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Cell Signaling Technology Inc cyclin a2
Knocking down SKA2 induces gastric cancer cell lines G2/M arrest (A and B) Cell cycle analysis of SKA2 knockdown in SNU638 and NUGC3 cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (C) Western blotting analysis of the expression of <t>Cyclin</t> D1, Cyclin <t>A2,</t> Cyclin B1, and SKA2 in SNU638 and NUGC3 SKA2-knockdown cell lines. α-Tubulin was used as the internal control. (D and E) Cell cycle analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (F) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using anti-Cyclin D1, anti-Cyclin A2, anti-Cyclin B1, and anti-SKA2 antibodies. α-Tubulin was used as the internal control. Representative flow cytometry histograms and blotting images are shown from 3 biologically independent experiments. Data in (A)–(B) and (D)–(E) are presented as mean ± SD, n = 3 biologically independent experiments. p values are based on a one-way ANOVA test. ns, no significance (∗∗ p < 0.01; ∗∗∗ p < 0.001).
Cyclin A2, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech china cyclin a
Knocking down SKA2 induces gastric cancer cell lines G2/M arrest (A and B) Cell cycle analysis of SKA2 knockdown in SNU638 and NUGC3 cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (C) Western blotting analysis of the expression of <t>Cyclin</t> D1, Cyclin <t>A2,</t> Cyclin B1, and SKA2 in SNU638 and NUGC3 SKA2-knockdown cell lines. α-Tubulin was used as the internal control. (D and E) Cell cycle analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (F) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using anti-Cyclin D1, anti-Cyclin A2, anti-Cyclin B1, and anti-SKA2 antibodies. α-Tubulin was used as the internal control. Representative flow cytometry histograms and blotting images are shown from 3 biologically independent experiments. Data in (A)–(B) and (D)–(E) are presented as mean ± SD, n = 3 biologically independent experiments. p values are based on a one-way ANOVA test. ns, no significance (∗∗ p < 0.01; ∗∗∗ p < 0.001).
China Cyclin A, supplied by Proteintech, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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R&D Systems antibodies against cyclin a
(A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and <t>cyclin</t> <t>A</t> expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.
Antibodies Against Cyclin A, supplied by R&D Systems, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Cell Signaling Technology Inc cyclin d1
(A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and <t>cyclin</t> <t>A</t> expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.
Cyclin D1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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(A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and <t>cyclin</t> <t>A</t> expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.
Cyclin A1, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Proteintech anticcne1
(A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and <t>cyclin</t> <t>A</t> expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.
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Proteintech anti ccna2
(A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and <t>cyclin</t> <t>A</t> expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.
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(A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and <t>cyclin</t> <t>A</t> expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.
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Image Search Results


Knocking down SKA2 induces gastric cancer cell lines G2/M arrest (A and B) Cell cycle analysis of SKA2 knockdown in SNU638 and NUGC3 cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (C) Western blotting analysis of the expression of Cyclin D1, Cyclin A2, Cyclin B1, and SKA2 in SNU638 and NUGC3 SKA2-knockdown cell lines. α-Tubulin was used as the internal control. (D and E) Cell cycle analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (F) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using anti-Cyclin D1, anti-Cyclin A2, anti-Cyclin B1, and anti-SKA2 antibodies. α-Tubulin was used as the internal control. Representative flow cytometry histograms and blotting images are shown from 3 biologically independent experiments. Data in (A)–(B) and (D)–(E) are presented as mean ± SD, n = 3 biologically independent experiments. p values are based on a one-way ANOVA test. ns, no significance (∗∗ p < 0.01; ∗∗∗ p < 0.001).

Journal: iScience

Article Title: SKA2 promotes gastric cancer progression by regulating glutathione metabolism

doi: 10.1016/j.isci.2026.115202

Figure Lengend Snippet: Knocking down SKA2 induces gastric cancer cell lines G2/M arrest (A and B) Cell cycle analysis of SKA2 knockdown in SNU638 and NUGC3 cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (C) Western blotting analysis of the expression of Cyclin D1, Cyclin A2, Cyclin B1, and SKA2 in SNU638 and NUGC3 SKA2-knockdown cell lines. α-Tubulin was used as the internal control. (D and E) Cell cycle analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines. Percentage of flow cytometric histogram images shows the effects of SKA2. (F) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using anti-Cyclin D1, anti-Cyclin A2, anti-Cyclin B1, and anti-SKA2 antibodies. α-Tubulin was used as the internal control. Representative flow cytometry histograms and blotting images are shown from 3 biologically independent experiments. Data in (A)–(B) and (D)–(E) are presented as mean ± SD, n = 3 biologically independent experiments. p values are based on a one-way ANOVA test. ns, no significance (∗∗ p < 0.01; ∗∗∗ p < 0.001).

Article Snippet: Cyclin A2 , Cell Signaling Technology , Cat#4656; RRID: AB_2071958.

Techniques: Cell Cycle Assay, Knockdown, Western Blot, Expressing, Control, Over Expression, Flow Cytometry

Knocking down SKA2-induced cell-cycle arrest and apoptosis through the SKA2/ROS/ATM axis in GC cell lines (A) Western blotting analysis of γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (B) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2. (C) Western blotting analysis of KU-55933 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), PARP, Cleaved-Caspase3, JNK, p -JNK (Thr183/Tyr185), ATM, p -ATM (Ser1981), and SKA2. (D) Western blotting analysis of BML-277 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), and SKA2. (E) Western blotting analysis of P38, p-P38 (Thr180/Tyr182), ERK, p -ERK1/2 (Thr202/Tyr204), JNK, p -JNK (Thr183/Tyr185), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (F) Western blotting analysis of the rescue effect of SKA2 overexpression on MAPK pathway markers (ERK, p -ERK1/2, JNK, and p -JNK) in SNU638 and NUGC3 SKA2-knockdown cell lines. (G) Western blotting analysis of JNK-IN-8 treatment in SNU638 SKA2-knockdown cell lines using antibodies against PARP, cleaved-caspase3, JNK, p -JNK (Thr183/Tyr185), and SKA2. α-Tubulin was used as the internal control for all blots. Representative blotting images are shown from 3 independent experiments.

Journal: iScience

Article Title: SKA2 promotes gastric cancer progression by regulating glutathione metabolism

doi: 10.1016/j.isci.2026.115202

Figure Lengend Snippet: Knocking down SKA2-induced cell-cycle arrest and apoptosis through the SKA2/ROS/ATM axis in GC cell lines (A) Western blotting analysis of γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (B) Western blotting analysis of SKA2 overexpression in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against γ-H2AX (Ser139), ATM, p -ATM (Ser1981), p -Chk2 (Thr68), and SKA2. (C) Western blotting analysis of KU-55933 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), PARP, Cleaved-Caspase3, JNK, p -JNK (Thr183/Tyr185), ATM, p -ATM (Ser1981), and SKA2. (D) Western blotting analysis of BML-277 treatment in SNU638 and NUGC3 SKA2-knockdown cell lines using antibodies against cyclin D1, cyclin A2, cyclin B1, p -Chk2 (Thr68), and SKA2. (E) Western blotting analysis of P38, p-P38 (Thr180/Tyr182), ERK, p -ERK1/2 (Thr202/Tyr204), JNK, p -JNK (Thr183/Tyr185), and SKA2 expression in SNU638 and NUGC3 SKA2-knockdown cell lines. (F) Western blotting analysis of the rescue effect of SKA2 overexpression on MAPK pathway markers (ERK, p -ERK1/2, JNK, and p -JNK) in SNU638 and NUGC3 SKA2-knockdown cell lines. (G) Western blotting analysis of JNK-IN-8 treatment in SNU638 SKA2-knockdown cell lines using antibodies against PARP, cleaved-caspase3, JNK, p -JNK (Thr183/Tyr185), and SKA2. α-Tubulin was used as the internal control for all blots. Representative blotting images are shown from 3 independent experiments.

Article Snippet: Cyclin A2 , Cell Signaling Technology , Cat#4656; RRID: AB_2071958.

Techniques: Western Blot, Expressing, Knockdown, Over Expression, Control

(A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and cyclin A expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.

Journal: bioRxiv

Article Title: Targeting Distinct Cell Cycle Nodes Overcomes KRAS/RAS Inhibitor Resistance

doi: 10.64898/2026.03.10.710937

Figure Lengend Snippet: (A) GSEA analysis illustrating the differential effect of MRTX849 on the genes associated with E2F target pathway and the proteins associated with G2/M checkpoint in cell cycle machinery. (B) Heat map represents the differential effect of MRTX849 in downregulating the indicated genes and proteins that are involved in cell cycle from MiaPaCa-2-WT and MiaPaca-2-MR cells following 48-hour treatment. (C) Biochemical analysis on the indicated sensitive (WT) and resistance cell lines to compare the effect of MRTX849 on RB phosphorylation and cyclin A expression at different doses after treating the cells for 48 hours. (D) GSEA analysis highlighting pathways associated with genes and proteins that are differentially expressed between MiaPaCa-2-MR and MiaPaCa-2-WT cells. (E) Volcano plots of differentially expressed genes and proteins in MiaPaCa-2-MR versus MiaPaCa-2-WT cells. (F) Heat map illustrating the effects of indicated targeted therapeutic agents on normalized fold change in cell growth in combination with DMSO or mutant-selective KRAS inhibitors. (G) Synergistic interactions between KRAS inhibitors and erlotinib or AZD4547 in AsPC-1-MR, UM53, and MiaPaCa-2-MR cells. Heat maps depict normalized fold change in growth rate following treatment with increasing concentrations of KRAS inhibitors in combination with erlotinib or AZD4547. Bliss synergy scores were calculated using the SynergyFinder online platform.

Article Snippet: Antibodies against Cyclin A (Cat# AF5999) and β-actin (Cat# MAB8929) were purchased from R&D Systems (Minneapolis, MN).

Techniques: Phospho-proteomics, Expressing, Mutagenesis