10058 f4 Search Results


10058 f4  (Selleck Chemicals)
95
Selleck Chemicals 10058 f4
mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated <t>with</t> <t>10058‐F4</t> or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.
10058 F4, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 95/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/10058+f4/pmc12936417-31-1-8?v=Selleck+Chemicals
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f4 80  (Thermo Fisher)
94
Thermo Fisher f4 80
mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated <t>with</t> <t>10058‐F4</t> or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.
F4 80, supplied by Thermo Fisher, 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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f4 80 - by Bioz Stars, 2026-07
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10058 f4  (Tocris)
93
Tocris 10058 f4
mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated <t>with</t> <t>10058‐F4</t> or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.
10058 F4, supplied by Tocris, 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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c myc max dimerization  (Tocris)
93
Tocris c myc max dimerization
mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated <t>with</t> <t>10058‐F4</t> or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.
C Myc Max Dimerization, supplied by Tocris, 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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10058 f4 treatment  (Santa Cruz Biotechnology)
92
Santa Cruz Biotechnology 10058 f4 treatment
mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated <t>with</t> <t>10058‐F4</t> or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.
10058 F4 Treatment, supplied by Santa Cruz Biotechnology, 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/10058+f4/us09155724-1228-14-20?v=Santa+Cruz+Biotechnology
Average 92 stars, based on 1 article reviews
10058 f4 treatment - by Bioz Stars, 2026-07
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10058-f4  (Cayman Chemical)
90
Cayman Chemical 10058-f4
mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated <t>with</t> <t>10058‐F4</t> or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.
10058 F4, supplied by Cayman Chemical, 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/10058+f4/pm37302654-297-34-39?v=Cayman+Chemical
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small-molecule inhibitor 10058-f4  (Merck KGaA)
90
Merck KGaA small-molecule inhibitor 10058-f4
mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated <t>with</t> <t>10058‐F4</t> or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.
Small Molecule Inhibitor 10058 F4, supplied by Merck KGaA, 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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10058-f4  (ApexBio)
90
ApexBio 10058-f4
mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated <t>with</t> <t>10058‐F4</t> or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.
10058 F4, supplied by ApexBio, 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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c-myc inhibitor 10058-f4  (Axon Medchem LLC)
90
Axon Medchem LLC c-myc inhibitor 10058-f4
Key Resources Table
C Myc Inhibitor 10058 F4, supplied by Axon Medchem LLC, 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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c-myc inhibitors 10058-f4  (Cayman Chemical)
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Cayman Chemical c-myc inhibitors 10058-f4
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C Myc Inhibitors 10058 F4, supplied by Cayman Chemical, 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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c-myc specific inhibitor 10058-f4  (ApexBio)
90
ApexBio c-myc specific inhibitor 10058-f4
Key Resources Table
C Myc Specific Inhibitor 10058 F4, supplied by ApexBio, 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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10058-f4  (AbMole Bioscience)
90
AbMole Bioscience 10058-f4
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10058 F4, supplied by AbMole Bioscience, 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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Image Search Results


mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated with 10058‐F4 or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.

Journal: Molecular Oncology

Article Title: Inhibition of CDK 9 enhances AML cell death induced by combined venetoclax and azacitidine

doi: 10.1002/1878-0261.70124

Figure Lengend Snippet: mTOR, c‐MYC, and MCL‐1 contribute to AraC‐resistant AML cell survival. (A) gsea comparing proteomics results of MV4‐11 and MV4‐11/AraC‐R cells (published in reference ) to the Hallmark gene set. (B) Whole cell lysates from AML cell lines, J000106565 PDX cells, and KCI48595 primary blasts were subjected to western blot and probed with anti‐p‐S6 and anti‐β‐actin antibodies. Densitometry measurements normalized to β‐actin and then compared to parental cell lines are shown below the corresponding blot. (C–H) AraC‐resistant AML cell lines were treated with 10058‐F4 or AZD5991 for 24 h; parental and AraC‐resistant AML cell lines were treated with rapamycin for 24 h. c‐MYC, MCL‐1, or p‐S6 protein levels, from whole cell lysates, were analyzed by western blot (panels C, E, and G). Densitometry measurements normalized to β‐actin and then compared to the control are shown below the corresponding blot. Annexin V‐fluorescein isothiocyanate (FITC)/propidium iodide (PI)‐stained cells were analyzed by flow cytometry (panels D, F, and H). Results are graphed as mean ± SEM from one experiment in triplicate. *** P < 0.001 compared to the control. The unpaired t ‐test was used to determine statistical significance. (I) AraC‐resistant AML cell lines were treated with AZD5991, 10058‐F4, or rapamycin, alone or in combination, for 24 h, then stained with annexin V‐FITC/PI and analyzed by flow cytometry. Results are graphed as mean ± SEM. *** P < 0.001 compared to the control. ### P < 0.001 compared to all corresponding single‐drug treatments. $$$ P < 0.001 compared to all corresponding 2‐drug combinations. One‐way ANOVA followed by Bonferroni's post hoc test was used to determine statistical significance. Western blotting and annexin V‐FITC/PI staining and flow cytometry analysis experiments were repeated in biological replicates.

Article Snippet: AZD4573, 10058‐F4, IACS‐010759, and AZA were purchased from Selleck Chemicals (Houston, TX, USA).

Techniques: Western Blot, Control, Staining, Flow Cytometry

Key Resources Table

Journal: Cell stem cell

Article Title: Deterministic Somatic Cell Reprogramming Involves Continuous Transcriptional Changes Governed by Myc and Epigenetic-Driven Modules

doi: 10.1016/j.stem.2018.11.014

Figure Lengend Snippet: Key Resources Table

Article Snippet: c-Myc inhibitor 10058-F4 , Axon Medchem , #2222.

Techniques: Recombinant, Protease Inhibitor, Sample Prep, Methylation, Transgenic Assay, Negative Control, Software