pan caspase inhibitor cas Search Results


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A) Schematic illustrating PP2A reactivation predisposed to MKI-induced SL in GB. B) Representative images of colony formation assay in T98G cells under PME-1 deletion (siRNA or CRISPR/Cas9) or NZ-8-061 treatment. Cells were treated with 25 nM UCN-01 (UCN) or left untreated (NT). Immunoblot analysis of PME-1 (lower panel). C) Viability of T98G cells treated with increasing concentration of NZ-8-061 either alone or in combination with 25 nM UCN-01 (UCN) for 72 h. ***P<0.001, Student’s t -test. D) Synergy plot showing the most synergistic area (yellow box) between NZ-8-061 and UCN-01 in T98G cells. The Bliss synergy score is calculated over the whole dose-response matrix. E) Viability of T98G wt and SV40 small t-antigen-expressing (T98G-ST) cells treated with 25 nM UCN-01 (UCN) and 8 µM NZ-8-061, alone or in combination for 72 h. Immunoblot analysis of SV40 small t-antigen (right panel). **P<0.01, ***P<0.001 Student’s t -test. F) <t>Caspase</t> 3/7 activity in T98G cells treated with 8 µM NZ-8-061 alone or in combination with 25 nM UCN-01 (UCN) under caspase inhibitor <t>Z-VAD-FMK</t> (20 µM) for 24 h. ***P<0.001, Student’s t -test. G) Structures of two different classes of SMAPs. H) Viability of T98G cells treated SMAPs, 10 µM DBK-794 and 5 µM DBK-1154, alone or in combination with 25 nM UCN-01 (UCN) for 72 h. **P<0.01, ***P<0.001, Student’s t -test. I) Representative images (left) and quantified data of colony formation assay (right) in U251, U118, A172 and U87MG cells treated with 8 µM NZ-8-061 alone or in combination with UCN-01 (UCN; 200 nM, 25 nM, 50 nM and 500 nM, respectively). n=2 independent experiments, *P<0.05, **P<0.01, ***P<0.001, Student’s t -test.
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A) Schematic illustrating PP2A reactivation predisposed to MKI-induced SL in GB. B) Representative images of colony formation assay in T98G cells under PME-1 deletion (siRNA or CRISPR/Cas9) or NZ-8-061 treatment. Cells were treated with 25 nM UCN-01 (UCN) or left untreated (NT). Immunoblot analysis of PME-1 (lower panel). C) Viability of T98G cells treated with increasing concentration of NZ-8-061 either alone or in combination with 25 nM UCN-01 (UCN) for 72 h. ***P<0.001, Student’s t -test. D) Synergy plot showing the most synergistic area (yellow box) between NZ-8-061 and UCN-01 in T98G cells. The Bliss synergy score is calculated over the whole dose-response matrix. E) Viability of T98G wt and SV40 small t-antigen-expressing (T98G-ST) cells treated with 25 nM UCN-01 (UCN) and 8 µM NZ-8-061, alone or in combination for 72 h. Immunoblot analysis of SV40 small t-antigen (right panel). **P<0.01, ***P<0.001 Student’s t -test. F) <t>Caspase</t> 3/7 activity in T98G cells treated with 8 µM NZ-8-061 alone or in combination with 25 nM UCN-01 (UCN) under caspase inhibitor <t>Z-VAD-FMK</t> (20 µM) for 24 h. ***P<0.001, Student’s t -test. G) Structures of two different classes of SMAPs. H) Viability of T98G cells treated SMAPs, 10 µM DBK-794 and 5 µM DBK-1154, alone or in combination with 25 nM UCN-01 (UCN) for 72 h. **P<0.01, ***P<0.001, Student’s t -test. I) Representative images (left) and quantified data of colony formation assay (right) in U251, U118, A172 and U87MG cells treated with 8 µM NZ-8-061 alone or in combination with UCN-01 (UCN; 200 nM, 25 nM, 50 nM and 500 nM, respectively). n=2 independent experiments, *P<0.05, **P<0.01, ***P<0.001, Student’s t -test.
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InvivoGen pan caspase inhibitor z vad fmk
A) Schematic illustrating PP2A reactivation predisposed to MKI-induced SL in GB. B) Representative images of colony formation assay in T98G cells under PME-1 deletion (siRNA or CRISPR/Cas9) or NZ-8-061 treatment. Cells were treated with 25 nM UCN-01 (UCN) or left untreated (NT). Immunoblot analysis of PME-1 (lower panel). C) Viability of T98G cells treated with increasing concentration of NZ-8-061 either alone or in combination with 25 nM UCN-01 (UCN) for 72 h. ***P<0.001, Student’s t -test. D) Synergy plot showing the most synergistic area (yellow box) between NZ-8-061 and UCN-01 in T98G cells. The Bliss synergy score is calculated over the whole dose-response matrix. E) Viability of T98G wt and SV40 small t-antigen-expressing (T98G-ST) cells treated with 25 nM UCN-01 (UCN) and 8 µM NZ-8-061, alone or in combination for 72 h. Immunoblot analysis of SV40 small t-antigen (right panel). **P<0.01, ***P<0.001 Student’s t -test. F) <t>Caspase</t> 3/7 activity in T98G cells treated with 8 µM NZ-8-061 alone or in combination with 25 nM UCN-01 (UCN) under caspase inhibitor <t>Z-VAD-FMK</t> (20 µM) for 24 h. ***P<0.001, Student’s t -test. G) Structures of two different classes of SMAPs. H) Viability of T98G cells treated SMAPs, 10 µM DBK-794 and 5 µM DBK-1154, alone or in combination with 25 nM UCN-01 (UCN) for 72 h. **P<0.01, ***P<0.001, Student’s t -test. I) Representative images (left) and quantified data of colony formation assay (right) in U251, U118, A172 and U87MG cells treated with 8 µM NZ-8-061 alone or in combination with UCN-01 (UCN; 200 nM, 25 nM, 50 nM and 500 nM, respectively). n=2 independent experiments, *P<0.05, **P<0.01, ***P<0.001, Student’s t -test.
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A) Schematic illustrating PP2A reactivation predisposed to MKI-induced SL in GB. B) Representative images of colony formation assay in T98G cells under PME-1 deletion (siRNA or CRISPR/Cas9) or NZ-8-061 treatment. Cells were treated with 25 nM UCN-01 (UCN) or left untreated (NT). Immunoblot analysis of PME-1 (lower panel). C) Viability of T98G cells treated with increasing concentration of NZ-8-061 either alone or in combination with 25 nM UCN-01 (UCN) for 72 h. ***P<0.001, Student’s t -test. D) Synergy plot showing the most synergistic area (yellow box) between NZ-8-061 and UCN-01 in T98G cells. The Bliss synergy score is calculated over the whole dose-response matrix. E) Viability of T98G wt and SV40 small t-antigen-expressing (T98G-ST) cells treated with 25 nM UCN-01 (UCN) and 8 µM NZ-8-061, alone or in combination for 72 h. Immunoblot analysis of SV40 small t-antigen (right panel). **P<0.01, ***P<0.001 Student’s t -test. F) <t>Caspase</t> 3/7 activity in T98G cells treated with 8 µM NZ-8-061 alone or in combination with 25 nM UCN-01 (UCN) under caspase inhibitor <t>Z-VAD-FMK</t> (20 µM) for 24 h. ***P<0.001, Student’s t -test. G) Structures of two different classes of SMAPs. H) Viability of T98G cells treated SMAPs, 10 µM DBK-794 and 5 µM DBK-1154, alone or in combination with 25 nM UCN-01 (UCN) for 72 h. **P<0.01, ***P<0.001, Student’s t -test. I) Representative images (left) and quantified data of colony formation assay (right) in U251, U118, A172 and U87MG cells treated with 8 µM NZ-8-061 alone or in combination with UCN-01 (UCN; 200 nM, 25 nM, 50 nM and 500 nM, respectively). n=2 independent experiments, *P<0.05, **P<0.01, ***P<0.001, Student’s t -test.
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A) Schematic illustrating PP2A reactivation predisposed to MKI-induced SL in GB. B) Representative images of colony formation assay in T98G cells under PME-1 deletion (siRNA or CRISPR/Cas9) or NZ-8-061 treatment. Cells were treated with 25 nM UCN-01 (UCN) or left untreated (NT). Immunoblot analysis of PME-1 (lower panel). C) Viability of T98G cells treated with increasing concentration of NZ-8-061 either alone or in combination with 25 nM UCN-01 (UCN) for 72 h. ***P<0.001, Student’s t -test. D) Synergy plot showing the most synergistic area (yellow box) between NZ-8-061 and UCN-01 in T98G cells. The Bliss synergy score is calculated over the whole dose-response matrix. E) Viability of T98G wt and SV40 small t-antigen-expressing (T98G-ST) cells treated with 25 nM UCN-01 (UCN) and 8 µM NZ-8-061, alone or in combination for 72 h. Immunoblot analysis of SV40 small t-antigen (right panel). **P<0.01, ***P<0.001 Student’s t -test. F) <t>Caspase</t> 3/7 activity in T98G cells treated with 8 µM NZ-8-061 alone or in combination with 25 nM UCN-01 (UCN) under caspase inhibitor <t>Z-VAD-FMK</t> (20 µM) for 24 h. ***P<0.001, Student’s t -test. G) Structures of two different classes of SMAPs. H) Viability of T98G cells treated SMAPs, 10 µM DBK-794 and 5 µM DBK-1154, alone or in combination with 25 nM UCN-01 (UCN) for 72 h. **P<0.01, ***P<0.001, Student’s t -test. I) Representative images (left) and quantified data of colony formation assay (right) in U251, U118, A172 and U87MG cells treated with 8 µM NZ-8-061 alone or in combination with UCN-01 (UCN; 200 nM, 25 nM, 50 nM and 500 nM, respectively). n=2 independent experiments, *P<0.05, **P<0.01, ***P<0.001, Student’s t -test.
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A) Schematic illustrating PP2A reactivation predisposed to MKI-induced SL in GB. B) Representative images of colony formation assay in T98G cells under PME-1 deletion (siRNA or CRISPR/Cas9) or NZ-8-061 treatment. Cells were treated with 25 nM UCN-01 (UCN) or left untreated (NT). Immunoblot analysis of PME-1 (lower panel). C) Viability of T98G cells treated with increasing concentration of NZ-8-061 either alone or in combination with 25 nM UCN-01 (UCN) for 72 h. ***P<0.001, Student’s t -test. D) Synergy plot showing the most synergistic area (yellow box) between NZ-8-061 and UCN-01 in T98G cells. The Bliss synergy score is calculated over the whole dose-response matrix. E) Viability of T98G wt and SV40 small t-antigen-expressing (T98G-ST) cells treated with 25 nM UCN-01 (UCN) and 8 µM NZ-8-061, alone or in combination for 72 h. Immunoblot analysis of SV40 small t-antigen (right panel). **P<0.01, ***P<0.001 Student’s t -test. F) <t>Caspase</t> 3/7 activity in T98G cells treated with 8 µM NZ-8-061 alone or in combination with 25 nM UCN-01 (UCN) under caspase inhibitor <t>Z-VAD-FMK</t> (20 µM) for 24 h. ***P<0.001, Student’s t -test. G) Structures of two different classes of SMAPs. H) Viability of T98G cells treated SMAPs, 10 µM DBK-794 and 5 µM DBK-1154, alone or in combination with 25 nM UCN-01 (UCN) for 72 h. **P<0.01, ***P<0.001, Student’s t -test. I) Representative images (left) and quantified data of colony formation assay (right) in U251, U118, A172 and U87MG cells treated with 8 µM NZ-8-061 alone or in combination with UCN-01 (UCN; 200 nM, 25 nM, 50 nM and 500 nM, respectively). n=2 independent experiments, *P<0.05, **P<0.01, ***P<0.001, Student’s t -test.
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Image Search Results


A) Schematic illustrating PP2A reactivation predisposed to MKI-induced SL in GB. B) Representative images of colony formation assay in T98G cells under PME-1 deletion (siRNA or CRISPR/Cas9) or NZ-8-061 treatment. Cells were treated with 25 nM UCN-01 (UCN) or left untreated (NT). Immunoblot analysis of PME-1 (lower panel). C) Viability of T98G cells treated with increasing concentration of NZ-8-061 either alone or in combination with 25 nM UCN-01 (UCN) for 72 h. ***P<0.001, Student’s t -test. D) Synergy plot showing the most synergistic area (yellow box) between NZ-8-061 and UCN-01 in T98G cells. The Bliss synergy score is calculated over the whole dose-response matrix. E) Viability of T98G wt and SV40 small t-antigen-expressing (T98G-ST) cells treated with 25 nM UCN-01 (UCN) and 8 µM NZ-8-061, alone or in combination for 72 h. Immunoblot analysis of SV40 small t-antigen (right panel). **P<0.01, ***P<0.001 Student’s t -test. F) Caspase 3/7 activity in T98G cells treated with 8 µM NZ-8-061 alone or in combination with 25 nM UCN-01 (UCN) under caspase inhibitor Z-VAD-FMK (20 µM) for 24 h. ***P<0.001, Student’s t -test. G) Structures of two different classes of SMAPs. H) Viability of T98G cells treated SMAPs, 10 µM DBK-794 and 5 µM DBK-1154, alone or in combination with 25 nM UCN-01 (UCN) for 72 h. **P<0.01, ***P<0.001, Student’s t -test. I) Representative images (left) and quantified data of colony formation assay (right) in U251, U118, A172 and U87MG cells treated with 8 µM NZ-8-061 alone or in combination with UCN-01 (UCN; 200 nM, 25 nM, 50 nM and 500 nM, respectively). n=2 independent experiments, *P<0.05, **P<0.01, ***P<0.001, Student’s t -test.

Journal: bioRxiv

Article Title: Pharmacological PP2A reactivation overcomes multikinase inhibitor tolerance across brain tumor cell models

doi: 10.1101/2022.05.31.494146

Figure Lengend Snippet: A) Schematic illustrating PP2A reactivation predisposed to MKI-induced SL in GB. B) Representative images of colony formation assay in T98G cells under PME-1 deletion (siRNA or CRISPR/Cas9) or NZ-8-061 treatment. Cells were treated with 25 nM UCN-01 (UCN) or left untreated (NT). Immunoblot analysis of PME-1 (lower panel). C) Viability of T98G cells treated with increasing concentration of NZ-8-061 either alone or in combination with 25 nM UCN-01 (UCN) for 72 h. ***P<0.001, Student’s t -test. D) Synergy plot showing the most synergistic area (yellow box) between NZ-8-061 and UCN-01 in T98G cells. The Bliss synergy score is calculated over the whole dose-response matrix. E) Viability of T98G wt and SV40 small t-antigen-expressing (T98G-ST) cells treated with 25 nM UCN-01 (UCN) and 8 µM NZ-8-061, alone or in combination for 72 h. Immunoblot analysis of SV40 small t-antigen (right panel). **P<0.01, ***P<0.001 Student’s t -test. F) Caspase 3/7 activity in T98G cells treated with 8 µM NZ-8-061 alone or in combination with 25 nM UCN-01 (UCN) under caspase inhibitor Z-VAD-FMK (20 µM) for 24 h. ***P<0.001, Student’s t -test. G) Structures of two different classes of SMAPs. H) Viability of T98G cells treated SMAPs, 10 µM DBK-794 and 5 µM DBK-1154, alone or in combination with 25 nM UCN-01 (UCN) for 72 h. **P<0.01, ***P<0.001, Student’s t -test. I) Representative images (left) and quantified data of colony formation assay (right) in U251, U118, A172 and U87MG cells treated with 8 µM NZ-8-061 alone or in combination with UCN-01 (UCN; 200 nM, 25 nM, 50 nM and 500 nM, respectively). n=2 independent experiments, *P<0.05, **P<0.01, ***P<0.001, Student’s t -test.

Article Snippet: After 24 hours, cells were treated with the indicated drugs in combination with pan-caspase inhibitor Z-VAD-FMK (10 mM, Promega).

Techniques: Colony Assay, CRISPR, Western Blot, Concentration Assay, Expressing, Activity Assay