histone h4 Search Results


histone h4  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology histone h4
Fig.1. Mn phosphorylates YY1 at serine residues via AurkB and CK2 in <t>H4</t> astrocytes. (A) Astrocytes were pre-treated with the AurkB inhibitor Hesperadin (Hesp, 250 nM,1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated with YY1 antibody, followed by western blotting for phosphoserine. (B) Astrocytes were pre-treated with the CK2 inhibitor CX-4945 (CX, 10 mM, 1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated for YY1, followed by western blotting for phosphoserine. (**p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).
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h4k16ac  (Cell Signaling Technology Inc)
95
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Fig.1. Mn phosphorylates YY1 at serine residues via AurkB and CK2 in <t>H4</t> astrocytes. (A) Astrocytes were pre-treated with the AurkB inhibitor Hesperadin (Hesp, 250 nM,1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated with YY1 antibody, followed by western blotting for phosphoserine. (B) Astrocytes were pre-treated with the CK2 inhibitor CX-4945 (CX, 10 mM, 1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated for YY1, followed by western blotting for phosphoserine. (**p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).
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anti h4  (Cell Signaling Technology Inc)
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Fig.1. Mn phosphorylates YY1 at serine residues via AurkB and CK2 in <t>H4</t> astrocytes. (A) Astrocytes were pre-treated with the AurkB inhibitor Hesperadin (Hesp, 250 nM,1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated with YY1 antibody, followed by western blotting for phosphoserine. (B) Astrocytes were pre-treated with the CK2 inhibitor CX-4945 (CX, 10 mM, 1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated for YY1, followed by western blotting for phosphoserine. (**p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).
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histone h4  (Cell Signaling Technology Inc)
95
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Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) <t>or</t> <t>anti-H3/H4</t> antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).
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acetyl histone h4 lys12 mab  (Cell Signaling Technology Inc)
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Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) <t>or</t> <t>anti-H3/H4</t> antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).
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h4k8 2594  (Cell Signaling Technology Inc)
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Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) <t>or</t> <t>anti-H3/H4</t> antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).
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anti ac histone h4 lys12 r  (Santa Cruz Biotechnology)
93
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Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) <t>or</t> <t>anti-H3/H4</t> antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).
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h4 cell signaling 13919  (Cell Signaling Technology Inc)
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Cell Signaling Technology Inc h4 cell signaling 13919
Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) <t>or</t> <t>anti-H3/H4</t> antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).
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rabbit anti histone h4ac16 antibody  (Bio-Rad)
85
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Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) <t>or</t> <t>anti-H3/H4</t> antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).
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acetyl histone 4  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc acetyl histone 4
Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) <t>or</t> <t>anti-H3/H4</t> antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).
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acetyl histone h4  (Cell Signaling Technology Inc)
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FIGURE 1. 15-LOX-1 promoter histone acetylation and 15-LOX-1 transcriptional activation. A and B, effects of depsipeptide on acetylation of histones H3 and <t>H4</t> in the 15-LOX-1 promoter. Caco-2 (A) and SW480 (B) cells were treated with depsipeptide (5 nM) or the vehicle solvent for depsipeptide (control). The cells were harvested 48 h after treatment and subjected to ChIP assays using <t>specific</t> <t>antibodies</t> against acetylated histone H3 (H3) or acetylated histone H4 (H4). and indicate immunoprecipitation with and without H3 or H4 antibodies, respectively, and Input indicates total DNA before immunoprecipitation. Depsipeptide induced H3 and H4 acetylation in the 15-LOX-1 promoter. C, kinetics of effects of depsipeptide on H3 acetylation. Caco-2 cells were treated with depsipeptide (5 nM), harvested at the indicated times, and subjected to ChIP/real-time PCR assays using specific acetylated H3 antibodies. The results are percentages of the respective input genomic DNA for the 15-LOX-1 promoter. The values are the means S.D. of triplicate measurements. D, effects of depsipeptide on 15-LOX-1 expression in colorectal cancer cells. Colorectal cancer cells were treated with either depsipeptide (5 nM) or solvent (control). The cells were harvested 24 h later and processed for 15-LOX-1 mRNA by real-time reverse transcription-PCR. The data are presented as the difference in 15-LOX-1 relative expression levels between depsipeptide- and control-treated cells. The values shown are the means S.D. of triplicate experiments. E, effects of SAHA on 15-LOX-1 expression in colorectal cancer cells. Colorectal cancer cells were treated with either SAHA (1 M) or solvent (control) and processed for 15-LOX-1 mRNA measurements as in D. The values shown are the means S.D. of triplicate experiments. F and G, effects of depsipeptide and SAHA on H3 acetylation in the 15-LOX-1 promoter. Colorectal cancer cells were treated with depsipeptide (F), SAHA (G), or solvent only (control). The cells were harvested and subjected to ChIP/real-time PCR using specific antibodies against acetylated histone H3. The data are presented as the difference in the H3 acetylation levels in the 15-LOX-1 promoter between depsipeptide- or SAHA-treated and control-treated cells. The values shown are the means S.D. of triplicate experiments. H and I, correlation between 15-LOX-1 expression and H3 acetylation in the 15-LOX-1 promoter in colorectal cancer cell lines. Scatter plots of the differences in 15-LOX-1 mRNA expression (treated control) in relation to those in 15-LOX-1 promoter H3 acetylation levels (treated control) in colorectal cancer cell lines treated with depsipeptide (H) or SAHA (I). The values shown are the means S.D. of triplicate experiments.
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anti h4 tetra ac  (Bethyl)
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FIGURE 1. 15-LOX-1 promoter histone acetylation and 15-LOX-1 transcriptional activation. A and B, effects of depsipeptide on acetylation of histones H3 and <t>H4</t> in the 15-LOX-1 promoter. Caco-2 (A) and SW480 (B) cells were treated with depsipeptide (5 nM) or the vehicle solvent for depsipeptide (control). The cells were harvested 48 h after treatment and subjected to ChIP assays using <t>specific</t> <t>antibodies</t> against acetylated histone H3 (H3) or acetylated histone H4 (H4). and indicate immunoprecipitation with and without H3 or H4 antibodies, respectively, and Input indicates total DNA before immunoprecipitation. Depsipeptide induced H3 and H4 acetylation in the 15-LOX-1 promoter. C, kinetics of effects of depsipeptide on H3 acetylation. Caco-2 cells were treated with depsipeptide (5 nM), harvested at the indicated times, and subjected to ChIP/real-time PCR assays using specific acetylated H3 antibodies. The results are percentages of the respective input genomic DNA for the 15-LOX-1 promoter. The values are the means S.D. of triplicate measurements. D, effects of depsipeptide on 15-LOX-1 expression in colorectal cancer cells. Colorectal cancer cells were treated with either depsipeptide (5 nM) or solvent (control). The cells were harvested 24 h later and processed for 15-LOX-1 mRNA by real-time reverse transcription-PCR. The data are presented as the difference in 15-LOX-1 relative expression levels between depsipeptide- and control-treated cells. The values shown are the means S.D. of triplicate experiments. E, effects of SAHA on 15-LOX-1 expression in colorectal cancer cells. Colorectal cancer cells were treated with either SAHA (1 M) or solvent (control) and processed for 15-LOX-1 mRNA measurements as in D. The values shown are the means S.D. of triplicate experiments. F and G, effects of depsipeptide and SAHA on H3 acetylation in the 15-LOX-1 promoter. Colorectal cancer cells were treated with depsipeptide (F), SAHA (G), or solvent only (control). The cells were harvested and subjected to ChIP/real-time PCR using specific antibodies against acetylated histone H3. The data are presented as the difference in the H3 acetylation levels in the 15-LOX-1 promoter between depsipeptide- or SAHA-treated and control-treated cells. The values shown are the means S.D. of triplicate experiments. H and I, correlation between 15-LOX-1 expression and H3 acetylation in the 15-LOX-1 promoter in colorectal cancer cell lines. Scatter plots of the differences in 15-LOX-1 mRNA expression (treated control) in relation to those in 15-LOX-1 promoter H3 acetylation levels (treated control) in colorectal cancer cell lines treated with depsipeptide (H) or SAHA (I). The values shown are the means S.D. of triplicate experiments.
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Image Search Results


Fig.1. Mn phosphorylates YY1 at serine residues via AurkB and CK2 in H4 astrocytes. (A) Astrocytes were pre-treated with the AurkB inhibitor Hesperadin (Hesp, 250 nM,1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated with YY1 antibody, followed by western blotting for phosphoserine. (B) Astrocytes were pre-treated with the CK2 inhibitor CX-4945 (CX, 10 mM, 1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated for YY1, followed by western blotting for phosphoserine. (**p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).

Journal: Toxicology letters

Article Title: Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes.

doi: 10.1016/j.toxlet.2021.11.007

Figure Lengend Snippet: Fig.1. Mn phosphorylates YY1 at serine residues via AurkB and CK2 in H4 astrocytes. (A) Astrocytes were pre-treated with the AurkB inhibitor Hesperadin (Hesp, 250 nM,1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated with YY1 antibody, followed by western blotting for phosphoserine. (B) Astrocytes were pre-treated with the CK2 inhibitor CX-4945 (CX, 10 mM, 1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated for YY1, followed by western blotting for phosphoserine. (**p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).

Article Snippet: Antibodies for YY1 (sc-7341), HDAC1 (sc-81598), HDAC3 (sc-376957), β-actin (sc-47778), and histone H4 (sc-25260) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA).

Techniques: Immunoprecipitation, Western Blot, Control

Fig. 2. Mn-induced YY1 phosphorylation via AurkB and CK2 leads to YY1 nuclear translocation. (A) Astrocytes were pre-treated with Hesp (250 nM, 1 h) and exposed to Mn (250 mM, 3 h), then cells were fractionated and analyzed for YY1 protein levels in the nuclear fraction by western blotting. Nuclear protein histone H4 was used as a loading control. (B) Astrocytes were pre-treated with CX (10 mM, 1 h) and exposed to Mn (250 mM, 3 h), then cells were fractionated and analyzed for YY1 protein expression in the nuclear fraction by western blotting. (C) Astrocytes were pre-treated with Hesp or CX and exposed to Mn for the indicated time periods, then analyzed via immunocytochemistry (ICC) for YY1 nuclear expression. Scale: 0-25 mM. (*p < 0.05, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).

Journal: Toxicology letters

Article Title: Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes.

doi: 10.1016/j.toxlet.2021.11.007

Figure Lengend Snippet: Fig. 2. Mn-induced YY1 phosphorylation via AurkB and CK2 leads to YY1 nuclear translocation. (A) Astrocytes were pre-treated with Hesp (250 nM, 1 h) and exposed to Mn (250 mM, 3 h), then cells were fractionated and analyzed for YY1 protein levels in the nuclear fraction by western blotting. Nuclear protein histone H4 was used as a loading control. (B) Astrocytes were pre-treated with CX (10 mM, 1 h) and exposed to Mn (250 mM, 3 h), then cells were fractionated and analyzed for YY1 protein expression in the nuclear fraction by western blotting. (C) Astrocytes were pre-treated with Hesp or CX and exposed to Mn for the indicated time periods, then analyzed via immunocytochemistry (ICC) for YY1 nuclear expression. Scale: 0-25 mM. (*p < 0.05, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).

Article Snippet: Antibodies for YY1 (sc-7341), HDAC1 (sc-81598), HDAC3 (sc-376957), β-actin (sc-47778), and histone H4 (sc-25260) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA).

Techniques: Phospho-proteomics, Translocation Assay, Western Blot, Control, Expressing, Immunocytochemistry

Fig. 3. Mn-induced YY1 phosphorylation increases interaction between YY1 and HDACs in H4 astrocytes. (A) Astrocytes were pre-treated with Hesp (250 nM, 1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated for YY1, followed by western blotting for HDAC1. (B) Astrocytes were pre-treated with CX (10 mM, 1 h), then exposed to Mn (250 mM, 3 h) and co-immunoprecipitated for YY1/HDAC3 interaction. (*p < 0.05, **p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ANOVA followed by Tukey’s post hoc test; N = 3).

Journal: Toxicology letters

Article Title: Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes.

doi: 10.1016/j.toxlet.2021.11.007

Figure Lengend Snippet: Fig. 3. Mn-induced YY1 phosphorylation increases interaction between YY1 and HDACs in H4 astrocytes. (A) Astrocytes were pre-treated with Hesp (250 nM, 1 h), then exposed to Mn (250 mM, 3 h) and immunoprecipitated for YY1, followed by western blotting for HDAC1. (B) Astrocytes were pre-treated with CX (10 mM, 1 h), then exposed to Mn (250 mM, 3 h) and co-immunoprecipitated for YY1/HDAC3 interaction. (*p < 0.05, **p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ANOVA followed by Tukey’s post hoc test; N = 3).

Article Snippet: Antibodies for YY1 (sc-7341), HDAC1 (sc-81598), HDAC3 (sc-376957), β-actin (sc-47778), and histone H4 (sc-25260) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA).

Techniques: Phospho-proteomics, Immunoprecipitation, Western Blot, Control

Fig. 4. Mn-induced YY1 phosphorylation via AurkB and CK2 increases YY1 binding to the EAAT2 promoter in H4 astrocytes. (A) Astrocytes were pre-treated with Hesp (250 nM, 1 h) and exposed to Mn (250 mM, 6 h), then cells were fractionated and the DAPA assay was performed to assess YY1 binding to the EAAT2 promoter. (B) Astrocytes were treated with Hesp and Mn for the indicated time periods, followed by the ChIP assay to assess YY1 binding to EAAT2 promoter. (C) Astrocytes were pre-treated with CX (10 mM,1 h) and exposed to Mn (250 mM, 6 h), then cells were fractionated and the DAPA assay was performed. (D) Astrocytes were treated with CX and Mn for the indicated time periods and the ChIP assay was performed. (*p < 0.05, **p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).

Journal: Toxicology letters

Article Title: Manganese phosphorylates Yin Yang 1 at serine residues to repress EAAT2 in human H4 astrocytes.

doi: 10.1016/j.toxlet.2021.11.007

Figure Lengend Snippet: Fig. 4. Mn-induced YY1 phosphorylation via AurkB and CK2 increases YY1 binding to the EAAT2 promoter in H4 astrocytes. (A) Astrocytes were pre-treated with Hesp (250 nM, 1 h) and exposed to Mn (250 mM, 6 h), then cells were fractionated and the DAPA assay was performed to assess YY1 binding to the EAAT2 promoter. (B) Astrocytes were treated with Hesp and Mn for the indicated time periods, followed by the ChIP assay to assess YY1 binding to EAAT2 promoter. (C) Astrocytes were pre-treated with CX (10 mM,1 h) and exposed to Mn (250 mM, 6 h), then cells were fractionated and the DAPA assay was performed. (D) Astrocytes were treated with CX and Mn for the indicated time periods and the ChIP assay was performed. (*p < 0.05, **p < 0.01, ***p < 0.001, compared to the control; #p < 0.05, ##p < 0.01, ANOVA followed by Tukey’s post hoc test; N = 3).

Article Snippet: Antibodies for YY1 (sc-7341), HDAC1 (sc-81598), HDAC3 (sc-376957), β-actin (sc-47778), and histone H4 (sc-25260) were obtained from Santa Cruz Biotechnology (Santa Cruz, CA).

Techniques: Phospho-proteomics, Binding Assay, Control

Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).

Journal: Cancer letters

Article Title: Macroautophagy/autophagy promotes resistance to KRAS G12D -targeted therapy through glutathione synthesis.

doi: 10.1016/j.canlet.2024.217258

Figure Lengend Snippet: Fig. 6. The combination of chloroquine and MRTX1133 induces histone-dependent immunogenic cell death to suppress tumor growth in immunocom petent mice. (A) A schematic diagram illustrating the experimental setup involving the subcutaneous implantation of the mouse KPC cell line in immunocompetent C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice were administered either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week) under conditions with or without chloroquine (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (B) Tumor growth curves of KPC cells implanted subcutaneously into C57BL6/J mice (n = 5 mice/group; *P < 0.05, two-way ANOVA test; data are presented as means ± SD). (C–F) The analysis included the quantification of cleaved CASP3 (C-CASP3) in isolated tumors, alongside measurements of serum H3 and H4 levels, as well as CD8+ T cell populations within isolated tumors at day 21 post-treatment in mice (n = 5 mice/group; *P < 0.05, one-way ANOVA with Tukey’s multiple comparisons test; data are presented as mean ± SD). (G) A schematic diagram illustrating the experimental setup involving the orthotopic implantation of KPC cells in C57BL6/J mice, followed by a 3-week treatment protocol. During this period, the mice received either a vehicle or MRTX1133 (10 mg/kg/i.p., twice daily, 5 days per week), under conditions with or without CQ (25 mg/kg/i.p., once daily, 5 days per week), GSH-MEE (10 mg/kg/p.o., once daily, 5 days per week) and/or anti-H3/H4 antibodies (10 mg/kg/mice/i.p., day 10, 13, 17, 20, and 27). (H) Survival curves of the indicated mice treated with vehicle or MRTX1133 in the absence or presence of CQ, GSH-MEE and/or anti-H3/H4 antibodies (n = 10 mice/group; *P < 0.05, log-rank tests).

Article Snippet: Antibodies to MAP1LC3B (2775 and 3868), p-MTOR (S2448; 2971), cleaved CASP3 (9664), ATG5 (12994), BECN1 (3495), CYCS (4280), TUBB (2128), TOMM20 (42406), ACTB (4970), histone H3 (14269), and histone H4 (2935) were obtained from Cell Signaling Technology.

Techniques: Isolation

FIGURE 1. 15-LOX-1 promoter histone acetylation and 15-LOX-1 transcriptional activation. A and B, effects of depsipeptide on acetylation of histones H3 and H4 in the 15-LOX-1 promoter. Caco-2 (A) and SW480 (B) cells were treated with depsipeptide (5 nM) or the vehicle solvent for depsipeptide (control). The cells were harvested 48 h after treatment and subjected to ChIP assays using specific antibodies against acetylated histone H3 (H3) or acetylated histone H4 (H4). and indicate immunoprecipitation with and without H3 or H4 antibodies, respectively, and Input indicates total DNA before immunoprecipitation. Depsipeptide induced H3 and H4 acetylation in the 15-LOX-1 promoter. C, kinetics of effects of depsipeptide on H3 acetylation. Caco-2 cells were treated with depsipeptide (5 nM), harvested at the indicated times, and subjected to ChIP/real-time PCR assays using specific acetylated H3 antibodies. The results are percentages of the respective input genomic DNA for the 15-LOX-1 promoter. The values are the means S.D. of triplicate measurements. D, effects of depsipeptide on 15-LOX-1 expression in colorectal cancer cells. Colorectal cancer cells were treated with either depsipeptide (5 nM) or solvent (control). The cells were harvested 24 h later and processed for 15-LOX-1 mRNA by real-time reverse transcription-PCR. The data are presented as the difference in 15-LOX-1 relative expression levels between depsipeptide- and control-treated cells. The values shown are the means S.D. of triplicate experiments. E, effects of SAHA on 15-LOX-1 expression in colorectal cancer cells. Colorectal cancer cells were treated with either SAHA (1 M) or solvent (control) and processed for 15-LOX-1 mRNA measurements as in D. The values shown are the means S.D. of triplicate experiments. F and G, effects of depsipeptide and SAHA on H3 acetylation in the 15-LOX-1 promoter. Colorectal cancer cells were treated with depsipeptide (F), SAHA (G), or solvent only (control). The cells were harvested and subjected to ChIP/real-time PCR using specific antibodies against acetylated histone H3. The data are presented as the difference in the H3 acetylation levels in the 15-LOX-1 promoter between depsipeptide- or SAHA-treated and control-treated cells. The values shown are the means S.D. of triplicate experiments. H and I, correlation between 15-LOX-1 expression and H3 acetylation in the 15-LOX-1 promoter in colorectal cancer cell lines. Scatter plots of the differences in 15-LOX-1 mRNA expression (treated control) in relation to those in 15-LOX-1 promoter H3 acetylation levels (treated control) in colorectal cancer cell lines treated with depsipeptide (H) or SAHA (I). The values shown are the means S.D. of triplicate experiments.

Journal: Journal of Biological Chemistry

Article Title: Chromatin Modification Requirements for 15-Lipoxygenase-1 Transcriptional Reactivation in Colon Cancer Cells

doi: 10.1074/jbc.m803729200

Figure Lengend Snippet: FIGURE 1. 15-LOX-1 promoter histone acetylation and 15-LOX-1 transcriptional activation. A and B, effects of depsipeptide on acetylation of histones H3 and H4 in the 15-LOX-1 promoter. Caco-2 (A) and SW480 (B) cells were treated with depsipeptide (5 nM) or the vehicle solvent for depsipeptide (control). The cells were harvested 48 h after treatment and subjected to ChIP assays using specific antibodies against acetylated histone H3 (H3) or acetylated histone H4 (H4). and indicate immunoprecipitation with and without H3 or H4 antibodies, respectively, and Input indicates total DNA before immunoprecipitation. Depsipeptide induced H3 and H4 acetylation in the 15-LOX-1 promoter. C, kinetics of effects of depsipeptide on H3 acetylation. Caco-2 cells were treated with depsipeptide (5 nM), harvested at the indicated times, and subjected to ChIP/real-time PCR assays using specific acetylated H3 antibodies. The results are percentages of the respective input genomic DNA for the 15-LOX-1 promoter. The values are the means S.D. of triplicate measurements. D, effects of depsipeptide on 15-LOX-1 expression in colorectal cancer cells. Colorectal cancer cells were treated with either depsipeptide (5 nM) or solvent (control). The cells were harvested 24 h later and processed for 15-LOX-1 mRNA by real-time reverse transcription-PCR. The data are presented as the difference in 15-LOX-1 relative expression levels between depsipeptide- and control-treated cells. The values shown are the means S.D. of triplicate experiments. E, effects of SAHA on 15-LOX-1 expression in colorectal cancer cells. Colorectal cancer cells were treated with either SAHA (1 M) or solvent (control) and processed for 15-LOX-1 mRNA measurements as in D. The values shown are the means S.D. of triplicate experiments. F and G, effects of depsipeptide and SAHA on H3 acetylation in the 15-LOX-1 promoter. Colorectal cancer cells were treated with depsipeptide (F), SAHA (G), or solvent only (control). The cells were harvested and subjected to ChIP/real-time PCR using specific antibodies against acetylated histone H3. The data are presented as the difference in the H3 acetylation levels in the 15-LOX-1 promoter between depsipeptide- or SAHA-treated and control-treated cells. The values shown are the means S.D. of triplicate experiments. H and I, correlation between 15-LOX-1 expression and H3 acetylation in the 15-LOX-1 promoter in colorectal cancer cell lines. Scatter plots of the differences in 15-LOX-1 mRNA expression (treated control) in relation to those in 15-LOX-1 promoter H3 acetylation levels (treated control) in colorectal cancer cell lines treated with depsipeptide (H) or SAHA (I). The values shown are the means S.D. of triplicate experiments.

Article Snippet: Antibodies against acetyl-histone H3, acetyl-histone H4, acetyl-histone H3 lysine 9 (H3K9ac), dimethyl-histone H3 lysine 4 (H3K4me2), monomethyl-histone H3 lysine 9 (H3K9me1), dimethyl-histone H3 lysine 9 (H3K9me2), trimethyl-histone H3 lysine 9 (H3K9me3), dimethyl-histone H3 lysine 27 (H3K27me2), trimethyl-histoneH3 lysine 27 (H3K27me3), and trimethyl-histone H4 lysine 20 (H4K20me3) were purchased fromUpstate Cell Signaling Solutions (Lake Placid, NY).

Techniques: Activation Assay, Solvent, Control, Immunoprecipitation, Real-time Polymerase Chain Reaction, Expressing, Reverse Transcription

FIGURE 2. Effects of KAT3B on 15-LOX-1 promoter histone acetylation and 15-LOX-1 transcriptional activation. A, effects of KAT3B siRNA transfection on KAT3B mRNA expression. Caco-2 cells were transfected with a pool of four siRNA duplexes for KAT3B (KAT3B siRNA), a nonspecific siRNA sequence (Nonspecific siRNA), or transfection medium only (Control) and then treated 24 h later with either depsipeptide (5 nM) or control solvent. The cells were harvested 48 h after transfection. KAT3B mRNA levels were measured by using real-time reverse transcription-PCR. The relative expression levels were calculated as the values relative to those of the calibrator samples (Nonspecific siRNA). B and C, effects of KAT3B knockdown on H3 (B) and H4 (C) acetylation in the 15-LOX-1 promoter. Caco-2 cells were transfected and treated as in A and then subjected to chromatin immunoprecipitation/real-time PCR. The results are presented as percentages of the respective input genomic DNA for the 15-LOX-1 promoter. The values are the means S.D. of triplicate measurements. D, effects of KAT3B knockdown on depsipeptide activation of 15-LOX-1 transcription. Caco-2 cells were transfected and treatedasdescribedinA,and15-LOX-1expressionwasmeasuredbyusingreal-timereversetranscription-PCR. The relative expression levels were calculated as the values relative to those of the calibrator samples (Control). The values shown are the means S.D. of triplicate experiments.

Journal: Journal of Biological Chemistry

Article Title: Chromatin Modification Requirements for 15-Lipoxygenase-1 Transcriptional Reactivation in Colon Cancer Cells

doi: 10.1074/jbc.m803729200

Figure Lengend Snippet: FIGURE 2. Effects of KAT3B on 15-LOX-1 promoter histone acetylation and 15-LOX-1 transcriptional activation. A, effects of KAT3B siRNA transfection on KAT3B mRNA expression. Caco-2 cells were transfected with a pool of four siRNA duplexes for KAT3B (KAT3B siRNA), a nonspecific siRNA sequence (Nonspecific siRNA), or transfection medium only (Control) and then treated 24 h later with either depsipeptide (5 nM) or control solvent. The cells were harvested 48 h after transfection. KAT3B mRNA levels were measured by using real-time reverse transcription-PCR. The relative expression levels were calculated as the values relative to those of the calibrator samples (Nonspecific siRNA). B and C, effects of KAT3B knockdown on H3 (B) and H4 (C) acetylation in the 15-LOX-1 promoter. Caco-2 cells were transfected and treated as in A and then subjected to chromatin immunoprecipitation/real-time PCR. The results are presented as percentages of the respective input genomic DNA for the 15-LOX-1 promoter. The values are the means S.D. of triplicate measurements. D, effects of KAT3B knockdown on depsipeptide activation of 15-LOX-1 transcription. Caco-2 cells were transfected and treatedasdescribedinA,and15-LOX-1expressionwasmeasuredbyusingreal-timereversetranscription-PCR. The relative expression levels were calculated as the values relative to those of the calibrator samples (Control). The values shown are the means S.D. of triplicate experiments.

Article Snippet: Antibodies against acetyl-histone H3, acetyl-histone H4, acetyl-histone H3 lysine 9 (H3K9ac), dimethyl-histone H3 lysine 4 (H3K4me2), monomethyl-histone H3 lysine 9 (H3K9me1), dimethyl-histone H3 lysine 9 (H3K9me2), trimethyl-histone H3 lysine 9 (H3K9me3), dimethyl-histone H3 lysine 27 (H3K27me2), trimethyl-histoneH3 lysine 27 (H3K27me3), and trimethyl-histone H4 lysine 20 (H4K20me3) were purchased fromUpstate Cell Signaling Solutions (Lake Placid, NY).

Techniques: Activation Assay, Transfection, Expressing, Sequencing, Control, Solvent, Reverse Transcription, Knockdown, Chromatin Immunoprecipitation, Real-time Polymerase Chain Reaction

FIGURE 4. Chromatin modification of 15-LOX-1 promoter during transcriptional activation. A, kinetics of depsipeptide effects on dimethyl-histone H3 lysine 4 (H3K4me2) in the 15-LOX-1 promoter. Caco-2 cells were treated with depsipeptide as indicated. ChIP/real-time PCR was performed with the use of specific H3K4me2 or acetylated histone H3 (acetylated H3) antibodies. The results are the means S.D. of four replicate experi- ments. B, effects of depsipeptide on H3 and H4 methylation patterns in the 15-LOX-1 promoter. Caco-2 cells were treated with depsipeptide (5 nM) or solvent control, harvested 30 min later, and processed for ChIP/real- time PCR using anti-H3K9me1, anti-H3K9me2, anti-H3K9me3, anti-H4K20me3, anti-H3K27me2, and anti- H3K27me3antibodies.TheresultsarethemeansS.D.oftriplicateexperiments.CandD,kineticsofdepsipep- tide effects on H3 acetylation and methylation. Caco-2 cells were treated with depsipeptide for the indicated times and processed for ChIP/real-time PCR using antibodies against H3K9me2 (C) and H3K9ac (D). The results are the means S.D. of four replicate experiments.

Journal: Journal of Biological Chemistry

Article Title: Chromatin Modification Requirements for 15-Lipoxygenase-1 Transcriptional Reactivation in Colon Cancer Cells

doi: 10.1074/jbc.m803729200

Figure Lengend Snippet: FIGURE 4. Chromatin modification of 15-LOX-1 promoter during transcriptional activation. A, kinetics of depsipeptide effects on dimethyl-histone H3 lysine 4 (H3K4me2) in the 15-LOX-1 promoter. Caco-2 cells were treated with depsipeptide as indicated. ChIP/real-time PCR was performed with the use of specific H3K4me2 or acetylated histone H3 (acetylated H3) antibodies. The results are the means S.D. of four replicate experi- ments. B, effects of depsipeptide on H3 and H4 methylation patterns in the 15-LOX-1 promoter. Caco-2 cells were treated with depsipeptide (5 nM) or solvent control, harvested 30 min later, and processed for ChIP/real- time PCR using anti-H3K9me1, anti-H3K9me2, anti-H3K9me3, anti-H4K20me3, anti-H3K27me2, and anti- H3K27me3antibodies.TheresultsarethemeansS.D.oftriplicateexperiments.CandD,kineticsofdepsipep- tide effects on H3 acetylation and methylation. Caco-2 cells were treated with depsipeptide for the indicated times and processed for ChIP/real-time PCR using antibodies against H3K9me2 (C) and H3K9ac (D). The results are the means S.D. of four replicate experiments.

Article Snippet: Antibodies against acetyl-histone H3, acetyl-histone H4, acetyl-histone H3 lysine 9 (H3K9ac), dimethyl-histone H3 lysine 4 (H3K4me2), monomethyl-histone H3 lysine 9 (H3K9me1), dimethyl-histone H3 lysine 9 (H3K9me2), trimethyl-histone H3 lysine 9 (H3K9me3), dimethyl-histone H3 lysine 27 (H3K27me2), trimethyl-histoneH3 lysine 27 (H3K27me3), and trimethyl-histone H4 lysine 20 (H4K20me3) were purchased fromUpstate Cell Signaling Solutions (Lake Placid, NY).

Techniques: Modification, Activation Assay, Real-time Polymerase Chain Reaction, Methylation, Solvent, Control