pgex-kg Search Results


pgex kg  (ATCC)
94
ATCC pgex kg
Pgex Kg, supplied by ATCC, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pGEX-KG/pm12921744-69-22-23
Average 94 stars, based on 1 article reviews
pgex kg - by Bioz Stars, 2026-10
94/100 stars
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pgex kg d4h mcherry  (Addgene inc)
93
Addgene inc pgex kg d4h mcherry
(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 <t>GST-D4H*–mCherry.</t> 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.
Pgex Kg D4h Mcherry, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pGEX-KG-D4H*-mCherry+(Plasmid+%23134604)/bio_rxiv__2025__03__31__646397-124-0-17
Average 93 stars, based on 1 article reviews
pgex kg d4h mcherry - by Bioz Stars, 2026-10
93/100 stars
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truncation mutant  (Addgene inc)
91
Addgene inc truncation mutant
(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 <t>GST-D4H*–mCherry.</t> 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.
Truncation Mutant, supplied by Addgene inc, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pGEX-KG-MmUbc6%2F2790+(Plasmid+%2311491)/pmc04850058-176-7-33
Average 91 stars, based on 1 article reviews
truncation mutant - by Bioz Stars, 2026-10
91/100 stars
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pgex kg gst yap construct  (Addgene inc)
93
Addgene inc pgex kg gst yap construct
(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 <t>GST-D4H*–mCherry.</t> 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.
Pgex Kg Gst Yap Construct, supplied by Addgene inc, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pGEX-KG-GST-YAP+(Plasmid+%2333052)/pmc05007193-188-12-14
Average 93 stars, based on 1 article reviews
pgex kg gst yap construct - by Bioz Stars, 2026-10
93/100 stars
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mers cov strain nrce hku270  (ATCC)
92
ATCC mers cov strain nrce hku270
(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 <t>GST-D4H*–mCherry.</t> 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.
Mers Cov Strain Nrce Hku270, supplied by ATCC, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pGEX-KG+plasmid%3B+in+E%2E+coli/pmc11367708-86-10-27
Average 92 stars, based on 1 article reviews
mers cov strain nrce hku270 - by Bioz Stars, 2026-10
92/100 stars
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pcdna3 3topo t7 hcas9  (Addgene inc)
91
Addgene inc pcdna3 3topo t7 hcas9
(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 <t>GST-D4H*–mCherry.</t> 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.
Pcdna3 3topo T7 Hcas9, supplied by Addgene inc, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pGEX-KG-GST-YAP+(Plasmid+%2338105)/pmc07757410-459-23-41
Average 91 stars, based on 1 article reviews
pcdna3 3topo t7 hcas9 - by Bioz Stars, 2026-10
91/100 stars
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pgex kg backbone  (Addgene inc)
92
Addgene inc pgex kg backbone
(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 <t>GST-D4H*–mCherry.</t> 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.
Pgex Kg Backbone, supplied by Addgene inc, used in various techniques. Bioz Stars score: 92/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pGEX-KG%2FNet1A+(Plasmid+%2328261)/pm37098770__ja3c01145_si_001-63-23-25
Average 92 stars, based on 1 article reviews
pgex kg backbone - by Bioz Stars, 2026-10
92/100 stars
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pgex-kg-vdr-l1  (Promega)
90
Promega pgex-kg-vdr-l1
(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 <t>GST-D4H*–mCherry.</t> 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.
Pgex Kg Vdr L1, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pgex+kg+vdr+l1/pmc06616526-45-3-29
Average 90 stars, based on 1 article reviews
pgex-kg-vdr-l1 - by Bioz Stars, 2026-10
90/100 stars
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pgexkg  (Promega)
90
Promega pgexkg
(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 <t>GST-D4H*–mCherry.</t> 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.
Pgexkg, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pgexkg/pmc00087335-90-26-27
Average 90 stars, based on 1 article reviews
pgexkg - by Bioz Stars, 2026-10
90/100 stars
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pgex-kg-vdr-l  (Promega)
90
Promega pgex-kg-vdr-l
(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 <t>GST-D4H*–mCherry.</t> 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.
Pgex Kg Vdr L, supplied by Promega, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pgex+kg+vdr+l/pmc06616526-45-1-29
Average 90 stars, based on 1 article reviews
pgex-kg-vdr-l - by Bioz Stars, 2026-10
90/100 stars
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pgex-kg/yyh1311079 expression plasmid  (HuiDa RC International Inc)
90
HuiDa RC International Inc pgex-kg/yyh1311079 expression plasmid
(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 <t>GST-D4H*–mCherry.</t> 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.
Pgex Kg/Yyh1311079 Expression Plasmid, supplied by HuiDa RC International Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/pgex-kg/pgex+kg+yyh1311079+expression+plasmid/pmc05395790-381-4-12
Average 90 stars, based on 1 article reviews
pgex-kg/yyh1311079 expression plasmid - by Bioz Stars, 2026-10
90/100 stars
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mutagenesis  (Eli Lilly)
86
Eli Lilly mutagenesis
(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 <t>GST-D4H*–mCherry.</t> 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.
Mutagenesis, supplied by Eli Lilly, 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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(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: pGEX-KG-D4H*-mCherry (#134604) and the lentiviral vectors; pLJM1-FLAG-GFP-OSBP (#134659), pLenti-EGFP-P4M-SidMx2 (#136997) and pLenti-EGFP-2xFYVE (#136996) were all obtained from Addgene.

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