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Visomitin induces cell cycle arrest in AML cells. (A) HL60 and U937 cells were treated with Visomitin (1 μM) for 24 h. Cell cycle was analyzed by FACS after PI staining. Expression levels of Cyclin D1 and <t>CDK4</t> (B) , as well as p21 and p16 (C) , were analyzed by Western blotting after treatment with 500 nM Visomitin for 24 h in U937 cells. β-actin was used as a loading control. All data are presented as mean ± SD and representative of three independent experiments and statistical analysis was performed using the two-tailed Mann–Whitney U test (*p < 0.05).
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Visomitin induces cell cycle arrest in AML cells. (A) HL60 and U937 cells were treated with Visomitin (1 μM) for 24 h. Cell cycle was analyzed by FACS after PI staining. Expression levels of Cyclin D1 and <t>CDK4</t> (B) , as well as p21 and p16 (C) , were analyzed by Western blotting after treatment with 500 nM Visomitin for 24 h in U937 cells. β-actin was used as a loading control. All data are presented as mean ± SD and representative of three independent experiments and statistical analysis was performed using the two-tailed Mann–Whitney U test (*p < 0.05).
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Visomitin induces cell cycle arrest in AML cells. (A) HL60 and U937 cells were treated with Visomitin (1 μM) for 24 h. Cell cycle was analyzed by FACS after PI staining. Expression levels of Cyclin D1 and <t>CDK4</t> (B) , as well as p21 and p16 (C) , were analyzed by Western blotting after treatment with 500 nM Visomitin for 24 h in U937 cells. β-actin was used as a loading control. All data are presented as mean ± SD and representative of three independent experiments and statistical analysis was performed using the two-tailed Mann–Whitney U test (*p < 0.05).
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Immunohistochemical localization of estrogen receptor, cyclin D1 and CDK 4 in the rat uterus (40X magnification). Rats were treated with or without 0.4 ppm arsenic for 28 days. The untreated uterus (A and C) showed prominent expression for estrogen receptor-α in the uterine epithelium as well as endometrium. Arsenic downregulated the estrogen receptors in the uterine epithelium (B) as well as endometrial stroma (D). Arsenic also downregulated Cyclin D1 and <t>CDK4</t> expression in the endometrial stroma (F and H) as compared to untreated uterus (E and G).
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Immunohistochemical localization of estrogen receptor, cyclin D1 and CDK 4 in the rat uterus (40X magnification). Rats were treated with or without 0.4 ppm arsenic for 28 days. The untreated uterus (A and C) showed prominent expression for estrogen receptor-α in the uterine epithelium as well as endometrium. Arsenic downregulated the estrogen receptors in the uterine epithelium (B) as well as endometrial stroma (D). Arsenic also downregulated Cyclin D1 and <t>CDK4</t> expression in the endometrial stroma (F and H) as compared to untreated uterus (E and G).
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Immunohistochemical localization of estrogen receptor, cyclin D1 and CDK 4 in the rat uterus (40X magnification). Rats were treated with or without 0.4 ppm arsenic for 28 days. The untreated uterus (A and C) showed prominent expression for estrogen receptor-α in the uterine epithelium as well as endometrium. Arsenic downregulated the estrogen receptors in the uterine epithelium (B) as well as endometrial stroma (D). Arsenic also downregulated Cyclin D1 and <t>CDK4</t> expression in the endometrial stroma (F and H) as compared to untreated uterus (E and G).
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Image Search Results


Visomitin induces cell cycle arrest in AML cells. (A) HL60 and U937 cells were treated with Visomitin (1 μM) for 24 h. Cell cycle was analyzed by FACS after PI staining. Expression levels of Cyclin D1 and CDK4 (B) , as well as p21 and p16 (C) , were analyzed by Western blotting after treatment with 500 nM Visomitin for 24 h in U937 cells. β-actin was used as a loading control. All data are presented as mean ± SD and representative of three independent experiments and statistical analysis was performed using the two-tailed Mann–Whitney U test (*p < 0.05).

Journal: Frontiers in Pharmacology

Article Title: Visomitin as a differentiation-inducing therapeutic agent through SYK inhibition in AML

doi: 10.3389/fphar.2026.1741351

Figure Lengend Snippet: Visomitin induces cell cycle arrest in AML cells. (A) HL60 and U937 cells were treated with Visomitin (1 μM) for 24 h. Cell cycle was analyzed by FACS after PI staining. Expression levels of Cyclin D1 and CDK4 (B) , as well as p21 and p16 (C) , were analyzed by Western blotting after treatment with 500 nM Visomitin for 24 h in U937 cells. β-actin was used as a loading control. All data are presented as mean ± SD and representative of three independent experiments and statistical analysis was performed using the two-tailed Mann–Whitney U test (*p < 0.05).

Article Snippet: The following primary antibodies were used for western blots: Cyclin D1 (Santa Cruz Biotechnology, Dallas, TX, United States; sc-8396), CDK4 (Santa Cruz Biotechnology; sc-23896), p16 (Cell Signaling Technology, Danvers, MA, United States; 80772S), p21 (Cell Signaling Technology; 2947S), Rb (Santa Cruz Biotechnology; sc-102), Mcl-1 (Santa Cruz Biotechnology; sc-12756), Bcl-xl (eBioscience, Vienna, Austria; 14-6994-81), Bak (Santa Cruz Biotechnology; sc-832), Bax (Santa Cruz Biotechnology; sc-7480), P-ATM (Cell Signaling Technology; 5883S), P-Histone H2A.X (Cell Signaling Technology; 9718S), SYK (Santa Cruz Biotechnology; sc-1240), phospho-SYK (Cell Signaling Technology; 2710S), and β-actin (Santa Cruz Biotechnology; sc-4778).

Techniques: Staining, Expressing, Western Blot, Control, Two Tailed Test, MANN-WHITNEY

Immunohistochemical localization of estrogen receptor, cyclin D1 and CDK 4 in the rat uterus (40X magnification). Rats were treated with or without 0.4 ppm arsenic for 28 days. The untreated uterus (A and C) showed prominent expression for estrogen receptor-α in the uterine epithelium as well as endometrium. Arsenic downregulated the estrogen receptors in the uterine epithelium (B) as well as endometrial stroma (D). Arsenic also downregulated Cyclin D1 and CDK4 expression in the endometrial stroma (F and H) as compared to untreated uterus (E and G).

Journal: Current Research in Toxicology

Article Title: Low-dose arsenic exposure disrupts rat uterine physiology independent of generation of oxidative stress

doi: 10.1016/j.crtox.2026.100289

Figure Lengend Snippet: Immunohistochemical localization of estrogen receptor, cyclin D1 and CDK 4 in the rat uterus (40X magnification). Rats were treated with or without 0.4 ppm arsenic for 28 days. The untreated uterus (A and C) showed prominent expression for estrogen receptor-α in the uterine epithelium as well as endometrium. Arsenic downregulated the estrogen receptors in the uterine epithelium (B) as well as endometrial stroma (D). Arsenic also downregulated Cyclin D1 and CDK4 expression in the endometrial stroma (F and H) as compared to untreated uterus (E and G).

Article Snippet: Sections were subsequently incubated with rabbit anti-ER and anti CDK4 IgG (sc-542, 1:500 dilution and sc-260 1:100 dilution), mouse anti Cyclin D1 (sc 8396, 1:500 dilution), all for 18 h at 4°C, followed by goat anti-rabbit HRP-conjugated secondary antibody (1:1000 dilution) (Santacruz biotechnology, sc-2004) for 1 h at room temperature.

Techniques: Immunohistochemical staining, Expressing

Effect of arsenic on expression of estrogen receptor, Cyclin D1 and CDK4 expression at the mRNA transcript levels relative to GAPDH. Rats were treated with or without 0.4 ppm arsenic for 28 days. Downregulation of the estrogen receptor as well as cell cycle regulatory proteins at the mRNA transcript levels were observed as determined by RT-PCR. The data shown is a representative of the experiments carried out in triplicates (three independent replicates per rat per assay). Mean ± SD *p < 0.01, **p < 0.05. as analyzed by T test.

Journal: Current Research in Toxicology

Article Title: Low-dose arsenic exposure disrupts rat uterine physiology independent of generation of oxidative stress

doi: 10.1016/j.crtox.2026.100289

Figure Lengend Snippet: Effect of arsenic on expression of estrogen receptor, Cyclin D1 and CDK4 expression at the mRNA transcript levels relative to GAPDH. Rats were treated with or without 0.4 ppm arsenic for 28 days. Downregulation of the estrogen receptor as well as cell cycle regulatory proteins at the mRNA transcript levels were observed as determined by RT-PCR. The data shown is a representative of the experiments carried out in triplicates (three independent replicates per rat per assay). Mean ± SD *p < 0.01, **p < 0.05. as analyzed by T test.

Article Snippet: Sections were subsequently incubated with rabbit anti-ER and anti CDK4 IgG (sc-542, 1:500 dilution and sc-260 1:100 dilution), mouse anti Cyclin D1 (sc 8396, 1:500 dilution), all for 18 h at 4°C, followed by goat anti-rabbit HRP-conjugated secondary antibody (1:1000 dilution) (Santacruz biotechnology, sc-2004) for 1 h at room temperature.

Techniques: Expressing, Reverse Transcription Polymerase Chain Reaction

Effect of arsenic on expression of estrogen receptor, Cyclin D1 and CDK4 expression at the protein expression levels relative to beta-tubulin . Rats were treated with or without 0.4 ppm arsenic for 28 days. Downregulation of the estrogen receptor as well as cell cycle regulatory proteins were observed as determined by western blot. The data shown is a representative of the experiments carried out in triplicates (three independent replicates per rat per assay). Mean ± SD *p < 0.01, **p < 0.05. as analyzed by T test.

Journal: Current Research in Toxicology

Article Title: Low-dose arsenic exposure disrupts rat uterine physiology independent of generation of oxidative stress

doi: 10.1016/j.crtox.2026.100289

Figure Lengend Snippet: Effect of arsenic on expression of estrogen receptor, Cyclin D1 and CDK4 expression at the protein expression levels relative to beta-tubulin . Rats were treated with or without 0.4 ppm arsenic for 28 days. Downregulation of the estrogen receptor as well as cell cycle regulatory proteins were observed as determined by western blot. The data shown is a representative of the experiments carried out in triplicates (three independent replicates per rat per assay). Mean ± SD *p < 0.01, **p < 0.05. as analyzed by T test.

Article Snippet: Sections were subsequently incubated with rabbit anti-ER and anti CDK4 IgG (sc-542, 1:500 dilution and sc-260 1:100 dilution), mouse anti Cyclin D1 (sc 8396, 1:500 dilution), all for 18 h at 4°C, followed by goat anti-rabbit HRP-conjugated secondary antibody (1:1000 dilution) (Santacruz biotechnology, sc-2004) for 1 h at room temperature.

Techniques: Expressing, Western Blot