U0126

Manufactured by Cell Signaling Technology

Sourced in United States, Germany, United Kingdom, China, France, Japan, Canada

U0126 is a specific inhibitor of the mitogen-activated protein kinase kinase (MEK1 and MEK2). It functions by blocking the activation of MAPK/ERK pathway.

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Lab products found in correlation

Ly294002, by Cell Signaling Technology (70 mentions) Sb203580, by Cell Signaling Technology (51 mentions) Fetal bovine serum (fbs), by Thermo Fisher Scientific (35 mentions) Sp600125, by Cell Signaling Technology (32 mentions) Pd98059, by Cell Signaling Technology (24 mentions) Dimethyl sulfoxide (dmso), by Merck Group (23 mentions) Sp600125, by Merck Group (20 mentions) Sb203580, by Merck Group (16 mentions) Penicillin streptomycin, by Thermo Fisher Scientific (15 mentions) Ly294002, by Merck Group (14 mentions) Dulbecco modified eagle medium (dmem), by Thermo Fisher Scientific (14 mentions) Wortmannin, by Cell Signaling Technology (13 mentions) Lipofectamine 2000, by Thermo Fisher Scientific (12 mentions) Cycloheximide (chx), by Merck Group (11 mentions) Rapamycin, by Merck Group (11 mentions) Wortmannin, by Merck Group (11 mentions) Penicillin, by Thermo Fisher Scientific (11 mentions) Streptomycin, by Thermo Fisher Scientific (11 mentions) Sb202190, by Cell Signaling Technology (9 mentions) β actin, by Cell Signaling Technology (9 mentions)

515 protocols using u0126

Protective Effects of (+)-Pentazocine and ERK Inhibitor on H2O2-Induced Oxidative Stress in ONHAs

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For MTT assay, ONHAs were seeded onto 96-well plates (10,000 cells/well). To determine (+)-pentazocine (Sigma, St. Louis, MO) toxicity to ONHA, ONHAs were exposed to increasing (+)-pentazocine concentrations (1, 3, 10, 50μM) for 24 hours. To determine H₂O₂ (Sigma, St. Louis, MO) toxicity to ONHA, ONHA were exposed to increasing H₂O₂ concentrations (50, 100, 150, 200, 250, 500μM) for 24 hours. To detect if (+)-pentazocine would protect ONHAs from H₂O₂ induced cell death, ONHAs were pre-treated with 10μM (+)-pentazocine for 1 hour followed by 100 μM H₂O₂ cotreatment with 10μM (+)-pentazocine for 24 hours. To detect if ERK inhibitor U0126 (Cell Signaling Technology, Danvers, MA) would protect ONHAs from H₂O₂ induced cell death, ONHAs were pre-treated with 10μM U0126 for 1 hour followed by 100 μM H₂O₂ cotreatment with 10μM U0126 for 24 hours.
To detect changes in phosphorylated ERK levels in ONHAs exposed to H₂O₂ and (+)-pentazocine, ONHAs were seeded onto 24 well plates at 20,000 cells /well. Cells were treated with 100μM H₂O₂ with or without 1-hour pre-treatment of 10μM (+)-pentazocine. After 15 minutes, 30 minutes, 1hour, 3 hours and 24 hours, cell lysates were collected for western blot to detect p-ERK, total ERK and GAPDH expression.

Zhao J., Mysona B.A., Wang J., Gonsalvez G.B., Smith S.B, & Bollinger K.E. (2017). Sigma 1 receptor regulates ERK activation and promotes survival of optic nerve head astrocytes. PLoS ONE, 12(9), e0184421.

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Muscle Incubation with Undercarboxylated Osteocalcin

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Muscles were evenly divided longitudinally into halves to improve the effusion of ucOC into muscle fiber ex vivo, similar to what has been performed in rat muscle in previous studies (16 (link)–18 (link)). The whole ucOC stimulation process is shown in Figure S1 in Supplementary Material. In experiments without the ERK inhibitor U0126, muscle samples were preincubated in 30°C baths containing carbogenated KHB buffer for 1 h. In experiments with U0126 (N = 5), after 30 min preincubation, muscle samples were exposed to the ERK inhibitor U0126 (1 µM) (Cell Signaling, MA, USA) or dimethyl sulfoxide (DMSO) vehicle (Sigma-Aldrich, MO, USA) for 30 min. Then, muscle samples were stimulated for 90 min with increasing doses [0 ng mL⁻¹ (N = 6), 0.3 ng mL⁻¹ (N = 10), 3 ng mL⁻¹ (N = 10), 10 ng mL⁻¹ (N = 14), or 30 ng mL⁻¹ (N = 10)] of recombinant ucOC (Bachem, Bubendorf, Switzerland). These doses of ucOC were chosen because they are within the physiological range in mice (7 (link), 31 (link)). In experiments without U0126, muscle halves from the same mouse were treated with KHB buffer control or ucOC. In experiments with U0126, muscle halves from the same mouse were treated with DMSO, DMSO with ucOC, U0126, and U0126 with ucOC, respectively.

Lin X., Parker L., Mclennan E., Zhang X., Hayes A., McConell G., Brennan-Speranza T.C, & Levinger I. (2017). Recombinant Uncarboxylated Osteocalcin Per Se Enhances Mouse Skeletal Muscle Glucose Uptake in both Extensor Digitorum Longus and Soleus Muscles. Frontiers in Endocrinology, 8, 330.

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OSCC Cell Culture and MAPK Inhibition

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Human HSC-3 OSCC cells (JCRB0623) were obtained from the Human Science Research Resources Bank, Japan Health Sciences Foundation (Tokyo, Japan). HSC-3 cells were cultured in Eagle's minimum essential medium (E-MEM; Wako Pure Chemical Industries, Ltd.) supplemented with 10% fetal bovine serum (FBS; Equitech-Bio, Inc.) at 37°C in a humidified atmosphere with 5% CO₂ and 95% air. U0126 (Cell Signaling Technology, Inc.), an inhibitor of mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK), was dissolved in dimethyl sulfoxide and added to the culture medium 1 h before MHT treatment (final concentration of U0126: 10 µM).

Tabuchi Y., Maekawa K., Torigoe M., Furusawa Y., Hirano T., Minagawa S., Yunoki T, & Hayashi A. (2020). HIKESHI silencing can enhance mild hyperthermia sensitivity in human oral squamous cell carcinoma HSC-3 cells. International Journal of Molecular Medicine, 46(1), 58-66.

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Neuroprotective Effects of Myrtenol in Rat MCAO Model

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Myrtenol was purchased from Sigma-Aldrich Corporation (W343900, CAS-No.19894-97-4, purity ≥95%; Figure 1). Seventy-five SD rats were randomly divided into five groups (n = 15): sham group: rats were treated with saline but without middle cerebral artery occlusion (MCAO). MCAO group: rats were given with saline alone with cerebral ischaemia/reperfusion (I/R) surgery. MCAO + Myr groups: rats were intraperitoneally injected with 10, 30, or 50 mg/kg Myrtenol after cerebral I/R surgery, respectively (Britto et al. 2018 (link)), once daily for seven consecutive days. The remaining 60 SD rats were randomly divided into four groups (n = 15): sham group, MCAO group, MCAO + Myr (50 mg/kg) group: rats were treated as above, MCAO + Myr + U0126 group: rats were intracerebroventricularly injected with 10 μL U0126 (Cell Signalling Technology, USA), a highly selective inhibitor of MEK (Ahnstedt et al. 2015 (link)), into the cerebral ischaemia side at 30 min prior to Myrtenol treatment, once daily for 7 consecutive days. The intracerebral ventricular injection and the dose of U0126 were based on the work of Ye et al. (2018 (link)).

Huang S., Tan Z., Cai J., Wang Z, & Tian Y. (2021). Myrtenol improves brain damage and promotes angiogenesis in rats with cerebral infarction by activating the ERK1/2 signalling pathway. Pharmaceutical Biology, 59(1), 582-591.

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Cardiac Fibroblast Isolation and Treatment

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One- to 3-day-old neonatal Sprague-Dawley rats were killed by decapitation. The hearts were tore into small pieces and predigested by 0.125% trypsogen for 5 minutes and then digested with 0.06% collagenase-II for 2 hours in a shaker at 37°C. Collected cells were plated onto a culture dish for 45 minutes. Then, unattached cells were removed. The remained cardiac fibroblasts were cultured in high glucose (4500 mg/L) Dulbecco’s modified Eagle’s medium (DMEM) supplemented with 10% fetal bovine serum in a humidified incubator with 5% CO₂ at 37°C. The purity of cardiac fibroblasts was greater than 98% as determined by positive staining for vimentin and negative staining for von Willebrand factor. Cells were cultured in serum-free DMEM for 24 hours before treatment. Cells were treated with (1) dimethyl sulfoxide (DMSO) (1 μL, Sigma-Aldrich) alone, (2) Ang II (100 nmol/L, Sigma-Aldrich), (3) apocynin (100 μmol/L) alone, (4) Ang II (100 nmol/L)+apocynin (100 μmol/L), (5) ERK1/2 inhibitor U0126 (10 μmol/L, Cell Signaling Technology), or (6) Ang II (100 nmol/L)+U0126 (10 μmol/L). apocynin and U0126 were dissolved in DMSO and added to cells for 1 hour before the stimulation of Ang II. Cells were treated with Ang II for 24 hours before detection of the expressions of procollagen I, procollagen III, transforming growth factor (TGF)-β and FGF-2.

Liu Y., Liu Y., Liu X., Chen J., Zhang K., Huang F., Wang J.F., Tang W, & Huang H. (2015). Apocynin Attenuates Cardiac Injury in Type 4 Cardiorenal Syndrome via Suppressing Cardiac Fibroblast Growth Factor-2 With Oxidative Stress Inhibition. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 4(7), e001598.

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Resveratrol and Pinostilbene Effects on Dopamine-Induced Toxicity

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Resveratrol was purchased from ChemPacific, Baltimore, MD. pinostilbene was synthesized by Dr. Cassia Mizuno in Dr. Agnes Rimando’s laboratory following published procedures. [31 ] Stock solutions of Resveratrol and pinostilbene were made in DMSO (Sigma Aldrich) and further diluted in serum-free media. SH-SY5Y cells were treated with 1 or 5 µM of Resveratrol, pinostilbene or DMSO (vehicle for Resveratrol and pinostilbene). DA (Sigma Aldrich) was dissolved in sterile water to an initial concentration of 100 mM. Following treatment with Resveratrol, pinostilbene, or DMSO (30 min), SH-SY5Y cells were treated with DA (50, 100, or 200 µM) or H₂O (vehicle for DA) for 24 hrs. U0126 (Cell Signaling) was dissolved in DMSO to an initial concentration of 10 mM. Cells were treated with U0126 (10 µM) or DMSO (vehicle) 1 hr prior to Resveratrol treatment/90 min prior to DA treatment.

Allen E.N., Potdar S., Tapias V., Parmar M., Mizuno C.S., Rimando A, & Cavanaugh J.E. (2017). Resveratrol and pinostilbene confer neuroprotection against aging-related deficits through an ERK1/2 dependent-mechanism. The Journal of nutritional biochemistry, 54, 77-86.

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TGFβ1-Induced Signaling Inhibition

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Recombinant TGFβ1 (R&D systems, Minneapolis, MN, USA) was reconstituted per the manufacturer’s instructions and used at 5–10 ng/ml. U0126 (Cell Signaling, Danvers, MA, USA) was dissolved in DMSO and used at 5 μM. Cells were incubated with U0126 for 60–120 min prior to treatment with either control media or media with Recombinant TGFβ1.

Principe D.R., Diaz A.M., Torres C., Mangan R.J., DeCant B., McKinney R., Tsao M.S., Lowy A., Munshi H.G., Jung B, & Grippo P.J. (2017). TGFβ engages MEK/ERK to differentially regulate benign and malignant pancreas cell function. Oncogene, 36(30), 4336-4348.

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Neonatal Intranasal E. coli Infection in Mice

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C57BL/6 mice were purchased from SLACS (Shanghai, China). This study was carried out in accordance with the guidelines of the Institutional Animal Care and Use Committee of the Institute for Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, China. The protocol was approved by the Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, China. C57BL/6 mice (5-day-old) were inoculated intranasally with 10 μL of bacterium solution containing 10⁵ cfu E. coli. The uninfected and U0126 control group were injected with 10 μL of isotonic saline. Both treatment and U0126 control group were subjected to 20 μL intraperitoneal injections of U0126 (Cell Signaling Technology, USA) at the dose of 3 mg/kg each, delivered at the following time points: 24 h prior to the inoculation of E. coli, at the time of inoculation, as well as 24 and 48 h after inoculation. After 72 h following the inoculation, the mice were euthanized and the brains were harvested. One half of each brain specimen was fixed in 4% PFA for histopathological analysis. The remaining half was homogenized for cytokine assays (Zwijnenburg et al., 2007 (link); Mittal et al., 2010 (link)).

Zhao M., Zhang L., Lv S., Zhang C., Wang L., Chen H., Zhou Y, & Lou J. (2017). IQGAP1 Mediates Hcp1-Promoted Escherichia coli Meningitis by Stimulating the MAPK Pathway. Frontiers in Cellular and Infection Microbiology, 7, 132.

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MEK1/2 Inhibitor Modulates HSV-1 Infection

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U0126, specific inhibitor of the MEK1/2^{48 (link)} was obtained from Cell Signaling Technology (Beverly, MA) and used at the final concentration of 5 µM. U0126 has been reconstituted in DMSO; the same percentage of DMSO, diluted in RPMI, was used in the untreated cells. HEp-2 cells, were pre-treated for 1 h at 37 °C with U0126 (5 µM), and infected with 10 PFU of HSV-1 in presence of the inhibitor. Phosphonoacetic acid (PAA) from Sigma-Aldrich, was used as an inhibitor of DNA synthesis in HSV-infected cells and was dissolved in the medium and used at 300 µg/ml during and after HSV-1 adsorption. At different time points post infection, defined in experimental designs, the cells were harvested and analyzed.

Colao I., Pennisi R., Venuti A., Nygårdas M., Heikkilä O., Hukkanen V, & Sciortino M.T. (2017). The ERK-1 function is required for HSV-1-mediated G1/S progression in HEP-2 cells and contributes to virus growth. Scientific Reports, 7, 9176.

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Intratumoral U0126 Administration

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U0126, a MAPK kinase (MEK) 1/2 inhibitor, was purchased from Cell Signaling Technology (#9903, Beverly, MA) and dissolved in dimethyl sulfoxide (DMSO) to a concentration of 0.1 mg/mL. U0126 suspension was freshly prepared and administered at a constant volume of 1 mL/100 g body weight every 3 days (1 mg/kg per 3 days, i.p.). The control group for this experiment was given the same volume of mixture without U0126.

Yu C., Tang L., Liang C., Chen X., Song S., Ding X., Zhang K., Song B., Zhao D., Zhu X., Li H, & Zhang Z. (2016). Angiotensin‐Converting Enzyme 3 (ACE3) Protects Against Pressure Overload‐Induced Cardiac Hypertrophy. Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, 5(2), e002680.

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