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10058 f4 c myc inhibitor

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10058-F4 is a c-Myc inhibitor, a type of lab equipment used for research purposes. It is a chemical compound that inhibits the activity of the c-Myc protein, which is involved in cell growth and proliferation. The core function of 10058-F4 is to serve as a tool for researchers to study the role of c-Myc in various biological processes.

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Lab products found in correlation

Crl 1658, by American Type Culture Collection (1 mentions) Cvt 313, by Enzo Life Sciences (1 mentions) μ slide 1, by Ibidi (1 mentions) Pd 0332991, by Chemietek (1 mentions) Celltiter 96 aqueous one solution cell proliferation assay mts, by Promega (1 mentions) Nfat inhibitor, by Cayman Chemical (1 mentions) Ac220, by Selleck Chemicals (1 mentions) Fingolimod, by Cayman Chemical (1 mentions) Tc g 24, by Bio-Techne (1 mentions) Azd1208, by Bio-Techne (1 mentions) Mk 2206, by Selleck Chemicals (1 mentions) Dspe peg2000, by Avanti Polar Lipids (1 mentions) Calf thymus dna, by Merck Group (1 mentions) Cisplatin, by Merck Group (1 mentions) Dotap, by Avanti Polar Lipids (1 mentions) Cholesterol, by Avanti Polar Lipids (1 mentions) Basic fibroblast growth factor (bfgf), by R&D Systems (1 mentions) Epidermal growth factor (egf), by R&D Systems (1 mentions) C myc, by Abcam (1 mentions) Tgf β, by R&D Systems (1 mentions)

Spelling variants of this product

C-Myc (65 citations) -myc inhibitor (2 citations)

4 protocols using 10058 f4 c myc inhibitor

1

E2F Dynamics Measurement in Synchronized Cells

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REF52 (an immortal line of postcrisis Fischer rat embryo cells)4 (link)62 (link)63 (link) and NIH3T3 mouse fibroblasts (CRL-1658, ATCC) were routinely grown in Minimum Essential Medium Alpha Medium (Gibco/Invitrogen) supplemented with 10% bovine growth medium (BGS, Hyclone/Thermo Scientific). For the preparation of E2F dynamics measurement by using time-lapse microscopy, cells were first trypsinized, resuspended at a density of 1 × 105 per ml and then seeded in μ-Slide I (tissue culture treated, ibidi) channel slides by adding 1 ml volume of the cell suspension. After overnight culturing, cells were synchronized in quiescence by shifting into Minimum Essential Medium Alpha medium with 0.02% BGS (starvation medium) for 36 h. For perturbation experiments, PD0332991 (CDK4/6 inhibitor, ChemieTek), CVT-313 (CDK2 inhibitor, Enzo Life Science), 10058-F4 (c-Myc inhibitor, Sigma Aldrich) and (+)-JQ1 (bromodomain and extra terminal domain inhibitor, Cayman Chemical) were added into cells immediately after cells were released from serum starvation (by adding 10% BGS) in either single or combined way. For 92 h perturbation experiment with both PD0332991 and CVT-313, cells were growing with replaced fresh medium with fresh inhibitors after the initial 48 h.
Dong P., Maddali M.V., Srimani J.K., Thélot F., Nevins J.R., Mathey-Prevot B, & You L. (2014). Division of labour between Myc and G1 cyclins in cell cycle commitment and pace control. Nature Communications, 5, 4750.
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2

Assessing UCS Cell Viability

Cited 1 time
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Viability of UCS cells was determined using the tetrazolium compound based CellTiter 96® AQueous One Solution Cell Proliferation (MTS) assay (Promega). Cells were plated in 96 well plate at density of 2.5x 103 cells per well. 4h post serum starvation cells were subjected to TGFβ-I (R&D Biosystems) treatment alone or in presence of LY2157299 [40 (link)] (TGFβR-I inhibitor, Selleck Chem), LY2109761 [41 (link)] (TGFβR-I/II inhibitor, Selleck Chem), 10058-F4 (c-Myc Inhibitor, Sigma Aldrich), NFAT inhibitor (Cay-man Chemicals). After 24h treatment MTS assay was done and viability was calculated using vehicle as 100%. [42 (link)].
Dhar Dwivedi S.K., McMeekin S.D., Slaughter K, & Bhattacharya R. (2015). Role of TGF-β signaling in uterine carcinosarcoma. Oncotarget, 6(16), 14646-14655.
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3

Inhibitors of FLT3, PP2A, and Signaling Pathways in AML

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Gilteritinib (4 (link)) (ASP2215; Active Biochem, Maplewood, NJ) and quizartinib (4 (link)) (AC220; Selleck Chemicals, Houston, TX), type I and II FLT3 inhibitors, respectively, clinically active in FLT3-ITD AML, were used at pharmacologically relevant concentrations (23 (link),24 (link)). The SET-sequestering PAD FTY720 (25 (link)) (Fingolimod; Cayman Chemical Company, Ann Arbor, MI) was also used at pharmacologically relevant concentrations. DT-061, an orally bioavailable small molecule activator of PP2A (SMAP) developed by reengineering tricyclic neuroleptics and proposed to directly bind the PP2A Aα subunit (26 (link)–29 (link)), was provided by Dr. Goutham Narla. The pan-Pim inhibitor AZD1208 and GSK-3β inhibitors TC-G 24 and TWS119 were from Tocris Bioscience, Minneapolis, MN, the c-Myc inhibitor 10058-F4 from Sigma-Aldrich, and the pan-AKT inhibitor MK-2206 from Selleck Chemicals, Houston, TX.
Scarpa M., Singh P., Bailey C.M., Lee J.K., Kapoor S., Lapidus R.G., Niyongere S., Sangodkar J., Wang Y., Perrotti D., Narla G, & Baer M.R. (2021). PP2A-activating drugs enhance FLT3 inhibitor efficacy through AKT inhibition-dependent GSK-3β-mediated c-Myc and Pim-1 proteasomal degradation. Molecular cancer therapeutics, 20(4), 676-690.
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4

Preparation and Characterization of Nanoparticles

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Antibodies used in this study were obtained from commercial sources and are described in Additional file 1: Table S1. Recombinant human proteins TGF-β, EGF and bFGF were obtained from R&D Systems, whereas c-Myc was purchased from Abcam. TβRI (type I TGF-β receptor) inhibitor SB431542, c-Myc inhibitor 10058-F4, cisplatin, doxorubicin (Dox), protamine sulfate and calf thymus DNA were purchased from Sigma-Aldrich (St Louis, MO). DOTAP, cholesterol and DSPE-PEG2000 were purchased from Avanti Polar Lipids (Alabaster, AL).
Chen H.Y., Chan S.J., Liu X., Wei A.C., Jian R.I., Huang K.W., Lang Y.D., Shih J.H., Liao C.C., Luan C.L., Kao Y.T., Chiang S.Y., Hsiao P.W., Jou Y.S., Chen Y, & Chen R.H. (2022). Long noncoding RNA Smyca coactivates TGF-β/Smad and Myc pathways to drive tumor progression. Journal of Hematology & Oncology, 15, 85.
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