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Cycloheximide chx n11534

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Cycloheximide (CHX; N11534) is a laboratory reagent used as a protein synthesis inhibitor. It functions by blocking the translocation step in eukaryotic protein synthesis, thereby preventing the translation of messenger RNA (mRNA) into proteins.

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Lab products found in correlation

Sorafenib, by Cell Signaling Technology (1 mentions) Chloroquine, by Merck Group (1 mentions) Z vad fmk 2163, by Bio-Techne (1 mentions) Mg132 s2619, by Selleck Chemicals (1 mentions) N ethylmaleimide e3876, by Merck Group (1 mentions) Iodoacetamide, by Merck Group (1 mentions) Voreloxin, by Selleck Chemicals (1 mentions) Docetaxel, by Selleck Chemicals (1 mentions) Etoposide, by Selleck Chemicals (1 mentions) Mln4924, by Selleck Chemicals (1 mentions) Doxorubicin, by Selleck Chemicals (1 mentions) Sn 38, by Selleck Chemicals (1 mentions) Bortezomib, by Selleck Chemicals (1 mentions) Mg132, by Selleck Chemicals (1 mentions)

2 protocols using cycloheximide chx n11534

1

Cellular Pathways Investigated Using Inhibitors

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SD70 (M60194-2s) was purchased from Xcessbio Biosciences Inc; Cycloheximide (CHX; N11534), Calpeptin (C8999), chloroquine (C6628), iodoacetamide (I1149), and N-ethylmaleimide (E-3876) were purchased from Sigma-Aldrich; Sorafenib (8705) was purchased from Cell Signaling Technology; MG-132 (S2619) was purchased from Selleck; Z-VAD-FMK (2163) was purchased from Tocris. Treatment conditions were described in detail in the text.
Shao N., Cheng J., Huang H., Gong X., Lu Y., Idris M., Peng X., Ong B.X., Zhang Q., Xu F, & Liu C. (2021). GASC1 promotes hepatocellular carcinoma progression by inhibiting the degradation of ROCK2. Cell Death & Disease, 12(3), 253.
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2

Immunoblotting analysis of drug-treated cells

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Drugs used in the study include: Bortezomib (S1013), MLN4924 (S7109), MG132 (S2619), Docetaxel (S1148), Doxorubicin (S1208), Etoposide (S1255), SN‐38 (S4908), and Voreloxin (S7518) from Selleckchem. Cycloheximide (CHX; N11534) was purchased from Sigma‐Aldrich. Drugs were dissolved in dimethyl sulfoxide (DMSO). Prior to drug treatment, cells were plated in six‐well plates. When cells reached 60% confluence, they were treated with indicated drugs for various length of time at the concentration described in corresponding figure legend. After treatment, cells were collected for protein extraction and immunoblotting analysis.
Shao N., Huang H., Idris M., Peng X., Xu F., Dong S, & Liu C. (2020). KEAP1 Mutations Drive Tumorigenesis by Suppressing SOX9 Ubiquitination and Degradation. Advanced Science, 7(21), 2001018.
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