Buy from Supplier

Structured Review

Proteintech cyclin e1

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).

Cyclin E1, supplied by Proteintech, used in various techniques. Bioz Stars score: 93/100, based on 55 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/cyclin+e1/Cyclin+E2+Antibody/pmc13040022-65-58-61
Average 93 stars, based on 55 article reviews

cyclin e1 - by Bioz Stars, 2026-10

93/100 stars

Images

1) Product Images from "Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma"

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

Journal: Cell Death & Disease

doi: 10.1038/s41419-026-08593-5

Figure Legend 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).

Techniques Used: DNA Synthesis, Staining, Western Blot

DNA Synthesis:

Article Title: Eugenol as a Novel Neuroblastoma Therapeutic Identified by an Online Prognostic Assessment Platform
Article Snippet: The c-Myc (#10828-1-AP, Dilution ratio 1:1000), GAPDH (#10494-1-AP, Dilution ratio 1:1000), cyclin-dependent kinase 2 (CDK2) (#10122-1-AP, Dilution ratio 1:2000), cyclin E1 (CCNE1; #11554-1-AP, Dilution ratio 1:500), and Tubulin (#14555-1-AP, Dilution ra- tio 1:1000) antibodies were purchased from Protein tech (Wuhan, China).

Article Title: ATP-binding cassette subfamily A member 5 suppresses pancreatic ductal adenocarcinoma progression and chemoresistance by promoting β-catenin ubiquitin-dependent degradation.
Article Snippet: Aims: Pancreatic ductal adenocarcinoma (PDAC) is one of the most aggressive and lethal malignancies characterized by poor prognosis and resistance to therapy.. Despite the most widely recognized role of ATP binding cassette (ABC) family transporters in multidrug resistance, emerging evidence suggests that ATP-binding cassette transporter A5 (ABCA5) acts as a tumor suppressor.. Nevertheless, the role and molecular mechanism of ABCA5 in PDAC have not yet been fully investigated.

Staining:

Western Blot:

Expressing:

EdU Assay:

Knockdown:

Immunofluorescence:

Image Search Results

CDK2 inhibition does not target RB in most of the HR + /HER2 − breast cancers. A and B, Western blot analysis with the indicated antibodies of lysates from the patient-derived HR + MBC cell lines MGH10035.1, MGH358.1, and MGH406.4, and the CCNE1 -amplified TNBC MDA-MB-157 and ovarian cancer OVCAR3 cell lines treated with different concentrations of CDK4/6 (palbociclib), CDK2/4/6 (PF-06873600), or CDK2 (PF-07104091) inhibitors. C, In vitro kinase assay using recombinant cyclin A2/CDK1, cyclin A2/CDK2, and cyclin D3/CDK2 after incubation with increased concentrations of PF-07104091 CDK2i. Data were normalized to incubation with DMSO, and error bars indicate standard deviations ( n = 3). IC 50 values were 1.370 nmol/L for cyclin A2/CDK1, 0.0821 nmol/L for cyclin A2/CDK2, and 3.062 nmol/L for cyclin D3/CDK2. IC 50 (nmol/L) was calculated using nonlinear regression of the dose–response inhibition. D and E, Cell viability of MGH10035.1 ( C ) and MCF7 ( D ) cells expressing shSCR or shRB1 and treated with CDK4/6is, CDK2/4/6is, or CDK2is for 7 days. Data were normalized to DMSO-treated cells. Error bars indicate standard deviations ( n = 3). F, Heatmaps presenting the CDK4/6i, CDK2/4/6i, or CDK2i log IC 50 (nmol/L) in MGH10035.1, MCF7, CAMA1, MDA-MB-361, and MDA-MB-415 HR + breast cancer cell lines. IC 50 was calculated using nonlinear regression of the dose–response inhibition.

Journal: Cancer research

Article Title: CDK2 Inhibition Exerts RB-Independent Antitumor Activity in CDK4/6 Inhibitor–Resistant HR + /HER2 − Breast Cancer

doi: 10.1158/0008-5472.CAN-25-1859

Figure Lengend Snippet: CDK2 inhibition does not target RB in most of the HR + /HER2 − breast cancers. A and B, Western blot analysis with the indicated antibodies of lysates from the patient-derived HR + MBC cell lines MGH10035.1, MGH358.1, and MGH406.4, and the CCNE1 -amplified TNBC MDA-MB-157 and ovarian cancer OVCAR3 cell lines treated with different concentrations of CDK4/6 (palbociclib), CDK2/4/6 (PF-06873600), or CDK2 (PF-07104091) inhibitors. C, In vitro kinase assay using recombinant cyclin A2/CDK1, cyclin A2/CDK2, and cyclin D3/CDK2 after incubation with increased concentrations of PF-07104091 CDK2i. Data were normalized to incubation with DMSO, and error bars indicate standard deviations ( n = 3). IC 50 values were 1.370 nmol/L for cyclin A2/CDK1, 0.0821 nmol/L for cyclin A2/CDK2, and 3.062 nmol/L for cyclin D3/CDK2. IC 50 (nmol/L) was calculated using nonlinear regression of the dose–response inhibition. D and E, Cell viability of MGH10035.1 ( C ) and MCF7 ( D ) cells expressing shSCR or shRB1 and treated with CDK4/6is, CDK2/4/6is, or CDK2is for 7 days. Data were normalized to DMSO-treated cells. Error bars indicate standard deviations ( n = 3). F, Heatmaps presenting the CDK4/6i, CDK2/4/6i, or CDK2i log IC 50 (nmol/L) in MGH10035.1, MCF7, CAMA1, MDA-MB-361, and MDA-MB-415 HR + breast cancer cell lines. IC 50 was calculated using nonlinear regression of the dose–response inhibition.

Article Snippet: CDK2 (cat. #sc-163, RRID: AB_631215), cyclin D1 (cat. #sc-753, RRID: AB_2070433), and cyclin E1 (cat. #sc-247, RRID: AB_627357) antibodies were purchased from Santa Cruz Biotechnology, and the tubulin (cat. #T9026, RRID: AB_477593) antibody was purchased from Sigma-Aldrich.

Techniques: Inhibition, Western Blot, Analysis, Derivative Assay, Amplification, In Vitro, Kinase Assay, Recombinant, Incubation, Expressing

A Representative western blot of HCC-1806 cells for cyclin E, CDK2, and pCDK1 (Y15) following CCNE1 or CDK2 knockdown. B Representative cell cycle profiling of HCC-1806 cells following CCNE1 knockdown and 48 hr treatment with indicated concentrations of TAK-931. C Quantification of cell cycle state from HCC-1806 cells following CCNE1 knockdown and 48 hr treatment with indicated concentrations of TAK-931 (n = 3; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect with significance determined for ≥ 4 N DNA; error bars represent SD). D HCC-1806 cells following CCNE1 knockdown and treatment with 125 nM (left) or 250 nM (right) TAK-931 for five days and monitored with Cellcyte or Incucyte live cell proliferative software ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). E IC 50 curves derived from live cell proliferative analyses as described in ( D ) ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). F Representative images captured at the end of five-day live cell proliferative analyses from HCC-1806 cells following CCNE1 knockdown and treatment with 125 nM TAK-931. G Representative colony outgrowth assay from HCC-1806 cells with CCNE1 CRISPR knockout or non-targeting control and treatment with indicated concentrations of TAK-931 for three cycles, with treatment replenishment every five days (left) and western blot of HCC-1806 CRISPR CCNE1 isogenic pair for cyclin E, CDK2, and pCDK1 (Y15) (right).

Journal: Oncogenesis

Article Title: Cyclin E modulates vulnerability to CDC7 kinase inhibition

doi: 10.1038/s41389-026-00613-5

Figure Lengend Snippet: A Representative western blot of HCC-1806 cells for cyclin E, CDK2, and pCDK1 (Y15) following CCNE1 or CDK2 knockdown. B Representative cell cycle profiling of HCC-1806 cells following CCNE1 knockdown and 48 hr treatment with indicated concentrations of TAK-931. C Quantification of cell cycle state from HCC-1806 cells following CCNE1 knockdown and 48 hr treatment with indicated concentrations of TAK-931 (n = 3; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect with significance determined for ≥ 4 N DNA; error bars represent SD). D HCC-1806 cells following CCNE1 knockdown and treatment with 125 nM (left) or 250 nM (right) TAK-931 for five days and monitored with Cellcyte or Incucyte live cell proliferative software ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). E IC 50 curves derived from live cell proliferative analyses as described in ( D ) ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). F Representative images captured at the end of five-day live cell proliferative analyses from HCC-1806 cells following CCNE1 knockdown and treatment with 125 nM TAK-931. G Representative colony outgrowth assay from HCC-1806 cells with CCNE1 CRISPR knockout or non-targeting control and treatment with indicated concentrations of TAK-931 for three cycles, with treatment replenishment every five days (left) and western blot of HCC-1806 CRISPR CCNE1 isogenic pair for cyclin E, CDK2, and pCDK1 (Y15) (right).

Article Snippet: Antibodies were obtained from the following vendors: Ph.RB (S807/811) (Cell Signaling Technology Cat# 8516, RRID:AB_11178658), CDK2 (Cell Signaling Technology Cat# 2546, RRID:AB_2276129), Ph.CDK1 (Y15) (Cell Signaling Technology Cat# 9111, RRID:AB_331460), CDK1 (Cell Signaling Technology Cat# 77055, RRID:AB_2716331), Cyclin B1 (Cell Signaling Technology Cat# 12231, RRID:AB_2783553), Cleaved PARP (Cell Signaling Technology Cat# 9542, RRID:AB_2160739), Ph.STAT1 (S727) (Cell Signaling Technology Cat# 8826, RRID:AB_2773718), STAT1 (Cell Signaling Technology Cat# 9172, RRID:AB_2198300), Ph.CHK1 (S317) (Cell Signaling Technology Cat# 2344, RRID:AB_331488), Ph.CHK1 (S345) (Cell Signaling Technology Cat# 2348, RRID:AB_331212), CHK1 (Cell Signaling Technology Cat# 2360, RRID:AB_2080320), CDK1 (Santa Cruz Biotechnology Cat# sc-54, RRID:AB_627224) (1:500), MCM-7 (Santa Cruz Biotechnology Cat# sc-9966, RRID:AB_627235) (1:500), Ph.MCM2 (S40/41) (Abcam Cat# ab70371, RRID:AB_2141957), Cyclin E (Bethyl Cat# A301-566A, RRID:AB_1039994), MCM-4 (Thermo Fisher Scientific Cat# MA5-52516, RRID:AB_3248993), β-actin (R and D Systems Cat# MAB8929, RRID:AB_3076436).

Techniques: Western Blot, Knockdown, Software, Derivative Assay, CRISPR, Knock-Out, Control

A Representative western blot of T-47D (left) and MDA-MB-231 (right) cells for cyclin E, CDK2, and pCDK1 (Y15) following CCNE1 induction. B Representative cell cycle profiling of T-47D cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931. C Quantification of cell cycle state from T-47D cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931 ( n = 3; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect with significance determined for ≥ 4 N DNA; error bars represent SD). D Representative cell cycle profiling of MDA-MB-231 cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931. E Quantification of cell cycle state from MDA-MB-231 cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931 ( n = 3; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect with significance determined for ≥ 4 N DNA; error bars represent SD). F T-47D cells following CCNE1 induction and treatment with 15.625 nM (left) or 31.25 nM (right) TAK-931 for five days and monitored with Cellcyte or Incucyte live cell proliferative software ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). G IC 50 curves derived from live cell proliferative analyses as described in ( F ) ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). H , MDA-MB-231 cells following CCNE1 induction and treatment with 62.5 nM (left) or 125 nM (right) TAK-931 for five days and monitored with Cellcyte or Incucyte live cell proliferative software ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). I IC 50 curves derived from live cell proliferative analyses as described in ( H ) ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). J Representative colony outgrowth assays from T-47D (left) and MDA-MB-231 (right) cells following CCNE1 induction and treatment with indicated concentrations of TAK-931 for three cycles, with doxycycline and treatment replenishment every five days. K Representative BrdU incorporation analysis of T-47D cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931.

Journal: Oncogenesis

Article Title: Cyclin E modulates vulnerability to CDC7 kinase inhibition

doi: 10.1038/s41389-026-00613-5

Figure Lengend Snippet: A Representative western blot of T-47D (left) and MDA-MB-231 (right) cells for cyclin E, CDK2, and pCDK1 (Y15) following CCNE1 induction. B Representative cell cycle profiling of T-47D cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931. C Quantification of cell cycle state from T-47D cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931 ( n = 3; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect with significance determined for ≥ 4 N DNA; error bars represent SD). D Representative cell cycle profiling of MDA-MB-231 cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931. E Quantification of cell cycle state from MDA-MB-231 cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931 ( n = 3; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect with significance determined for ≥ 4 N DNA; error bars represent SD). F T-47D cells following CCNE1 induction and treatment with 15.625 nM (left) or 31.25 nM (right) TAK-931 for five days and monitored with Cellcyte or Incucyte live cell proliferative software ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). G IC 50 curves derived from live cell proliferative analyses as described in ( F ) ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). H , MDA-MB-231 cells following CCNE1 induction and treatment with 62.5 nM (left) or 125 nM (right) TAK-931 for five days and monitored with Cellcyte or Incucyte live cell proliferative software ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). I IC 50 curves derived from live cell proliferative analyses as described in ( H ) ( n = 4; two-way ANOVA with Tukey’s multiple comparisons test accounting for gene and drug effect using endpoint normalized GFP counts; error bars represent SEM). J Representative colony outgrowth assays from T-47D (left) and MDA-MB-231 (right) cells following CCNE1 induction and treatment with indicated concentrations of TAK-931 for three cycles, with doxycycline and treatment replenishment every five days. K Representative BrdU incorporation analysis of T-47D cells following CCNE1 induction and 48 hr treatment with indicated concentrations of TAK-931.

Techniques: Western Blot, Software, Derivative Assay, BrdU Incorporation Assay

A Representative western blot of HCC-1806 cells for total MCM-4, 7, and cyclin E following CCNE1 knockdown. B Representative flow cytometric MCM-4 chromatin binding assay from HCC-1806 cells following CCNE1 knockdown and 48 hr treatment with 125 nM TAK-931. C Representative flow cytometric MCM-7 chromatin binding assay from HCC-1806 cells following CCNE1 knockdown and 48 hr treatment with 125 nM TAK-931. D Representative flow cytometric MCM-4 chromatin binding assay from T-47D cells following CCNE1 induction and 48 hr treatment with 62.5 nM TAK-931. E Representative flow cytometric MCM-7 chromatin binding assay from T-47D cells following CCNE1 induction and 48 hr treatment with 62.5 nM TAK-931.

Journal: Oncogenesis

Article Title: Cyclin E modulates vulnerability to CDC7 kinase inhibition

doi: 10.1038/s41389-026-00613-5

Figure Lengend Snippet: A Representative western blot of HCC-1806 cells for total MCM-4, 7, and cyclin E following CCNE1 knockdown. B Representative flow cytometric MCM-4 chromatin binding assay from HCC-1806 cells following CCNE1 knockdown and 48 hr treatment with 125 nM TAK-931. C Representative flow cytometric MCM-7 chromatin binding assay from HCC-1806 cells following CCNE1 knockdown and 48 hr treatment with 125 nM TAK-931. D Representative flow cytometric MCM-4 chromatin binding assay from T-47D cells following CCNE1 induction and 48 hr treatment with 62.5 nM TAK-931. E Representative flow cytometric MCM-7 chromatin binding assay from T-47D cells following CCNE1 induction and 48 hr treatment with 62.5 nM TAK-931.

Techniques: Western Blot, Knockdown, Binding Assay

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

Identification and biomarkers (A–C) PPI network: The interaction of 23 candidate genes (A), CCNE1 (B), and UGT1A6 (C). (D–F) The top 15 genes acquired by Radiality (D), Closeness (E), and Degree algorithms (F). (G) Venn diagram of intersecting genes from the above 3 algorithms with the module genes. (H–I) Box plot analysis indicated the hub genes in the training set and validation set.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: Identification and biomarkers (A–C) PPI network: The interaction of 23 candidate genes (A), CCNE1 (B), and UGT1A6 (C). (D–F) The top 15 genes acquired by Radiality (D), Closeness (E), and Degree algorithms (F). (G) Venn diagram of intersecting genes from the above 3 algorithms with the module genes. (H–I) Box plot analysis indicated the hub genes in the training set and validation set.

Article Snippet: Primary antibodies against Cyclin E1 (HUABIO, ET1612–16; 1:2000), EZH2 (HUABIO, HA722095; 1:2000), E2F1 (HUABIO, ET1701–73; 1:2000), CDK1 (Affinity, DF6024; 1:2000), E-cadherin (Abcam, ab314063; 1:1000), vimentin (Abcam, ab8978; 1:2000), MMP2 (Abcam, ab92536; 1:2000), MMP9 (HUABIO, ET1704–69; 1:4000), and GADPH (HUABIO, HA721136; 1:20,000) were used.

Techniques: Biomarker Discovery

Pathways enriched with biomarkers in BRCA (A–D) GSEA revealed the enriched pathway of (A) CDK1, (B) E2F1, (C) EZH2, and (D) CCNE1.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: Pathways enriched with biomarkers in BRCA (A–D) GSEA revealed the enriched pathway of (A) CDK1, (B) E2F1, (C) EZH2, and (D) CCNE1.

Techniques:

The binding ability of MEP to biomarkers Molecular docking models of (A) CDK1, (B) E2F1, (C) EZH2, and (D) CCNE1 with MEP. (E) RMSD analysis of protein backbone atoms during 100 ns MD simulations. (F) RMSF analysis of protein backbone atoms during 100 ns MD simulations. (G) Rg analysis of protein backbone atoms during 100 ns simulations.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: The binding ability of MEP to biomarkers Molecular docking models of (A) CDK1, (B) E2F1, (C) EZH2, and (D) CCNE1 with MEP. (E) RMSD analysis of protein backbone atoms during 100 ns MD simulations. (F) RMSF analysis of protein backbone atoms during 100 ns MD simulations. (G) Rg analysis of protein backbone atoms during 100 ns simulations.

Techniques: Binding Assay

Key cells in the scRNA-seq data (A, B) Relative comparison of spatial clusters between the BRCA and the control samples. (C–F) The violin plot revealed the expression level of (C) CDK1, (D) E2F1, (E) EZH2, and (F) CCNE1 in different cell subsets between the BRCA samples versus. controls. (G) KEGG results for fibroblasts between the BRCA samples versus. controls.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: Key cells in the scRNA-seq data (A, B) Relative comparison of spatial clusters between the BRCA and the control samples. (C–F) The violin plot revealed the expression level of (C) CDK1, (D) E2F1, (E) EZH2, and (F) CCNE1 in different cell subsets between the BRCA samples versus. controls. (G) KEGG results for fibroblasts between the BRCA samples versus. controls.

Techniques: Comparison, Control, Expressing

MEP promote the malignant biological behavior of MCF-7 (A) qRT-PCR data showing CDK1, EZH2, E2F1, and CCNE1 mRNA expression. (B) Western blots showing CDK1, EZH2, E2F1, and CCNE1 expression. (C) Macrographs of colony formation and quantitative analysis. (D) Flow cytometry showing cell cycle distribution and cell percentages in different phases. (E) Wound healing assay with quantitative analysis was performed to assess the migratory capacity. Scale bar 650 μm. (F) Representative cell migration images and migration index. Scale bar 275 μm. (G) Phalloidin staining was employed to evaluate F-actin reorganization. Scale bar 25 μm. (H) Western blots showing E-cadherin, Vimentin, MMP2, and MMP9 expression. Data are presented as the mean ± standard deviation ( n = 3), * P < 0.05, ** P < 0.01, *** P < 0.001 and **** P < 0.0001 when compared with control cells.

Journal: ACS Omega

Article Title: Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments

doi: 10.1021/acsomega.5c11680

Figure Lengend Snippet: MEP promote the malignant biological behavior of MCF-7 (A) qRT-PCR data showing CDK1, EZH2, E2F1, and CCNE1 mRNA expression. (B) Western blots showing CDK1, EZH2, E2F1, and CCNE1 expression. (C) Macrographs of colony formation and quantitative analysis. (D) Flow cytometry showing cell cycle distribution and cell percentages in different phases. (E) Wound healing assay with quantitative analysis was performed to assess the migratory capacity. Scale bar 650 μm. (F) Representative cell migration images and migration index. Scale bar 275 μm. (G) Phalloidin staining was employed to evaluate F-actin reorganization. Scale bar 25 μm. (H) Western blots showing E-cadherin, Vimentin, MMP2, and MMP9 expression. Data are presented as the mean ± standard deviation ( n = 3), * P < 0.05, ** P < 0.01, *** P < 0.001 and **** P < 0.0001 when compared with control cells.

Techniques: Quantitative RT-PCR, Expressing, Western Blot, Flow Cytometry, Wound Healing Assay, Migration, Staining, Standard Deviation, Control

Review

cyclin e1 (Proteintech)

Structured Review

Images

1) Product Images from "Dual targeting of PI3Kδ and PPARα enhances antitumor activity via FoxO1 activation in follicular lymphoma"

Related Articles

DNA Synthesis:

Staining:

Western Blot:

Expressing:

EdU Assay:

Knockdown:

Immunofluorescence:

Similar Products

Image Search Results