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96
Selleck Chemicals etoposide
The pBcl‐2/Bcl‐2 model predicts the MOMP in response to ABT‐199 or <t>etoposide.</t> (A, B) The experimentally derived CI values for the ABT‐199/paclitaxel combination were plotted against those predicted from the pBcl‐2/Bcl‐2 model, using MDA‐MB‐231 (A) and T49D cells (B), with and without SP600125. Data are the mean ± SD (n = 5). Spearman's correlation (r) and P values are shown. (C, D) Upper panel: Expression of p‐PKCα/β, p‐ERK and Bcl‐2 proteins in the five AML cell lines (A) before and after ABT‐199 treatment (0.2 μM for OCI‐AML2 and KG‐1; 4 μM for THP‐1 and NB4; 10 μM for OCI‐AML3; 24 h) and in the five colorectal cancer cell lines (B) before or after etoposide treatment (1 μM for LoVo and HCT‐116; 2 μM for SW480; 4 μM for DLD1 and HT29; 24 h). Equal loading was confirmed by stripping the immunoblot and reprobing it for actin. Lower panel: The experimental IC50 values for apoptosis induced by ABT‐199 or etoposide treatment after 48 h were plotted against the dose ω predicted by the pBcl‐2/Bcl‐2 model or the Bcl‐2 model Correlations (r values shown) between the experimental IC50 values and the predicted dose ω predicted by pBcl‐2/Bcl‐2 model were statistically significant whereas those using the Bcl‐2 model were not significant .
Etoposide, supplied by Selleck Chemicals, 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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96
MathWorks Inc partial differential equations pdes
The pBcl‐2/Bcl‐2 model predicts the MOMP in response to ABT‐199 or <t>etoposide.</t> (A, B) The experimentally derived CI values for the ABT‐199/paclitaxel combination were plotted against those predicted from the pBcl‐2/Bcl‐2 model, using MDA‐MB‐231 (A) and T49D cells (B), with and without SP600125. Data are the mean ± SD (n = 5). Spearman's correlation (r) and P values are shown. (C, D) Upper panel: Expression of p‐PKCα/β, p‐ERK and Bcl‐2 proteins in the five AML cell lines (A) before and after ABT‐199 treatment (0.2 μM for OCI‐AML2 and KG‐1; 4 μM for THP‐1 and NB4; 10 μM for OCI‐AML3; 24 h) and in the five colorectal cancer cell lines (B) before or after etoposide treatment (1 μM for LoVo and HCT‐116; 2 μM for SW480; 4 μM for DLD1 and HT29; 24 h). Equal loading was confirmed by stripping the immunoblot and reprobing it for actin. Lower panel: The experimental IC50 values for apoptosis induced by ABT‐199 or etoposide treatment after 48 h were plotted against the dose ω predicted by the pBcl‐2/Bcl‐2 model or the Bcl‐2 model Correlations (r values shown) between the experimental IC50 values and the predicted dose ω predicted by pBcl‐2/Bcl‐2 model were statistically significant whereas those using the Bcl‐2 model were not significant .
Partial Differential Equations Pdes, supplied by MathWorks 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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Average 96 stars, based on 1 article reviews
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96
Selleck Chemicals abt 199
The pBcl‐2/Bcl‐2 model predicts the MOMP in response to ABT‐199 or <t>etoposide.</t> (A, B) The experimentally derived CI values for the ABT‐199/paclitaxel combination were plotted against those predicted from the pBcl‐2/Bcl‐2 model, using MDA‐MB‐231 (A) and T49D cells (B), with and without SP600125. Data are the mean ± SD (n = 5). Spearman's correlation (r) and P values are shown. (C, D) Upper panel: Expression of p‐PKCα/β, p‐ERK and Bcl‐2 proteins in the five AML cell lines (A) before and after ABT‐199 treatment (0.2 μM for OCI‐AML2 and KG‐1; 4 μM for THP‐1 and NB4; 10 μM for OCI‐AML3; 24 h) and in the five colorectal cancer cell lines (B) before or after etoposide treatment (1 μM for LoVo and HCT‐116; 2 μM for SW480; 4 μM for DLD1 and HT29; 24 h). Equal loading was confirmed by stripping the immunoblot and reprobing it for actin. Lower panel: The experimental IC50 values for apoptosis induced by ABT‐199 or etoposide treatment after 48 h were plotted against the dose ω predicted by the pBcl‐2/Bcl‐2 model or the Bcl‐2 model Correlations (r values shown) between the experimental IC50 values and the predicted dose ω predicted by pBcl‐2/Bcl‐2 model were statistically significant whereas those using the Bcl‐2 model were not significant .
Abt 199, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 96/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/abt 199/product/Selleck Chemicals
Average 96 stars, based on 1 article reviews
abt 199 - by Bioz Stars, 2026-05
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The pBcl‐2/Bcl‐2 model predicts the MOMP in response to ABT‐199 or etoposide. (A, B) The experimentally derived CI values for the ABT‐199/paclitaxel combination were plotted against those predicted from the pBcl‐2/Bcl‐2 model, using MDA‐MB‐231 (A) and T49D cells (B), with and without SP600125. Data are the mean ± SD (n = 5). Spearman's correlation (r) and P values are shown. (C, D) Upper panel: Expression of p‐PKCα/β, p‐ERK and Bcl‐2 proteins in the five AML cell lines (A) before and after ABT‐199 treatment (0.2 μM for OCI‐AML2 and KG‐1; 4 μM for THP‐1 and NB4; 10 μM for OCI‐AML3; 24 h) and in the five colorectal cancer cell lines (B) before or after etoposide treatment (1 μM for LoVo and HCT‐116; 2 μM for SW480; 4 μM for DLD1 and HT29; 24 h). Equal loading was confirmed by stripping the immunoblot and reprobing it for actin. Lower panel: The experimental IC50 values for apoptosis induced by ABT‐199 or etoposide treatment after 48 h were plotted against the dose ω predicted by the pBcl‐2/Bcl‐2 model or the Bcl‐2 model Correlations (r values shown) between the experimental IC50 values and the predicted dose ω predicted by pBcl‐2/Bcl‐2 model were statistically significant whereas those using the Bcl‐2 model were not significant .

Journal: British Journal of Pharmacology

Article Title: Systems analysis of phosphorylation‐regulated Bcl‐2 interactions establishes a model to reconcile the controversy over the significance of Bcl‐2 phosphorylation

doi: 10.1111/bph.14555

Figure Lengend Snippet: The pBcl‐2/Bcl‐2 model predicts the MOMP in response to ABT‐199 or etoposide. (A, B) The experimentally derived CI values for the ABT‐199/paclitaxel combination were plotted against those predicted from the pBcl‐2/Bcl‐2 model, using MDA‐MB‐231 (A) and T49D cells (B), with and without SP600125. Data are the mean ± SD (n = 5). Spearman's correlation (r) and P values are shown. (C, D) Upper panel: Expression of p‐PKCα/β, p‐ERK and Bcl‐2 proteins in the five AML cell lines (A) before and after ABT‐199 treatment (0.2 μM for OCI‐AML2 and KG‐1; 4 μM for THP‐1 and NB4; 10 μM for OCI‐AML3; 24 h) and in the five colorectal cancer cell lines (B) before or after etoposide treatment (1 μM for LoVo and HCT‐116; 2 μM for SW480; 4 μM for DLD1 and HT29; 24 h). Equal loading was confirmed by stripping the immunoblot and reprobing it for actin. Lower panel: The experimental IC50 values for apoptosis induced by ABT‐199 or etoposide treatment after 48 h were plotted against the dose ω predicted by the pBcl‐2/Bcl‐2 model or the Bcl‐2 model Correlations (r values shown) between the experimental IC50 values and the predicted dose ω predicted by pBcl‐2/Bcl‐2 model were statistically significant whereas those using the Bcl‐2 model were not significant .

Article Snippet: Subsequently, ODEs were solved using MATLAB 7.3 (MathWorks, R2007b) function ode 15 s at time point t = 300 min. Materials Paclitaxel, ABT‐199 and etoposide were purchased from Selleck Chemicals (S1150, S8048 and S1225, Houston, TX, USA).

Techniques: Derivative Assay, Expressing, Stripping Membranes, Western Blot