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mouse anti bcl2 c2  (Santa Cruz Biotechnology)


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    Structured Review

    Santa Cruz Biotechnology mouse anti bcl2 c2
    ML329 decreases cell viability; reduces the expression of MITF, KIT, <t>BCL2,</t> and CDK2; and impairs the cell cycle in GIST cell lines GIST cells: GIST-T1 (A) and GIST 430/654 (G) were incubated with various concentrations of ML329 on different days. Cell viability was measured (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; two-way ANOVA analysis of significance, Tukey’s multiple comparisons test). Sigmoidal 4PL representations of cytotoxicity for GIST-T1 after 3 days of ML329 incubation (5 μM) (B) and for GIST 430/654 after 10 days of ML329 incubation (5 μM) were performed (H). MITF activity was measured using the TRPM-1-luciferase gene reporter in GIST-T1 after 1 day of ML329 incubation (5 μM) (C) and in GIST 430/654 after 8 days of ML329 incubation (5 μM) (I) (∗∗ p < 0.01; unpaired t test). Caspase 3/7 activity was measured in GIST-T1 (D) and GIST 430/657(J), incubated with 10 μM ML329 after 24 h of administration (∗∗ p < 0.01, ∗∗∗ p < 0.001; unpaired t test). The relative number of cells (%) was plotted, showing cell-cycle phases in GIST-T1 treated with ML329 (5 μM) at days 5 and 7 (E) and GIST 430/654 treated with ML329 (10 μM) at days 7 and 10 (K). Results were analyzed using the Dean/Jett/Fox model and FlowJo 7.0 software. (∗ p < 0.05, ∗∗ p < 0.01; unpaired t test.) Western blots for KIT, MITF, BCL2, and CDK2 are shown after treatment with ML329 in GIST-T1 after 3 days and GIST 430/654 after 10 days (F and L, respectively). β-actin was used as a loading control. Ratios of proteins blotted versus β-actin are shown. All experiments were performed at least three times, and the blots represent the results of several experiments.
    Mouse Anti Bcl2 C2, supplied by Santa Cruz Biotechnology, used in various techniques. Bioz Stars score: 96/100, based on 13681 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "Preclinical study of microphthalmia-associated transcription factor inhibitor ML329 in gastrointestinal stromal tumor growth"

    Article Title: Preclinical study of microphthalmia-associated transcription factor inhibitor ML329 in gastrointestinal stromal tumor growth

    Journal: Molecular Therapy Oncology

    doi: 10.1016/j.omton.2025.200983

    ML329 decreases cell viability; reduces the expression of MITF, KIT, BCL2, and CDK2; and impairs the cell cycle in GIST cell lines GIST cells: GIST-T1 (A) and GIST 430/654 (G) were incubated with various concentrations of ML329 on different days. Cell viability was measured (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; two-way ANOVA analysis of significance, Tukey’s multiple comparisons test). Sigmoidal 4PL representations of cytotoxicity for GIST-T1 after 3 days of ML329 incubation (5 μM) (B) and for GIST 430/654 after 10 days of ML329 incubation (5 μM) were performed (H). MITF activity was measured using the TRPM-1-luciferase gene reporter in GIST-T1 after 1 day of ML329 incubation (5 μM) (C) and in GIST 430/654 after 8 days of ML329 incubation (5 μM) (I) (∗∗ p < 0.01; unpaired t test). Caspase 3/7 activity was measured in GIST-T1 (D) and GIST 430/657(J), incubated with 10 μM ML329 after 24 h of administration (∗∗ p < 0.01, ∗∗∗ p < 0.001; unpaired t test). The relative number of cells (%) was plotted, showing cell-cycle phases in GIST-T1 treated with ML329 (5 μM) at days 5 and 7 (E) and GIST 430/654 treated with ML329 (10 μM) at days 7 and 10 (K). Results were analyzed using the Dean/Jett/Fox model and FlowJo 7.0 software. (∗ p < 0.05, ∗∗ p < 0.01; unpaired t test.) Western blots for KIT, MITF, BCL2, and CDK2 are shown after treatment with ML329 in GIST-T1 after 3 days and GIST 430/654 after 10 days (F and L, respectively). β-actin was used as a loading control. Ratios of proteins blotted versus β-actin are shown. All experiments were performed at least three times, and the blots represent the results of several experiments.
    Figure Legend Snippet: ML329 decreases cell viability; reduces the expression of MITF, KIT, BCL2, and CDK2; and impairs the cell cycle in GIST cell lines GIST cells: GIST-T1 (A) and GIST 430/654 (G) were incubated with various concentrations of ML329 on different days. Cell viability was measured (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; two-way ANOVA analysis of significance, Tukey’s multiple comparisons test). Sigmoidal 4PL representations of cytotoxicity for GIST-T1 after 3 days of ML329 incubation (5 μM) (B) and for GIST 430/654 after 10 days of ML329 incubation (5 μM) were performed (H). MITF activity was measured using the TRPM-1-luciferase gene reporter in GIST-T1 after 1 day of ML329 incubation (5 μM) (C) and in GIST 430/654 after 8 days of ML329 incubation (5 μM) (I) (∗∗ p < 0.01; unpaired t test). Caspase 3/7 activity was measured in GIST-T1 (D) and GIST 430/657(J), incubated with 10 μM ML329 after 24 h of administration (∗∗ p < 0.01, ∗∗∗ p < 0.001; unpaired t test). The relative number of cells (%) was plotted, showing cell-cycle phases in GIST-T1 treated with ML329 (5 μM) at days 5 and 7 (E) and GIST 430/654 treated with ML329 (10 μM) at days 7 and 10 (K). Results were analyzed using the Dean/Jett/Fox model and FlowJo 7.0 software. (∗ p < 0.05, ∗∗ p < 0.01; unpaired t test.) Western blots for KIT, MITF, BCL2, and CDK2 are shown after treatment with ML329 in GIST-T1 after 3 days and GIST 430/654 after 10 days (F and L, respectively). β-actin was used as a loading control. Ratios of proteins blotted versus β-actin are shown. All experiments were performed at least three times, and the blots represent the results of several experiments.

    Techniques Used: Expressing, Incubation, Activity Assay, Luciferase, Software, Western Blot, Control



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    ML329 decreases cell viability; reduces the expression of MITF, KIT, <t>BCL2,</t> and CDK2; and impairs the cell cycle in GIST cell lines GIST cells: GIST-T1 (A) and GIST 430/654 (G) were incubated with various concentrations of ML329 on different days. Cell viability was measured (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; two-way ANOVA analysis of significance, Tukey’s multiple comparisons test). Sigmoidal 4PL representations of cytotoxicity for GIST-T1 after 3 days of ML329 incubation (5 μM) (B) and for GIST 430/654 after 10 days of ML329 incubation (5 μM) were performed (H). MITF activity was measured using the TRPM-1-luciferase gene reporter in GIST-T1 after 1 day of ML329 incubation (5 μM) (C) and in GIST 430/654 after 8 days of ML329 incubation (5 μM) (I) (∗∗ p < 0.01; unpaired t test). Caspase 3/7 activity was measured in GIST-T1 (D) and GIST 430/657(J), incubated with 10 μM ML329 after 24 h of administration (∗∗ p < 0.01, ∗∗∗ p < 0.001; unpaired t test). The relative number of cells (%) was plotted, showing cell-cycle phases in GIST-T1 treated with ML329 (5 μM) at days 5 and 7 (E) and GIST 430/654 treated with ML329 (10 μM) at days 7 and 10 (K). Results were analyzed using the Dean/Jett/Fox model and FlowJo 7.0 software. (∗ p < 0.05, ∗∗ p < 0.01; unpaired t test.) Western blots for KIT, MITF, BCL2, and CDK2 are shown after treatment with ML329 in GIST-T1 after 3 days and GIST 430/654 after 10 days (F and L, respectively). β-actin was used as a loading control. Ratios of proteins blotted versus β-actin are shown. All experiments were performed at least three times, and the blots represent the results of several experiments.
    Mouse Anti Bcl2 C2, supplied by Santa Cruz Biotechnology, 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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    ML329 decreases cell viability; reduces the expression of MITF, KIT, <t>BCL2,</t> and CDK2; and impairs the cell cycle in GIST cell lines GIST cells: GIST-T1 (A) and GIST 430/654 (G) were incubated with various concentrations of ML329 on different days. Cell viability was measured (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; two-way ANOVA analysis of significance, Tukey’s multiple comparisons test). Sigmoidal 4PL representations of cytotoxicity for GIST-T1 after 3 days of ML329 incubation (5 μM) (B) and for GIST 430/654 after 10 days of ML329 incubation (5 μM) were performed (H). MITF activity was measured using the TRPM-1-luciferase gene reporter in GIST-T1 after 1 day of ML329 incubation (5 μM) (C) and in GIST 430/654 after 8 days of ML329 incubation (5 μM) (I) (∗∗ p < 0.01; unpaired t test). Caspase 3/7 activity was measured in GIST-T1 (D) and GIST 430/657(J), incubated with 10 μM ML329 after 24 h of administration (∗∗ p < 0.01, ∗∗∗ p < 0.001; unpaired t test). The relative number of cells (%) was plotted, showing cell-cycle phases in GIST-T1 treated with ML329 (5 μM) at days 5 and 7 (E) and GIST 430/654 treated with ML329 (10 μM) at days 7 and 10 (K). Results were analyzed using the Dean/Jett/Fox model and FlowJo 7.0 software. (∗ p < 0.05, ∗∗ p < 0.01; unpaired t test.) Western blots for KIT, MITF, BCL2, and CDK2 are shown after treatment with ML329 in GIST-T1 after 3 days and GIST 430/654 after 10 days (F and L, respectively). β-actin was used as a loading control. Ratios of proteins blotted versus β-actin are shown. All experiments were performed at least three times, and the blots represent the results of several experiments.
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    MDM4 binds <t>BCL2</t> and facilitates binding between mitochondrial p53 and BCL2. (A, B) p53−/−Mdm4−/−MEFs were transfected with indicated plasmids (molar plasmid ratio of p53:BCL2, 1:2; P53:BCL2:MDM4 0.5:2:1) and p53 and BCL2 immunocomplexes analysed after immunoprecipitation of 600 μg of WCE with α-p53, FL393 (A) or α-BCL2, <t>C2</t> antibodies (B). Wb indicates analysis of 1/10 of WCEs. (C, D) p53−/−Mdm4−/−MEFs were transfected with equimolar amounts of the indicated plasmids and MDM4 and BCL2 immunocomplexes analysed after immunoprecipitation of 600 μg of WCE with α-MDM4, BL-1258 (C) or α-BCL2, C2 antibodies (D). (E) Analysis of MDM4 immunocomplexes in mitochondria of MCF7 cells transfected with siCTL or siMDM4. 100 μg of mitochondrial lysates were immunoprecipitated with α-MDM4, BL1258 and proteins present in the immunocomplex analysed by Wb. (F) Analysis of MDM4 immunocomplexes in MCF7 cells either untreated or treated with UV 40 J/m2. After 3 h from UV, 2 mg of WCEs or 100 μg of mitochondrial lysates were immunoprecipitated with α-MDM4, BL1258 and proteins present in the immunocomplex analysed by Wb. (G) Analysis of p53 immunocomplexes in MCF7 cells transfected with siCTL or siMDM4 and treated with UV 40 J/m2. After 7 h, 200 μg of mitochondrial lysates were immunoprecipitated with α-p53, PAb-421 and proteins present in the immunocomplex analysed by Wb.
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    Image Search Results


    ML329 decreases cell viability; reduces the expression of MITF, KIT, BCL2, and CDK2; and impairs the cell cycle in GIST cell lines GIST cells: GIST-T1 (A) and GIST 430/654 (G) were incubated with various concentrations of ML329 on different days. Cell viability was measured (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; two-way ANOVA analysis of significance, Tukey’s multiple comparisons test). Sigmoidal 4PL representations of cytotoxicity for GIST-T1 after 3 days of ML329 incubation (5 μM) (B) and for GIST 430/654 after 10 days of ML329 incubation (5 μM) were performed (H). MITF activity was measured using the TRPM-1-luciferase gene reporter in GIST-T1 after 1 day of ML329 incubation (5 μM) (C) and in GIST 430/654 after 8 days of ML329 incubation (5 μM) (I) (∗∗ p < 0.01; unpaired t test). Caspase 3/7 activity was measured in GIST-T1 (D) and GIST 430/657(J), incubated with 10 μM ML329 after 24 h of administration (∗∗ p < 0.01, ∗∗∗ p < 0.001; unpaired t test). The relative number of cells (%) was plotted, showing cell-cycle phases in GIST-T1 treated with ML329 (5 μM) at days 5 and 7 (E) and GIST 430/654 treated with ML329 (10 μM) at days 7 and 10 (K). Results were analyzed using the Dean/Jett/Fox model and FlowJo 7.0 software. (∗ p < 0.05, ∗∗ p < 0.01; unpaired t test.) Western blots for KIT, MITF, BCL2, and CDK2 are shown after treatment with ML329 in GIST-T1 after 3 days and GIST 430/654 after 10 days (F and L, respectively). β-actin was used as a loading control. Ratios of proteins blotted versus β-actin are shown. All experiments were performed at least three times, and the blots represent the results of several experiments.

    Journal: Molecular Therapy Oncology

    Article Title: Preclinical study of microphthalmia-associated transcription factor inhibitor ML329 in gastrointestinal stromal tumor growth

    doi: 10.1016/j.omton.2025.200983

    Figure Lengend Snippet: ML329 decreases cell viability; reduces the expression of MITF, KIT, BCL2, and CDK2; and impairs the cell cycle in GIST cell lines GIST cells: GIST-T1 (A) and GIST 430/654 (G) were incubated with various concentrations of ML329 on different days. Cell viability was measured (∗∗∗ p < 0.001, ∗∗∗∗ p < 0.0001; two-way ANOVA analysis of significance, Tukey’s multiple comparisons test). Sigmoidal 4PL representations of cytotoxicity for GIST-T1 after 3 days of ML329 incubation (5 μM) (B) and for GIST 430/654 after 10 days of ML329 incubation (5 μM) were performed (H). MITF activity was measured using the TRPM-1-luciferase gene reporter in GIST-T1 after 1 day of ML329 incubation (5 μM) (C) and in GIST 430/654 after 8 days of ML329 incubation (5 μM) (I) (∗∗ p < 0.01; unpaired t test). Caspase 3/7 activity was measured in GIST-T1 (D) and GIST 430/657(J), incubated with 10 μM ML329 after 24 h of administration (∗∗ p < 0.01, ∗∗∗ p < 0.001; unpaired t test). The relative number of cells (%) was plotted, showing cell-cycle phases in GIST-T1 treated with ML329 (5 μM) at days 5 and 7 (E) and GIST 430/654 treated with ML329 (10 μM) at days 7 and 10 (K). Results were analyzed using the Dean/Jett/Fox model and FlowJo 7.0 software. (∗ p < 0.05, ∗∗ p < 0.01; unpaired t test.) Western blots for KIT, MITF, BCL2, and CDK2 are shown after treatment with ML329 in GIST-T1 after 3 days and GIST 430/654 after 10 days (F and L, respectively). β-actin was used as a loading control. Ratios of proteins blotted versus β-actin are shown. All experiments were performed at least three times, and the blots represent the results of several experiments.

    Article Snippet: Mouse anti-C-KIT (E1) (clone Ab81), mouse anti-BCL2 (C2), and mouse anti-CDK2 (Clone D-12) were purchased from Santa Cruz Biotechnology, Inc. (Santa Cruz, CA, USA).

    Techniques: Expressing, Incubation, Activity Assay, Luciferase, Software, Western Blot, Control

    MDM4 binds BCL2 and facilitates binding between mitochondrial p53 and BCL2. (A, B) p53−/−Mdm4−/−MEFs were transfected with indicated plasmids (molar plasmid ratio of p53:BCL2, 1:2; P53:BCL2:MDM4 0.5:2:1) and p53 and BCL2 immunocomplexes analysed after immunoprecipitation of 600 μg of WCE with α-p53, FL393 (A) or α-BCL2, C2 antibodies (B). Wb indicates analysis of 1/10 of WCEs. (C, D) p53−/−Mdm4−/−MEFs were transfected with equimolar amounts of the indicated plasmids and MDM4 and BCL2 immunocomplexes analysed after immunoprecipitation of 600 μg of WCE with α-MDM4, BL-1258 (C) or α-BCL2, C2 antibodies (D). (E) Analysis of MDM4 immunocomplexes in mitochondria of MCF7 cells transfected with siCTL or siMDM4. 100 μg of mitochondrial lysates were immunoprecipitated with α-MDM4, BL1258 and proteins present in the immunocomplex analysed by Wb. (F) Analysis of MDM4 immunocomplexes in MCF7 cells either untreated or treated with UV 40 J/m2. After 3 h from UV, 2 mg of WCEs or 100 μg of mitochondrial lysates were immunoprecipitated with α-MDM4, BL1258 and proteins present in the immunocomplex analysed by Wb. (G) Analysis of p53 immunocomplexes in MCF7 cells transfected with siCTL or siMDM4 and treated with UV 40 J/m2. After 7 h, 200 μg of mitochondrial lysates were immunoprecipitated with α-p53, PAb-421 and proteins present in the immunocomplex analysed by Wb.

    Journal:

    Article Title: MDM4 (MDMX) localizes at the mitochondria and facilitates the p53-mediated intrinsic-apoptotic pathway

    doi: 10.1038/emboj.2009.154

    Figure Lengend Snippet: MDM4 binds BCL2 and facilitates binding between mitochondrial p53 and BCL2. (A, B) p53−/−Mdm4−/−MEFs were transfected with indicated plasmids (molar plasmid ratio of p53:BCL2, 1:2; P53:BCL2:MDM4 0.5:2:1) and p53 and BCL2 immunocomplexes analysed after immunoprecipitation of 600 μg of WCE with α-p53, FL393 (A) or α-BCL2, C2 antibodies (B). Wb indicates analysis of 1/10 of WCEs. (C, D) p53−/−Mdm4−/−MEFs were transfected with equimolar amounts of the indicated plasmids and MDM4 and BCL2 immunocomplexes analysed after immunoprecipitation of 600 μg of WCE with α-MDM4, BL-1258 (C) or α-BCL2, C2 antibodies (D). (E) Analysis of MDM4 immunocomplexes in mitochondria of MCF7 cells transfected with siCTL or siMDM4. 100 μg of mitochondrial lysates were immunoprecipitated with α-MDM4, BL1258 and proteins present in the immunocomplex analysed by Wb. (F) Analysis of MDM4 immunocomplexes in MCF7 cells either untreated or treated with UV 40 J/m2. After 3 h from UV, 2 mg of WCEs or 100 μg of mitochondrial lysates were immunoprecipitated with α-MDM4, BL1258 and proteins present in the immunocomplex analysed by Wb. (G) Analysis of p53 immunocomplexes in MCF7 cells transfected with siCTL or siMDM4 and treated with UV 40 J/m2. After 7 h, 200 μg of mitochondrial lysates were immunoprecipitated with α-p53, PAb-421 and proteins present in the immunocomplex analysed by Wb.

    Article Snippet: The following primary antibody were used: rabbit anti-MDM4 polyclonal antibody BL1258 (Bethyl laboratory), mouse anti-MDM4 monoclonal antibody 6B1A, mouse anti-MDM4 monoclonal antibody C82 (Sigma), mouse anti-BCL2 monoclonal antibody C2 (Santa Cruz), mouse anti-His Tag 4D11 (Upstate), mouse anti-c-myc monoclonal antibody 9E10 (Pharmingen), rabbit anti-BCL2 polyclonal antibody (N19 Santa Cruz Biotechnology), rabbit anti-p53 polyclonal antibody FL393 (Santa Cruz), sheep anti-p53 polyclonal antibody Ab7 (Oncogene Science), rabbit anti-p53S46 P and anti-p53S15 P polyclonal antibodies (Cell Signaling), mouse anti-p53 monoclonal antibody Ab1 (Calbiochem), mouse anti-MDM2 monoclonal antibody 2A10, mouse anti-α-tubulin monoclonal antibody DM1A (Sigma), mouse anti-mHsp70 monoclonal antibody JG1 (Affinity Bioreagent), mouse anti-Cytochrome C monoclonal antibody 7H8 (Santa Cruz), mouse anti-CoxIV monoclonal antibody 1D6 (Molecular Probes-Invitrogen), mouse anti-actin monoclonal antibody C-40 (Sigma) and rabbit anti-Sp1 polyclonal antibody PEP2 (Santa Cruz).

    Techniques: Binding Assay, Transfection, Plasmid Preparation, Immunoprecipitation

    In the presence of MDM4, BCL2 binds p53Ser46P preferentially. (A) p53−/−Mdm4−/−MEFs were transfected with p53, p53S46D or p53S46A and BCL2, and MDM4 (molar plasmid ratio of p53:BCL2, 1:2; P53:BCL2:MDM4 0.5:2:1), and BCL2 immunocomplexes analysed after immunoprecipitation of 600 μg of WCE with α-BCL2, C2 antibody. (B) Wb of cytosolic and mitochondrial fractions of p53−/−Mdm4−/−MEFs transfected with the indicated plasmids (molar plasmid ratio of p53:MDM4, 1:2).

    Journal:

    Article Title: MDM4 (MDMX) localizes at the mitochondria and facilitates the p53-mediated intrinsic-apoptotic pathway

    doi: 10.1038/emboj.2009.154

    Figure Lengend Snippet: In the presence of MDM4, BCL2 binds p53Ser46P preferentially. (A) p53−/−Mdm4−/−MEFs were transfected with p53, p53S46D or p53S46A and BCL2, and MDM4 (molar plasmid ratio of p53:BCL2, 1:2; P53:BCL2:MDM4 0.5:2:1), and BCL2 immunocomplexes analysed after immunoprecipitation of 600 μg of WCE with α-BCL2, C2 antibody. (B) Wb of cytosolic and mitochondrial fractions of p53−/−Mdm4−/−MEFs transfected with the indicated plasmids (molar plasmid ratio of p53:MDM4, 1:2).

    Article Snippet: The following primary antibody were used: rabbit anti-MDM4 polyclonal antibody BL1258 (Bethyl laboratory), mouse anti-MDM4 monoclonal antibody 6B1A, mouse anti-MDM4 monoclonal antibody C82 (Sigma), mouse anti-BCL2 monoclonal antibody C2 (Santa Cruz), mouse anti-His Tag 4D11 (Upstate), mouse anti-c-myc monoclonal antibody 9E10 (Pharmingen), rabbit anti-BCL2 polyclonal antibody (N19 Santa Cruz Biotechnology), rabbit anti-p53 polyclonal antibody FL393 (Santa Cruz), sheep anti-p53 polyclonal antibody Ab7 (Oncogene Science), rabbit anti-p53S46 P and anti-p53S15 P polyclonal antibodies (Cell Signaling), mouse anti-p53 monoclonal antibody Ab1 (Calbiochem), mouse anti-MDM2 monoclonal antibody 2A10, mouse anti-α-tubulin monoclonal antibody DM1A (Sigma), mouse anti-mHsp70 monoclonal antibody JG1 (Affinity Bioreagent), mouse anti-Cytochrome C monoclonal antibody 7H8 (Santa Cruz), mouse anti-CoxIV monoclonal antibody 1D6 (Molecular Probes-Invitrogen), mouse anti-actin monoclonal antibody C-40 (Sigma) and rabbit anti-Sp1 polyclonal antibody PEP2 (Santa Cruz).

    Techniques: Transfection, Plasmid Preparation, Immunoprecipitation