Mek inhibitor pd0325901

Manufactured by Merck Group

MEK inhibitor PD0325901 is a small molecule that targets the MEK enzyme, a key component of the MAPK/ERK signaling pathway. It acts as a potent and selective inhibitor of MEK1 and MEK2. PD0325901 is commonly used as a research tool to study the role of the MAPK/ERK pathway in various biological processes.

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4 protocols using mek inhibitor pd0325901

Epigenetic Regulation in Mouse Embryonic Stem Cells

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Rw4 murine (male,129X1/SvJ) embryonic stem cells (mESCs) were cultured feeder-free in 0.1% gelatin-coated dishes. Serum condition: Knockout DMEM (Life Technologies), 2 mM Glutamax (GIBCO), 0.1 mM non-essential amino acids (GIBCO), 15% ESC-grade fetal bovine serum (FBS) (GIBCO), 0.1 mM β-mercaptoethanol, and leukemia inhibitory factor (LIF) (Millipore), 2i/Serum condition: above medium supplemented with 2i; 1 μM MEK inhibitor PD0325901 (Sigma) and 3 μM GSK3 inhibitor CHIR99021 (Sigma). 2i condition: serum free ESGRO Complete Basal medium (Millipore) with 0.1mM LIF and 2i as described above. For drug treatment, mESCs were grown in respective medium supplemented with 10 μM GSK-J4 (Sigma) for 96 h, 50 μM Zebularin for 96 h or 10 μM EPZ-6438 (BioVision) for 7 days. For all conditions cells were passaged in 48 h intervals, using accutase (Sigma) for detachment. Cell line was tested for mycoplasma contamination.

Kumar B, & Elsässer S.J. (2019). Quantitative Multiplexed ChIP Reveals Global Alterations that Shape Promoter Bivalency in Ground State Embryonic Stem Cells. Cell Reports, 28(12), 3274-3284.e5.

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Myeloid Precursor Expansion and Differentiation Assay

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Myeloid hematopoietic precursors were expanded from BM cells using granulocyte-monocyte-colony stimulating factor (GM-CSF), stem cell factor (SCF) and leukaemia inhibitory factor (LIF) for 2 to 3 days, following published conditions [8 (link), 30 (link)]. Then, myeloid precursors were seeded on two L8 cell culture chambers for the xCELLingence RTCA monitoring system (ACEA biosciences), at a density of 200000 cells per well. DC or B16-MDSC differentiation medium was added to myeloid precursors, and treatments were carried out simultaneously in duplicates. After 30 min, the indicated chemical inhibitors were added at concentrations reported to be cytotoxic to cancer cells. Control wells were treated with carrier solution (either water or DMSO). The following inhibitors were used: AKT inhibitor X (Calbiochem), tyrosine kinase inhibitor TX-1123 (Calbiochem), MEK inhibitor PD0325901 (SIGMA), ERK inhibitors SCH772984 and VTX-11e [31 (link)], broad PKC inhibitor GÖ 6983 (Santa Cruz Biotechnology), PKC inhibitor NPC-15437 dihydrochloride (Santa Cruz Biotechnology), selective LCK and FYN inhibitor PP2 (Santa Cruz Biotechnology), and the SRC and FYN inhibitor Saracatinib (MedChem Express). IC50s for each inhibitor were calculated using the RTCA data and analysis software, using duplicates for each drug treatment.

Gato-Cañas M., de Morentin X.M., Blanco-Luquin I., Fernandez-Irigoyen J., Zudaire I., Liechtenstein T., Arasanz H., Lozano T., Casares N., Chaikuad A., Knapp S., Guerrero-Setas D., Escors D., Kochan G, & Santamaría E. (2015). A core of kinase-regulated interactomes defines the neoplastic MDSC lineage. Oncotarget, 6(29), 27160-27175.

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Intestinal Organoids for Serotonin Analysis

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Tph1^CFP mice aged 6–10 weeks were used to generate intestinal organoids, as previously reported (Sato et al., 2009 (link)). Briefly, the small intestine was isolated and washed with cold PBS and crypts were isolated following dissociation in EDTA. Isolated crypts were suspended in Matrigel. Following polymerization, IntestiCult™ Organoid Growth Medium (Stemcell) was added and refreshed every 3–4 days. Organoids were maintained at 37 °C, 5% CO2 and propagated weekly. For the induction of EC cell enriched differentiation, organoids were cultured in standard culture conditions plating in Matrigel for 2 days. The organoids were cultured in the media the cocktails for EC cell enriched differentiation including IWP2 (1.5 mM; Sigma Aldrich), DAPT (10 mM, Sigma Aldrich) and MEK inhibitor PD0325901 (1 mM; Sigma Aldrich) for 7 days. For serotonin measurement, the media was harvested before the treatments and used as control in the quantification of the 5-HT amounts after the treatments.

Chen Z., Luo J., Li J., Kim G., Stewart A., Urban JF J.r., Huang Y., Chen S., Wu L.G., Chesler A., Trinchieri G., Li W, & Wu C. (2020). Interleukin-33 promotes serotonin release from enterochromaffin cells for intestinal homeostasis. Immunity, 54(1), 151-163.e6.

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Retinoic Acid-Induced Differentiation Assay

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Retinoic acid (RA) differentiation experiments were performed as previously described in Semrau et al., 2017. Explicitly, prior to differentiation cells were grown for at least 2 passages in 2i medium plus LIF (2i/L): DMEM/F12 (Gibco) supplemented with 0.5x N2 supplement, 0.5x B27 supplement, 0.5 mM L-glutamine, 20 µg/ml human insulin (Sigma-Aldrich), 1 × 100 U/ml penicillin/streptomycin, 0.5x MEM Non- Essential Amino Acids, 0.1 mM 2-Mercaptoethanol, 1 µM MEK inhibitor (PD0325901, Sigma-Aldrich), 3 µM GSK3 inhibitor (CHIR99021, Sigma-Aldrich), 1000 U/ml mouse LIF (Peprotech). Cells were seeded at a density of 2.5 × 10⁵ per 10 cm dish and grown over night (12 h). The next day cells were washed twice with PBS and medium was replaced with basal N2B27 medium (2i/L medium without inhibitors, LIF and the additional insulin) supplemented with 0.25 μM all-trans retinoic acid (Sigma-Aldrich). Medium was being refreshed every 48H.

Athanasouli P., Balli M., De Jaime-Soguero A., Boel A., Papanikolaou S., van der Veer B.K., Janiszewski A., Vanhessche T., Francis A., El Laithy Y., Nigro A.L., Aulicino F., Koh K.P., Pasque V., Cosma M.P., Verfaillie C., Zwijsen A., Heindryckx B., Nikolaou C, & Lluis F. (2023). The Wnt/TCF7L1 transcriptional repressor axis drives primitive endoderm formation by antagonizing naive and formative pluripotency. Nature Communications, 14, 1210.

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