pe cy7 conjugated rabbit anti ps6 ser235 ser236 antibody Search Results


phospho-erk  (Cell Signaling Technology Inc)
90
Cell Signaling Technology Inc phospho-erk
Phospho Erk, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti phospho s6  (Cell Signaling Technology Inc)
98
Cell Signaling Technology Inc anti phospho s6
Anti Phospho S6, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Average 98 stars, based on 1 article reviews
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phospho s6 ser235 236  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc phospho s6 ser235 236
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Phospho S6 Ser235 236, 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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phospho s6 ser235 236 - by Bioz Stars, 2026-03
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protein s6  (Cell Signaling Technology Inc)
98
Cell Signaling Technology Inc protein s6
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Protein S6, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 98/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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rps6  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc rps6
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Rps6, supplied by Cell Signaling Technology Inc, 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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anti phospho s6 ribosomal protein mab  (Cell Signaling Technology Inc)
93
Cell Signaling Technology Inc anti phospho s6 ribosomal protein mab
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Anti Phospho S6 Ribosomal Protein Mab, supplied by Cell Signaling Technology Inc, 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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loading controls  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc loading controls
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Loading Controls, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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anti phospho s6 ribosomal protein  (Cell Signaling Technology Inc)
97
Cell Signaling Technology Inc anti phospho s6 ribosomal protein
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Anti Phospho S6 Ribosomal Protein, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 97/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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phospho s6 p s6 ser235 236  (Cell Signaling Technology Inc)
96
Cell Signaling Technology Inc phospho s6 p s6 ser235 236
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Phospho S6 P S6 Ser235 236, 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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mouse santa cruz sc 47778 wb prps6 ps6rp  (Cell Signaling Technology Inc)
94
Cell Signaling Technology Inc mouse santa cruz sc 47778 wb prps6 ps6rp
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Mouse Santa Cruz Sc 47778 Wb Prps6 Ps6rp, supplied by Cell Signaling Technology Inc, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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pe anti human p s6k  (Thermo Fisher)
86
Thermo Fisher pe anti human p s6k
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Pe Anti Human P S6k, supplied by Thermo Fisher, 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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phospho s6rp  (Santa Cruz Biotechnology)
93
Santa Cruz Biotechnology phospho s6rp
(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 <t>(Ser235/236)</t> and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Phospho S6rp, supplied by Santa Cruz Biotechnology, 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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Image Search Results


(A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 (Ser235/236) and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Journal: bioRxiv

Article Title: Senescent cell survival relies on upregulation of lysosomal quality control mechanisms

doi: 10.1101/2025.03.31.646397

Figure Lengend Snippet: (A) Representative immunoblot analysis of dose-dependent activation of mTORC1 by LDL in proliferative or senescent cells. IMR90 ER:RasV12 primary fibroblasts were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were depleted of sterol with methyl-β cyclodextrin (MCD, 0.5% w/v) for 2 hours and then stimulated for 2 hours with increasing concentrations (0 to 100 μg/ml) of low-density lipoprotein (LDL). Cell lysates were analysed for phosphorylation of S6 (Ser235/236) and ULK1 (Ser757). (B) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (C) Representative immunoblot analysis of activation of mTORC1 signalling by cholesterol. Proliferative or senescent cells were treated as stated in (A), however stimulated for 2 hours with increasing concentrations (0 to 100 μM) of MCD:cholesterol. (D) Phosphorylation of S6 (Ser235/236) was quantified as in (B). (E) Proliferating or senescent cells were fixed, permeabilised using a liquid-nitrogen pulse and subjected to cholesterol labelling by GST-D4H*–mCherry. Scale bar, 10 μm. The quantification of D4H*–mCherry signal intensity is shown in (F). The quantification represents the mean intensity ± SEM compared by Student’s t test (unpaired); n = 3 independent experiments with at least 5 fields of view per experimental repeat. (G) Proliferative or senescent cells were fixed and immunostained for antibodies against LDLR (green) and LAMP2 (magenta), scale bar, 20 μm. (H) Colocalisation analysis of endogenous LDLR and LAMP2. The graph represents means ± SEM. Pearson’s correlation; n = 3 independent experiments with ≥ 6 fields of view per experimental repeat. Student’s t test (unpaired). (I) Proliferating and senescent cells were surface biotinylated, and streptavidin agarose was used to capture biotinylated membrane proteins. Surface abundance of the indicated proteins was assessed by immunoblotting. (J) The quantification shows the mean ± SEM surface levels in senescent cells presented relative to proliferating cells (dashed line); n = 2 independent experiments for LDLR n = 4 independent experiments for CD36. *, P < 0.05; **, P < 0.01; ***, P < 0.001.

Article Snippet: The following primary antibodies were used: mouse monoclonal antibodies raised against Lamp1 (H4A3, DSHB, 1:2000), PI4K2A (sc-390026, Santa Cruz, 1:2000), β-Actin (8H10D10, 3700, Cell Signalling Technology, 1:5000), GAPDH (D4C6R, 97166, Cell Signalling Technology, 1:2000), integrin beta 1/CD29 (610467, BD Biosciences, 1:2000), transferrin receptor/CD71 (3B8 2A1, sc-32272, Santa Cruz, 1:1000), GFP (7.1/13.1, Roche, 11814460001, 1:2000), rabbit monoclonal antibodies raised against cathepsin B (D1C7Y, 31718, Cell Signalling Technology, 1:2000), CI-MPR (EPR6599, 124767, Abcam, 1:2000), Lamp1 (D2D11 9091, Cell Signalling Technology, 1:2000), phospho-S6 Ser235/236 (4856, Cell Signaling Technology, 1:2000), S6 (2217, Cell Signaling Technology, 1:1000), phospho-ULK1 Ser757 (D7O6U, 14202, Cell Signaling Technology, 1:1000), ULK1 (D8H5, 8054, Cell Signaling Technology, 1:1000), integrin alpha 5 (EPR7854, ab150361, Abcam, 1:2000), rabbit polyclonal antibodies raised against PI4K2A (15318-1-AP, Proteintech, 1:1000), LDLR (10785-1-AP, Proteintech, 1:2000), CD36 (18836-1-AP, Proteintech, 1:1000), VAPA (15275-1-AP, Proteintech, 1:2000).

Techniques: Western Blot, Activation Assay, Cell Culture, Expressing, Comparison, Membrane

(A) IMR90 ER:RasV12 primary fibroblasts expressing GFP-OSBP were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were fixed and immunostained with an antibody against LAMP2 (magenta), scale bar, 10 μm. (B) The number of GFP-OSBP puncta (defined as 0.5-0.05 μm 3 ) per cell were plotted as mean ± SEM, n = 2 independent experiments with at least 14 cells per experimental repeat. (C) Proliferating and senescent cells were serum starved overnight, then treated with DMSO or OSW-1 for 4 hours and incubated with EBSS or stimulated with complete media (DMEM) for the last hour of treatment. Cell lysate were analysed for phosphorylation of S6 (Ser235/236) (D) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (E) and (F) DRAQ7 intensity measured by flow cytometry reported the death of proliferating (E) and senescent (F) following 4 hours treatment with DMSO or 50 nM OSW-1. (G) Proliferating and senescent cell viability was measured (% DRAQ7 negative cells) following 4 hours treatment with increasing concentrations (0 to 800 nM) of OSW-1. (H) Cell viability after 4 hours treatment with 50 nM OSW-1 was analysed by two-way ANOVA followed by Šídák’s multiple comparison. Quantification represents mean ± SEM; n = 3 independent experiments. *, P < 0.05; ***, P < 0.001.

Journal: bioRxiv

Article Title: Senescent cell survival relies on upregulation of lysosomal quality control mechanisms

doi: 10.1101/2025.03.31.646397

Figure Lengend Snippet: (A) IMR90 ER:RasV12 primary fibroblasts expressing GFP-OSBP were cultured in the presence of EtOH (Prol; proliferative) or 100 nM 4OHT for 6–8 days to induce RasV12 expression and oncogene-induced senescence (Sen; senescent). Cells were fixed and immunostained with an antibody against LAMP2 (magenta), scale bar, 10 μm. (B) The number of GFP-OSBP puncta (defined as 0.5-0.05 μm 3 ) per cell were plotted as mean ± SEM, n = 2 independent experiments with at least 14 cells per experimental repeat. (C) Proliferating and senescent cells were serum starved overnight, then treated with DMSO or OSW-1 for 4 hours and incubated with EBSS or stimulated with complete media (DMEM) for the last hour of treatment. Cell lysate were analysed for phosphorylation of S6 (Ser235/236) (D) Quantification represents mean ± SEM; n = 3 independent experiments; two-way ANOVA followed by Dunnett’s multiple comparison. (E) and (F) DRAQ7 intensity measured by flow cytometry reported the death of proliferating (E) and senescent (F) following 4 hours treatment with DMSO or 50 nM OSW-1. (G) Proliferating and senescent cell viability was measured (% DRAQ7 negative cells) following 4 hours treatment with increasing concentrations (0 to 800 nM) of OSW-1. (H) Cell viability after 4 hours treatment with 50 nM OSW-1 was analysed by two-way ANOVA followed by Šídák’s multiple comparison. Quantification represents mean ± SEM; n = 3 independent experiments. *, P < 0.05; ***, P < 0.001.

Article Snippet: The following primary antibodies were used: mouse monoclonal antibodies raised against Lamp1 (H4A3, DSHB, 1:2000), PI4K2A (sc-390026, Santa Cruz, 1:2000), β-Actin (8H10D10, 3700, Cell Signalling Technology, 1:5000), GAPDH (D4C6R, 97166, Cell Signalling Technology, 1:2000), integrin beta 1/CD29 (610467, BD Biosciences, 1:2000), transferrin receptor/CD71 (3B8 2A1, sc-32272, Santa Cruz, 1:1000), GFP (7.1/13.1, Roche, 11814460001, 1:2000), rabbit monoclonal antibodies raised against cathepsin B (D1C7Y, 31718, Cell Signalling Technology, 1:2000), CI-MPR (EPR6599, 124767, Abcam, 1:2000), Lamp1 (D2D11 9091, Cell Signalling Technology, 1:2000), phospho-S6 Ser235/236 (4856, Cell Signaling Technology, 1:2000), S6 (2217, Cell Signaling Technology, 1:1000), phospho-ULK1 Ser757 (D7O6U, 14202, Cell Signaling Technology, 1:1000), ULK1 (D8H5, 8054, Cell Signaling Technology, 1:1000), integrin alpha 5 (EPR7854, ab150361, Abcam, 1:2000), rabbit polyclonal antibodies raised against PI4K2A (15318-1-AP, Proteintech, 1:1000), LDLR (10785-1-AP, Proteintech, 1:2000), CD36 (18836-1-AP, Proteintech, 1:1000), VAPA (15275-1-AP, Proteintech, 1:2000).

Techniques: Expressing, Cell Culture, Incubation, Comparison, Flow Cytometry