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Cell Signaling Technology Inc rabbit anti cyclin a2 ccna2

Post-mitotic iPSC-derived motor neurons from C9orf72 carriers aberrantly enter cell-cycle (A) Representative images of control and C9orf72 motor neuron cultures. Scale bars, 100 μm. (B–C) mRNA levels of Ki67 and GMNN at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (D) Representative western blot images of GMNN and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (E–F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from control (lines: 35L5, 35L11, and 37L20) and C9orf72 (lines: 16L14, 40L3, and 42L11). (G) Percentage of neurons in S-phase from controls and C9orf72 neurons. (H and I) mRNA levels of <t>CCNA2</t> and CCNB2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (J and K) mRNA levels of CDK2 and CDK4 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (L) Representative western blot images of CCNA2 and GAPDH and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (M) Representative western blot images of CDK4 and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. Data are presented as mean ± SEM (B–D, G–M). Data presented in (B–D) is from 3 control and 3 C9orf72 iPSC iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. Data presented in (G) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05. Data presented in (H–K) 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05 and ∗∗ p < 0.01. Data presented in (L and M) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ∗ p < 0.05. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

Rabbit Anti Cyclin A2 Ccna2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 95/100, based on 69 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 95 stars, based on 69 article reviews

rabbit anti cyclin a2 ccna2 - by Bioz Stars, 2026-09

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1) Product Images from "Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD"

Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD

Journal: iScience

doi: 10.1016/j.isci.2025.114596

Figure Legend Snippet: Post-mitotic iPSC-derived motor neurons from C9orf72 carriers aberrantly enter cell-cycle (A) Representative images of control and C9orf72 motor neuron cultures. Scale bars, 100 μm. (B–C) mRNA levels of Ki67 and GMNN at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (D) Representative western blot images of GMNN and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (E–F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from control (lines: 35L5, 35L11, and 37L20) and C9orf72 (lines: 16L14, 40L3, and 42L11). (G) Percentage of neurons in S-phase from controls and C9orf72 neurons. (H and I) mRNA levels of CCNA2 and CCNB2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (J and K) mRNA levels of CDK2 and CDK4 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (L) Representative western blot images of CCNA2 and GAPDH and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (M) Representative western blot images of CDK4 and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. Data are presented as mean ± SEM (B–D, G–M). Data presented in (B–D) is from 3 control and 3 C9orf72 iPSC iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. Data presented in (G) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05. Data presented in (H–K) 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05 and ∗∗ p < 0.01. Data presented in (L and M) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ∗ p < 0.05. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

Techniques Used: Derivative Assay, Control, Western Blot, Flow Cytometry, Staining, Two Tailed Test, Membrane

Poly (GR) induces an increase in cyclins and CDKs levels (A) Schematic representation of the CRISPR/Cas9 strategy to generate C9orf72 homozygous and heterozygous lines from a healthy control line. (B) Generation of C9orf72 heterozygous and homozygous knockout iPSC lines by CRISPR Cas9. (C) Representative western blot image of C9orf72 protein levels in homozygous (line 3) and heterozygous (line 8) knockout lines by CRISPR Cas9. (D–G) mRNA levels of Ki67, GMNN, CDK4, and CCNA2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (H) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GR). Scale bars, 200 μm. (I and J) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (K) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GP). Scale bars, 200 μm. (L and M) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (N) Representative western blot image of control iPSC-derived neurons treated with Poly (GR) and poly (GP). (O and P) Quantification of protein levels of CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR) and poly (GP). Data are presented as mean ± SEM (D–G, I and J, L and M, O and P). Data presented in (D–G) is from 3 independent differentiation experiments of a control iPSC line (parental line) and one C9orf72 heterozygous and one homozygous knockout line. Two-tailed t test with Welch’s correction was applied. ns, not significant. Data in (I and J, L and M) is from 3 control iPSC lines treated with DPRs from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. Data in (O and P) is from 3 control iPSC lines treated with DPRs from 2 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

Figure Legend Snippet: Poly (GR) induces an increase in cyclins and CDKs levels (A) Schematic representation of the CRISPR/Cas9 strategy to generate C9orf72 homozygous and heterozygous lines from a healthy control line. (B) Generation of C9orf72 heterozygous and homozygous knockout iPSC lines by CRISPR Cas9. (C) Representative western blot image of C9orf72 protein levels in homozygous (line 3) and heterozygous (line 8) knockout lines by CRISPR Cas9. (D–G) mRNA levels of Ki67, GMNN, CDK4, and CCNA2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (H) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GR). Scale bars, 200 μm. (I and J) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (K) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GP). Scale bars, 200 μm. (L and M) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (N) Representative western blot image of control iPSC-derived neurons treated with Poly (GR) and poly (GP). (O and P) Quantification of protein levels of CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR) and poly (GP). Data are presented as mean ± SEM (D–G, I and J, L and M, O and P). Data presented in (D–G) is from 3 independent differentiation experiments of a control iPSC line (parental line) and one C9orf72 heterozygous and one homozygous knockout line. Two-tailed t test with Welch’s correction was applied. ns, not significant. Data in (I and J, L and M) is from 3 control iPSC lines treated with DPRs from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. Data in (O and P) is from 3 control iPSC lines treated with DPRs from 2 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

Techniques Used: CRISPR, Control, Knock-Out, Western Blot, Derivative Assay, Immunostaining, Two Tailed Test, Membrane

CDK4/6 inhibitor Palbociclib (PD33002291) prevents cell-cycle reentry in iPSC-derived motor neuron from C9orf72 carriers (A and B) Western blot and quantification of protein levels of phosphorylated RB and topoisomerase II α (TopoII) in 2-month-old iPSC-derived motor neurons from C9orf72 carriers treated with Palbociclib 1 and 5 μM. (C–E) mRNA levels of Ki67 and CCNA2 and CDK1 in 2-month-old C9orf72 iPSC-derived motor neurons treated with Palbociclib 5 μM. (F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from controls, C9orf72 and C9orf72 neurons treated with Palbociclib 5 μM. (G) Quantification of the percentage of C9orf72 iPSC-derived motor neurons in S-phase. Data are presented as mean ± SEM (A–E, G). Data presented in (A and B) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 treated with Palbociclib 1 and 5 μM from 2 differentiation experiments, one-way ANOVA with Newman-Keuls post hoc test was applied ∗ p < 0.05.∗∗ p < 0.01 and ∗∗∗ p < 0.001. Data presented in (C–E) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 neurons with Palbociclib 5 μM from 2 differentiation experiments. Two-tailed t test with Welch’s correction was applied ∗ p < 0.05 and ∗∗ p < 0.01. Data in (G) is from iPSC-derived neurons from 3 controls, 3 C9orf72 , and 3 C9orf72 treated with Palbociclib from 1 differentiation experiment, one-way ANOVA with Newman-Keuls post hoc test was applied ∗∗ p < 0.01. See also .

Figure Legend Snippet: CDK4/6 inhibitor Palbociclib (PD33002291) prevents cell-cycle reentry in iPSC-derived motor neuron from C9orf72 carriers (A and B) Western blot and quantification of protein levels of phosphorylated RB and topoisomerase II α (TopoII) in 2-month-old iPSC-derived motor neurons from C9orf72 carriers treated with Palbociclib 1 and 5 μM. (C–E) mRNA levels of Ki67 and CCNA2 and CDK1 in 2-month-old C9orf72 iPSC-derived motor neurons treated with Palbociclib 5 μM. (F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from controls, C9orf72 and C9orf72 neurons treated with Palbociclib 5 μM. (G) Quantification of the percentage of C9orf72 iPSC-derived motor neurons in S-phase. Data are presented as mean ± SEM (A–E, G). Data presented in (A and B) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 treated with Palbociclib 1 and 5 μM from 2 differentiation experiments, one-way ANOVA with Newman-Keuls post hoc test was applied ∗ p < 0.05.∗∗ p < 0.01 and ∗∗∗ p < 0.001. Data presented in (C–E) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 neurons with Palbociclib 5 μM from 2 differentiation experiments. Two-tailed t test with Welch’s correction was applied ∗ p < 0.05 and ∗∗ p < 0.01. Data in (G) is from iPSC-derived neurons from 3 controls, 3 C9orf72 , and 3 C9orf72 treated with Palbociclib from 1 differentiation experiment, one-way ANOVA with Newman-Keuls post hoc test was applied ∗∗ p < 0.01. See also .

Techniques Used: Derivative Assay, Western Blot, Flow Cytometry, Staining, Two Tailed Test

Derivative Assay:

Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD
Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

Control:

Western Blot:

Flow Cytometry:

Staining:

Two Tailed Test:

Membrane:

CRISPR:

Knock-Out:

Immunostaining:

Image Search Results

Journal: iScience

Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD

doi: 10.1016/j.isci.2025.114596

Figure Lengend Snippet: Post-mitotic iPSC-derived motor neurons from C9orf72 carriers aberrantly enter cell-cycle (A) Representative images of control and C9orf72 motor neuron cultures. Scale bars, 100 μm. (B–C) mRNA levels of Ki67 and GMNN at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (D) Representative western blot images of GMNN and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (E–F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from control (lines: 35L5, 35L11, and 37L20) and C9orf72 (lines: 16L14, 40L3, and 42L11). (G) Percentage of neurons in S-phase from controls and C9orf72 neurons. (H and I) mRNA levels of CCNA2 and CCNB2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (J and K) mRNA levels of CDK2 and CDK4 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (L) Representative western blot images of CCNA2 and GAPDH and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. (M) Representative western blot images of CDK4 and actin and quantification of protein levels from 2-month-old control and C9orf72 iPSC-derived motor neurons. Data are presented as mean ± SEM (B–D, G–M). Data presented in (B–D) is from 3 control and 3 C9orf72 iPSC iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05, ∗∗ p < 0.01, and ∗∗∗ p < 0.001. Data presented in (G) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05. Data presented in (H–K) 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗ p < 0.05 and ∗∗ p < 0.01. Data presented in (L and M) is from 3 control and 3 C9orf72 iPSC-derived neuron cultures from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ∗ p < 0.05. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

Techniques: Derivative Assay, Control, Western Blot, Flow Cytometry, Staining, Two Tailed Test, Membrane

Journal: iScience

Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD

doi: 10.1016/j.isci.2025.114596

Figure Lengend Snippet: Poly (GR) induces an increase in cyclins and CDKs levels (A) Schematic representation of the CRISPR/Cas9 strategy to generate C9orf72 homozygous and heterozygous lines from a healthy control line. (B) Generation of C9orf72 heterozygous and homozygous knockout iPSC lines by CRISPR Cas9. (C) Representative western blot image of C9orf72 protein levels in homozygous (line 3) and heterozygous (line 8) knockout lines by CRISPR Cas9. (D–G) mRNA levels of Ki67, GMNN, CDK4, and CCNA2 at 1-, 1.5-, and 2-month-old control and C9orf72 iPSC-derived motor neurons. (H) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GR). Scale bars, 200 μm. (I and J) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (K) Representative immunostaining images of iPSC-derived motor neurons cultures treated with 1 and 2 μM of poly (GP). Scale bars, 200 μm. (L and M) Quantification of protein levels of CCND1 and CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR). (N) Representative western blot image of control iPSC-derived neurons treated with Poly (GR) and poly (GP). (O and P) Quantification of protein levels of CDK4 in 2-month-old control iPSC-derived motor neurons treated with 1 and 2 μM of poly (GR) and poly (GP). Data are presented as mean ± SEM (D–G, I and J, L and M, O and P). Data presented in (D–G) is from 3 independent differentiation experiments of a control iPSC line (parental line) and one C9orf72 heterozygous and one homozygous knockout line. Two-tailed t test with Welch’s correction was applied. ns, not significant. Data in (I and J, L and M) is from 3 control iPSC lines treated with DPRs from 3 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. Data in (O and P) is from 3 control iPSC lines treated with DPRs from 2 independent differentiation experiments. Two-tailed t test with Welch’s correction was applied. ns, not significant, ∗∗ p < 0.01. In cases where the loading control was located above the target protein on the original membrane, the band was repositioned below for consistency and clarity.

Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

Techniques: CRISPR, Control, Knock-Out, Western Blot, Derivative Assay, Immunostaining, Two Tailed Test, Membrane

Journal: iScience

Article Title: Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD

doi: 10.1016/j.isci.2025.114596

Figure Lengend Snippet: CDK4/6 inhibitor Palbociclib (PD33002291) prevents cell-cycle reentry in iPSC-derived motor neuron from C9orf72 carriers (A and B) Western blot and quantification of protein levels of phosphorylated RB and topoisomerase II α (TopoII) in 2-month-old iPSC-derived motor neurons from C9orf72 carriers treated with Palbociclib 1 and 5 μM. (C–E) mRNA levels of Ki67 and CCNA2 and CDK1 in 2-month-old C9orf72 iPSC-derived motor neurons treated with Palbociclib 5 μM. (F) Flow cytometry of propidium iodide-stained 2-month-old iPSC-derived motor neurons from controls, C9orf72 and C9orf72 neurons treated with Palbociclib 5 μM. (G) Quantification of the percentage of C9orf72 iPSC-derived motor neurons in S-phase. Data are presented as mean ± SEM (A–E, G). Data presented in (A and B) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 treated with Palbociclib 1 and 5 μM from 2 differentiation experiments, one-way ANOVA with Newman-Keuls post hoc test was applied ∗ p < 0.05.∗∗ p < 0.01 and ∗∗∗ p < 0.001. Data presented in (C–E) is from iPSC-derived neurons from 3 C9orf72 and 3 C9orf72 neurons with Palbociclib 5 μM from 2 differentiation experiments. Two-tailed t test with Welch’s correction was applied ∗ p < 0.05 and ∗∗ p < 0.01. Data in (G) is from iPSC-derived neurons from 3 controls, 3 C9orf72 , and 3 C9orf72 treated with Palbociclib from 1 differentiation experiment, one-way ANOVA with Newman-Keuls post hoc test was applied ∗∗ p < 0.01. See also .

Article Snippet: Rabbit anti-Cyclin A2 (CCNA2) , Cell Signaling , Cat# 67955; RRID:AB_2909603.

Techniques: Derivative Assay, Western Blot, Flow Cytometry, Staining, Two Tailed Test

Expression of CCNA2 in CRC and its effect on biological behavior of CRC cells . A , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by immunohistochemistry assay. B , the mRNA expressions of CCNA2 were detected in paracancerous and CRC tissues by quantitative PCR (qPCR) assay. C , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by Western blotting. D , the protein expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by Western blotting. E , the mRNA expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by qPCR assay. F , the interference efficiency of knockdown CCNA2 expression in the HCT116 and HT29 stable cell lines was evaluated by Western blotting. G , CCK-8 assay showed that knockdown of CCNA2 expression inhibited the proliferation of HT29 and HCT116 cells. H , wound scratch assay demonstrated that hat knockdown of CCNA2 expression inhibited the migration of HT29 and HCT116 cells. I , Transwell assay revealed that knockdown of CCNA2 expression inhibited the invasion of HT29 and HCT116 cells. J , flow cytometry assay indicated that knockdown of CCNA2 expression induced the apoptosis of HT29 and HCT116 cells. K – L , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in HT29 and HCT116 cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

Journal: The Journal of Biological Chemistry

Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

doi: 10.1016/j.jbc.2025.110216

Figure Lengend Snippet: Expression of CCNA2 in CRC and its effect on biological behavior of CRC cells . A , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by immunohistochemistry assay. B , the mRNA expressions of CCNA2 were detected in paracancerous and CRC tissues by quantitative PCR (qPCR) assay. C , the protein expressions of CCNA2 were detected in paracancerous and CRC tissues by Western blotting. D , the protein expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by Western blotting. E , the mRNA expressions of CCNA2 were detected in normal human colonic epithelial and CRC cell lines by qPCR assay. F , the interference efficiency of knockdown CCNA2 expression in the HCT116 and HT29 stable cell lines was evaluated by Western blotting. G , CCK-8 assay showed that knockdown of CCNA2 expression inhibited the proliferation of HT29 and HCT116 cells. H , wound scratch assay demonstrated that hat knockdown of CCNA2 expression inhibited the migration of HT29 and HCT116 cells. I , Transwell assay revealed that knockdown of CCNA2 expression inhibited the invasion of HT29 and HCT116 cells. J , flow cytometry assay indicated that knockdown of CCNA2 expression induced the apoptosis of HT29 and HCT116 cells. K – L , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in HT29 and HCT116 cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

Article Snippet: The slides were treated with primary antibody against CCNA2 (1:500 dilution, #67955; Cell Signaling Technology), primary antibody against ki67 (1:500 dilution, #GB111499-100; ServiceBio) or primary antibody against caspase 3 (1:500 dilution, #GB115600-100; ServiceBio) at 4°C overnight.

Techniques: Expressing, Immunohistochemistry, Real-time Polymerase Chain Reaction, Western Blot, Knockdown, Stable Transfection, CCK-8 Assay, Wound Healing Assay, Migration, Transwell Assay, Flow Cytometry, Cell Counting

The miR-548x-3p– CCNA2 axis regulates the biological behavior of CRC cells . A , correlation analysis of miR-548x-3p and CCNA2 mRNA expression in CRC. B , validation of the targeting relationship between miR-548x-3p and CCNA2 through dual-luciferase reporter assays in CRC cells. C , the effect of miR-548x-3p on the targeted regulation of CCNA2 protein expression in CRC cells was analyzed by Western blotting. D , the effect of miR-548x-3p on the targeted regulation of CCNA2 mRNA expression in CRC cells was analyzed by quantitative PCR (qPCR) assay. E , CCK-8 assays demonstrated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the proliferation in CRC cells. F , wound scratch assay indicated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the migration of CRC cells. G , transwell assay showed that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the invasion of CRC cells. H and I , the effect of CCNA2 on miR-548x-3p regulation of the EMT-signaling pathway–associated biomarkers in CRC cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

Journal: The Journal of Biological Chemistry

Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

doi: 10.1016/j.jbc.2025.110216

Figure Lengend Snippet: The miR-548x-3p– CCNA2 axis regulates the biological behavior of CRC cells . A , correlation analysis of miR-548x-3p and CCNA2 mRNA expression in CRC. B , validation of the targeting relationship between miR-548x-3p and CCNA2 through dual-luciferase reporter assays in CRC cells. C , the effect of miR-548x-3p on the targeted regulation of CCNA2 protein expression in CRC cells was analyzed by Western blotting. D , the effect of miR-548x-3p on the targeted regulation of CCNA2 mRNA expression in CRC cells was analyzed by quantitative PCR (qPCR) assay. E , CCK-8 assays demonstrated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the proliferation in CRC cells. F , wound scratch assay indicated that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the migration of CRC cells. G , transwell assay showed that overexpression of CCNA2 rescued the inhibitory effect of miR-548x-3p on the invasion of CRC cells. H and I , the effect of CCNA2 on miR-548x-3p regulation of the EMT-signaling pathway–associated biomarkers in CRC cells was analyzed by Western blotting. The data in the bar plots were shown as the mean ± SD. ∗ or # represented p < 0.05; ∗∗ or ## represented p < 0.01; and ∗∗∗ or ### represented p < 0.001. CCK-8, Cell Counting Kit-8; CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

Techniques: Expressing, Biomarker Discovery, Luciferase, Western Blot, Real-time Polymerase Chain Reaction, CCK-8 Assay, Over Expression, Wound Healing Assay, Migration, Transwell Assay, Cell Counting

The effect of CCNA2 on biological behavior of CRC cells in vivo . A , the nude mice with subcutaneous tumorigenesis of shNC and sh CCNA2 CRC cells. B , statistical results of subcutaneous tumor xenograft volume in shNC and sh CCNA2 groups of nude mice. C , the appearance of subcutaneous tumor xenografts in shNC and sh CCNA2 groups of nude mice. D , statistical results of subcutaneous tumor xenograft weight in shNC and sh CCNA2 groups of nude mice. E and F , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in subcutaneous tumor xenografts was analyzed by Western blotting. G , the H&E staining results of subcutaneous tumor xenografts. H and I , the effect of CCNA2 on proliferation and apoptosis-associated biomarkers in subcutaneous tumor xenografts was analyzed by immunohistochemistry. The data in the bar plots were shown as the mean ± SD. ∗ represented p < 0.05; ∗∗ represented p < 0.01; and ∗∗∗ represented p < 0.001. CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

Journal: The Journal of Biological Chemistry

Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

doi: 10.1016/j.jbc.2025.110216

Figure Lengend Snippet: The effect of CCNA2 on biological behavior of CRC cells in vivo . A , the nude mice with subcutaneous tumorigenesis of shNC and sh CCNA2 CRC cells. B , statistical results of subcutaneous tumor xenograft volume in shNC and sh CCNA2 groups of nude mice. C , the appearance of subcutaneous tumor xenografts in shNC and sh CCNA2 groups of nude mice. D , statistical results of subcutaneous tumor xenograft weight in shNC and sh CCNA2 groups of nude mice. E and F , the effect of CCNA2 on the EMT-signaling pathway–associated biomarkers in subcutaneous tumor xenografts was analyzed by Western blotting. G , the H&E staining results of subcutaneous tumor xenografts. H and I , the effect of CCNA2 on proliferation and apoptosis-associated biomarkers in subcutaneous tumor xenografts was analyzed by immunohistochemistry. The data in the bar plots were shown as the mean ± SD. ∗ represented p < 0.05; ∗∗ represented p < 0.01; and ∗∗∗ represented p < 0.001. CCNA2 , cyclin A2; CRC, colorectal cancer; EMT, epithelial–mesenchymal transition.

Techniques: In Vivo, Western Blot, Staining, Immunohistochemistry

Journal: The Journal of Biological Chemistry

Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

doi: 10.1016/j.jbc.2025.110216

Article Snippet: The PVDF membranes were blocked with 5% skim milk, and the PVDF membranes were incubated with primary antibodies CCNA2 (1:1000 dilution, #67955; Cell Signaling Technology), E-cadherin (1:1000 dilution, #3195; Cell Signaling Technology), N-cadherin (1:1000 dilution, #13116; Cell Signaling Technology), GAPDH (1:3000 dilution, #AC002; Abclonal), and β-Actin (1:4000 dilution, #90422; SIGMA) at 4°C overnight.

Journal: The Journal of Biological Chemistry

Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

doi: 10.1016/j.jbc.2025.110216

Journal: The Journal of Biological Chemistry

Article Title: Exploring the regulatory mechanism of CCNA2 in colorectal cancer: Insights from multiomics and experimental analysis

doi: 10.1016/j.jbc.2025.110216

Techniques: In Vivo, Western Blot, Staining, Immunohistochemistry

Cell cycle regulator proteins expression in different CTR groups. A–H the expression of CCNA2, CCNB1, CCND1, TP53, P16, P21, TOP2A, and pRb in lung adenocarcinoma with different CTR. CTR, consolidation-to-tumour ratio

Journal: Respiratory Research

Article Title: Analysis of tumor cell proliferation (Ki-67) and cell cycle regulator proteins in lung adenocarcinoma with different radiological subtypes

doi: 10.1186/s12931-025-03217-6

Figure Lengend Snippet: Cell cycle regulator proteins expression in different CTR groups. A–H the expression of CCNA2, CCNB1, CCND1, TP53, P16, P21, TOP2A, and pRb in lung adenocarcinoma with different CTR. CTR, consolidation-to-tumour ratio

Article Snippet: The antibodies used for the IHC analyses were as follows: CCNB1 (Ab32053, 1:250 dilution; Abcam, MA, USA), P16 (Ab108349, 1:1000 dilution; Abcam, MA, USA), P21 (Ab109520, 1:1000 dilution; Abcam, MA, USA), Cyclin D1 (CCND1) (clone# 5506S, 1:1000 dilution; Cell Signaling Technology, MA, USA), Cyclin A2 (CCNA2) (clone# 67955, 1:1600 dilution; Cell Signaling Technology, MA, USA), TOP2A (12286 T, 1:400 dilution; Cell Signaling Technology, MA, USA), pRb (clone# 8516 T, 1:800 dilution; Cell Signaling Technology, MA, USA), and p53 (Santa Cruz, clone DO1 SC-126, 1:800 dilution; USA).

Techniques: Expressing

Differences in the positive expression rate of cell cycle regulatory proteins among different CTR groups. A the TMA constructed using clinical samples (HE staining); B the positive expression rates of GGO-LUAD and SN-LUAD on eight cell cycle regulatory proteins (CCNA2, CCNB1, CCND1, P16, P21, TOP2A, TP53, and pRb). CTR consolidation-to-tumour ratio, TMA tissue microarrays

Journal: Respiratory Research

Article Title: Analysis of tumor cell proliferation (Ki-67) and cell cycle regulator proteins in lung adenocarcinoma with different radiological subtypes

doi: 10.1186/s12931-025-03217-6

Figure Lengend Snippet: Differences in the positive expression rate of cell cycle regulatory proteins among different CTR groups. A the TMA constructed using clinical samples (HE staining); B the positive expression rates of GGO-LUAD and SN-LUAD on eight cell cycle regulatory proteins (CCNA2, CCNB1, CCND1, P16, P21, TOP2A, TP53, and pRb). CTR consolidation-to-tumour ratio, TMA tissue microarrays

Techniques: Expressing, Construct, Staining

Associations between Ki-67 and cell cycle regulator proteins expression. A – D the expression of the following four cell cycle regulator proteins showed a positive correlation with Ki-67 expression, namely CCNA2 , TOP2A, TP53, and pRb, E – H the expression of the remaining four cell cycle regulator proteins (included CCNB1, CCND1, P16 and P21) is not correlated with Ki-67 expression

Journal: Respiratory Research

Article Title: Analysis of tumor cell proliferation (Ki-67) and cell cycle regulator proteins in lung adenocarcinoma with different radiological subtypes

doi: 10.1186/s12931-025-03217-6

Figure Lengend Snippet: Associations between Ki-67 and cell cycle regulator proteins expression. A – D the expression of the following four cell cycle regulator proteins showed a positive correlation with Ki-67 expression, namely CCNA2 , TOP2A, TP53, and pRb, E – H the expression of the remaining four cell cycle regulator proteins (included CCNB1, CCND1, P16 and P21) is not correlated with Ki-67 expression

Techniques: Expressing

Cdk1 regulates Cyclin B accumulation in G2 phase (A) Schematic. Cdk1 and Plk1 activities that induce mitosis are detected at the S/G2 border and increase gradually throughout G2 phase. (B) Example of unsynchronized U2OS Cyclin B1-YFP cells growing on micropatterns. Lighter colors indicate higher Cyclin B1-YFP fluorescence. Arrows indicate addition of DMSO or inhibitors. Time lapse 30 min. Scale bar 20 μm. (C) Schematic of the in silico synchronization setup. DMSO-treated cells are synchronized in mitosis (top). The resulting Cyclin B1-YFP fluorescence curve (top right) is used to fit Cyclin B1-YFP fluorescence of individual cells before kinase inhibitor treatment (bottom). (D) Quantification of Cyclin B1-YFP fluorescence of cells growing on micropatterns, treated with DMSO or indicated kinase inhibitors after in silico synchronization as in (B) and (C). Graph shows average and standard error of Cyclin B1-YFP fluorescence (At least 15 cells per condition are showed. Data are representative of 4 additional independent experiments, except for Plk1 inhibitor that is present in 2 additional independent experiments). Please note that only Cyclin B1-YFP fluorescence after kinase inhibitor addition is plotted. (E) Quantification of Cyclin B1, Aurora A, and Aurora B immunofluorescence in 4N U2OS Cdk1as cells after 2 h treatment with 1NMPP1. At least 420 cells per condition are showed. Data are representative of 3 independent experiments. ∗∗∗ p < 0.001, using Student’s t test. Interquartile range and median values are indicated within violin plots.

Journal: iScience

Article Title: Preparation for mitosis requires gradual CDK1 activation

doi: 10.1016/j.isci.2025.112292

Figure Lengend Snippet: Cdk1 regulates Cyclin B accumulation in G2 phase (A) Schematic. Cdk1 and Plk1 activities that induce mitosis are detected at the S/G2 border and increase gradually throughout G2 phase. (B) Example of unsynchronized U2OS Cyclin B1-YFP cells growing on micropatterns. Lighter colors indicate higher Cyclin B1-YFP fluorescence. Arrows indicate addition of DMSO or inhibitors. Time lapse 30 min. Scale bar 20 μm. (C) Schematic of the in silico synchronization setup. DMSO-treated cells are synchronized in mitosis (top). The resulting Cyclin B1-YFP fluorescence curve (top right) is used to fit Cyclin B1-YFP fluorescence of individual cells before kinase inhibitor treatment (bottom). (D) Quantification of Cyclin B1-YFP fluorescence of cells growing on micropatterns, treated with DMSO or indicated kinase inhibitors after in silico synchronization as in (B) and (C). Graph shows average and standard error of Cyclin B1-YFP fluorescence (At least 15 cells per condition are showed. Data are representative of 4 additional independent experiments, except for Plk1 inhibitor that is present in 2 additional independent experiments). Please note that only Cyclin B1-YFP fluorescence after kinase inhibitor addition is plotted. (E) Quantification of Cyclin B1, Aurora A, and Aurora B immunofluorescence in 4N U2OS Cdk1as cells after 2 h treatment with 1NMPP1. At least 420 cells per condition are showed. Data are representative of 3 independent experiments. ∗∗∗ p < 0.001, using Student’s t test. Interquartile range and median values are indicated within violin plots.

Article Snippet: Rabbit polyclonal anti- Cyclin A2 , Atlas antibodies , Cat# HPA020626, RRID: AB_1847376.

Techniques: Fluorescence, In Silico, Immunofluorescence

Cdk1 regulates transcription of mitotic factors (A) Quantification of Cyclin B1 immunofluorescence in 4N U2OS cells treated with Cdk1 inhibitor (RO3306), cycloheximide, or both for 2 h. The G2 population was separated in silico based on DAPI. At least 520 cells per condition are showed. Data are representative of 2 independent experiments; ∗∗∗ p < 0.001, using ANOVA. Interquartile range and median values are indicated within violin plots. (B) Schematic of the setup for RNA sequencing. HeLa cells were released after double thymidine synchronization. After 4.5 h Cdk1 inhibitor (RO3306) or DMSO was added. After 2 h cells were harvested for RNA sequencing analysis. (C and D) Volcano plots show log2 fold change between treated (RO3306) and non-treated (DMSO) normalized gene expressions (x axis), plotted versus the p value (y axis). Orange circles represent differentially expressed genes, and blue circles represent genes with similar expression (data from 3 independent experiments). (E) Schematic containing a selection of key components involved in direct, inner, and outer feedback regulating Cdk activity. (F) Gene Ontology and p values based on (C).

Journal: iScience

Article Title: Preparation for mitosis requires gradual CDK1 activation

doi: 10.1016/j.isci.2025.112292

Figure Lengend Snippet: Cdk1 regulates transcription of mitotic factors (A) Quantification of Cyclin B1 immunofluorescence in 4N U2OS cells treated with Cdk1 inhibitor (RO3306), cycloheximide, or both for 2 h. The G2 population was separated in silico based on DAPI. At least 520 cells per condition are showed. Data are representative of 2 independent experiments; ∗∗∗ p < 0.001, using ANOVA. Interquartile range and median values are indicated within violin plots. (B) Schematic of the setup for RNA sequencing. HeLa cells were released after double thymidine synchronization. After 4.5 h Cdk1 inhibitor (RO3306) or DMSO was added. After 2 h cells were harvested for RNA sequencing analysis. (C and D) Volcano plots show log2 fold change between treated (RO3306) and non-treated (DMSO) normalized gene expressions (x axis), plotted versus the p value (y axis). Orange circles represent differentially expressed genes, and blue circles represent genes with similar expression (data from 3 independent experiments). (E) Schematic containing a selection of key components involved in direct, inner, and outer feedback regulating Cdk activity. (F) Gene Ontology and p values based on (C).

Article Snippet: Rabbit polyclonal anti- Cyclin A2 , Atlas antibodies , Cat# HPA020626, RRID: AB_1847376.

Techniques: Immunofluorescence, In Silico, RNA Sequencing, Expressing, Selection, Activity Assay

Mathematical model of the cell cycle (A) Schematic representation of the mathematical model. (B) Model prediction (red line) of protein level dynamics after parameter estimation based on quantitative immunofluorescence of indicated proteins in U2OS cells from Akopyan et al. (blue dots). Please note that experimental data are only used until mitotic entry. The decrease of protein levels in mitosis is added to the model to mark mitosis upon full activation of Cdk1. (C) Model estimation of selected cell-cycle activities. Model time refers to number of calculation steps with a fixed duration. (D) Model prediction of Cyclin B level dynamics after inhibition of Cdk1, Cdk2, or Plk1.

Journal: iScience

Article Title: Preparation for mitosis requires gradual CDK1 activation

doi: 10.1016/j.isci.2025.112292

Figure Lengend Snippet: Mathematical model of the cell cycle (A) Schematic representation of the mathematical model. (B) Model prediction (red line) of protein level dynamics after parameter estimation based on quantitative immunofluorescence of indicated proteins in U2OS cells from Akopyan et al. (blue dots). Please note that experimental data are only used until mitotic entry. The decrease of protein levels in mitosis is added to the model to mark mitosis upon full activation of Cdk1. (C) Model estimation of selected cell-cycle activities. Model time refers to number of calculation steps with a fixed duration. (D) Model prediction of Cyclin B level dynamics after inhibition of Cdk1, Cdk2, or Plk1.

Article Snippet: Rabbit polyclonal anti- Cyclin A2 , Atlas antibodies , Cat# HPA020626, RRID: AB_1847376.

Techniques: Immunofluorescence, Activation Assay, Inhibition

Mitotic duration after Wee1 inhibition depends on when in G2 phase Wee1 inhibitors are added (A) Model prediction of G2 duration after Wee1 inhibition at different time points in G2 phase. Time when Wee1i added same as in (B) and (C). G2 phase starts approximately at model time 740, and 20 model time corresponds approximately to 30 min. How activities change relative to model time is visible in <xref ref-type=

Figure 3 . (B) Model prediction of accumulated FoxM activity at mitotic entry after Wee1 inhibition at different time points in G2 phase. 100% denotes mitotic levels in absence of Wee1 inhibition. (C) Model prediction of Cyclin B level at mitotic entry after Wee1 inhibition at different time points in G2 phase. 100% denotes mitotic levels in absence of Wee1 inhibition. Striped line indicates apparent minimum Cyclin B levels at mitotic entry. (D and E) U2OS Cyclin B1-YFP cells were monitored by time-lapse microscopy upon addition of Wee1 inhibitors. Three different inhibitors were used: MK1775 (1 μM), PD0166285 (1 μM), and PD407824 (5 μM). (D) Duration of mitosis (x axis) is plotted versus Cyclin B1-YFP level at mitotic entry (y axis). 100% denotes median mitotic levels in absence of Wee1 inhibition. (E) Duration of mitosis (y axis) is plotted versus estimated time before mitosis should Wee1 inhibitors have not been added (x axis). The estimate is based on Cyclin B1-YFP accumulation of control cells in the same experiment ( Figures S3 E and S3F). 31–70 cells per condition are showed. The data are representative of 3 independent experiments. " width="100%" height="100%">

Journal: iScience

Article Title: Preparation for mitosis requires gradual CDK1 activation

doi: 10.1016/j.isci.2025.112292

Figure Lengend Snippet: Mitotic duration after Wee1 inhibition depends on when in G2 phase Wee1 inhibitors are added (A) Model prediction of G2 duration after Wee1 inhibition at different time points in G2 phase. Time when Wee1i added same as in (B) and (C). G2 phase starts approximately at model time 740, and 20 model time corresponds approximately to 30 min. How activities change relative to model time is visible in Figure 3 . (B) Model prediction of accumulated FoxM activity at mitotic entry after Wee1 inhibition at different time points in G2 phase. 100% denotes mitotic levels in absence of Wee1 inhibition. (C) Model prediction of Cyclin B level at mitotic entry after Wee1 inhibition at different time points in G2 phase. 100% denotes mitotic levels in absence of Wee1 inhibition. Striped line indicates apparent minimum Cyclin B levels at mitotic entry. (D and E) U2OS Cyclin B1-YFP cells were monitored by time-lapse microscopy upon addition of Wee1 inhibitors. Three different inhibitors were used: MK1775 (1 μM), PD0166285 (1 μM), and PD407824 (5 μM). (D) Duration of mitosis (x axis) is plotted versus Cyclin B1-YFP level at mitotic entry (y axis). 100% denotes median mitotic levels in absence of Wee1 inhibition. (E) Duration of mitosis (y axis) is plotted versus estimated time before mitosis should Wee1 inhibitors have not been added (x axis). The estimate is based on Cyclin B1-YFP accumulation of control cells in the same experiment ( Figures S3 E and S3F). 31–70 cells per condition are showed. The data are representative of 3 independent experiments.

Article Snippet: Rabbit polyclonal anti- Cyclin A2 , Atlas antibodies , Cat# HPA020626, RRID: AB_1847376.

Techniques: Inhibition, Activity Assay, Time-lapse Microscopy, Control

Wee1 inhibition in G2 phase leads to a de-coupling of Cdk1 and Plk1 activities (A) Model prediction of Plk1 activity at mitotic entry after Wee1 inhibition at different time points in G2 phase. 100% denotes mitotic levels in absence of Wee1 inhibition. G2 phase starts approximately at model time 740, and 20 model time corresponds approximately to 30 min. How activities change relative to model time is visible in <xref ref-type=

Figure 3 . (B) Model prediction of Cyclin B level, Plk1 level, Plk1 activity, and Cdk1 activity after inhibition of Wee1 at different time points in G2 phase. The dotted line in each graph represents the levels at mitotic entry when Wee1 is not artificially inhibited. Mit indicates mitosis. (C) Flow cytometry analysis of Plk1 levels and Plk1-mediated phosphorylation of TCTP (pTCTP) in mitotic U2OS cells. STLC (10 μM), to block cells in mitosis, was added with or without Wee1i for 2 h before harvest. Graph shows mitotic cells, gated as in Figure S5 A. Wee1i, cells treated with the Wee1 inhibitor MK1775 (1 μM) together with STLC; DMSO, cells treated with DMSO together with STLC. At least 2,000 mitotic cells were quantified per condition in two independent experiments. " width="100%" height="100%">

Journal: iScience

Article Title: Preparation for mitosis requires gradual CDK1 activation

doi: 10.1016/j.isci.2025.112292

Figure Lengend Snippet: Wee1 inhibition in G2 phase leads to a de-coupling of Cdk1 and Plk1 activities (A) Model prediction of Plk1 activity at mitotic entry after Wee1 inhibition at different time points in G2 phase. 100% denotes mitotic levels in absence of Wee1 inhibition. G2 phase starts approximately at model time 740, and 20 model time corresponds approximately to 30 min. How activities change relative to model time is visible in Figure 3 . (B) Model prediction of Cyclin B level, Plk1 level, Plk1 activity, and Cdk1 activity after inhibition of Wee1 at different time points in G2 phase. The dotted line in each graph represents the levels at mitotic entry when Wee1 is not artificially inhibited. Mit indicates mitosis. (C) Flow cytometry analysis of Plk1 levels and Plk1-mediated phosphorylation of TCTP (pTCTP) in mitotic U2OS cells. STLC (10 μM), to block cells in mitosis, was added with or without Wee1i for 2 h before harvest. Graph shows mitotic cells, gated as in Figure S5 A. Wee1i, cells treated with the Wee1 inhibitor MK1775 (1 μM) together with STLC; DMSO, cells treated with DMSO together with STLC. At least 2,000 mitotic cells were quantified per condition in two independent experiments.

Article Snippet: Rabbit polyclonal anti- Cyclin A2 , Atlas antibodies , Cat# HPA020626, RRID: AB_1847376.

Techniques: Inhibition, Activity Assay, Flow Cytometry, Phospho-proteomics, Blocking Assay

Journal: iScience

Article Title: Preparation for mitosis requires gradual CDK1 activation

doi: 10.1016/j.isci.2025.112292

Figure Lengend Snippet:

Article Snippet: Rabbit polyclonal anti- Cyclin A2 , Atlas antibodies , Cat# HPA020626, RRID: AB_1847376.

Techniques: Recombinant, Gene Expression, RNA Sequencing, Software

Review

rabbit anti cyclin a2 ccna2 (Cell Signaling Technology Inc)

Structured Review

Images

1) Product Images from "Aberrant CDK4/6-driven cell-cycle reentry drives neuronal loss and defines a therapeutic target in C9orf72 ALS/FTD"

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