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N ethyl n nitrosourea enu

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N-ethyl-N-nitrosourea (ENU) is a chemical compound that is commonly used as a laboratory tool in research and experimentation. It serves as a mutagenic agent, capable of inducing genetic mutations in cells and organisms. ENU's core function is to facilitate the study of genetic processes and the impact of genetic modifications, without providing any interpretation or recommendations for its intended use.

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Lab products found in correlation

Lb 100, by Selleck Chemicals (1 mentions) Clove oil, by Merck Group (1 mentions) Bendamustine, by Selleck Chemicals (1 mentions) Prednisolone, by Fujifilm (1 mentions) Vincristine, by Selleck Chemicals (1 mentions) Sodium pyruvate, by Thermo Fisher Scientific (1 mentions) Doxorubicin, by Selleck Chemicals (1 mentions) Z vad fmk, by Merck Group (1 mentions) Hepes, by Merck Group (1 mentions) Dimethyl sulfoxide (dmso), by Merck Group (1 mentions) Fetal bovine serum (fbs), by Merck Group (1 mentions) Rpmi 1640, by Merck Group (1 mentions) D glucose, by Merck Group (1 mentions)

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N-ethyl-N-nitrosourea

5 protocols using n ethyl n nitrosourea enu

1

ENU-Induced Carcinogenesis Protocol

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The n-ethyl-n-nitrosourea (ENU) was purchased from Sigma Aldrich (St. Louis, MO, USA). It was stored at −20 °C until needed for the experiment. The chemical carcinogen was prepared freshly on each of the administration day by dissolving the required quantity according to the average bodyweight of the mice in the treatment group in the required volume of normal saline. The dissolved powder was mixed thoroughly by vortex to dissolve the solute properly. Eighty (80) mg/kg bodyweight of the dissolved powder was injected to each of the mice in the treatment group via intraperitoneal route using an insulin syringe with a 26-gauge needle. The mice were injected twice with the same dose at one-week interval [35 (link)]. The mice were closely monitored for any signs of toxicity and/or mortality. Feed and water were made available for the mice ad libitum.
Aliyu A., Shaari M.R., Ahmad Sayuti N.S., Reduan M.F., Sithambaram S., Noordin M.M., Shaari K, & Hamzah H. (2020). N-Ethyl-n-Nitrosourea Induced Leukaemia in a Mouse Model through Upregulation of Vascular Endothelial Growth Factor and Evading Apoptosis. Cancers, 12(3), 678.
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2

Mutagenesis Screen for EGFR Inhibitor Resistance

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N-ethyl-N-nitrosourea (ENU) was purchased from Sigma Aldrich and mutagenesis studies were carried as previously described (25 (link)). Briefly, 1×106 cells/ml of L858R and L858R/T790M Ba/F3 cells were treated with 50μg/ml of ENU for 24 hours before the cells were washed in RPMI media and allowed to expand. 1×104 cells per well were plated in 96 wells and 5 plates were plated per condition. These cells were treated continuously with either DMSO, 1μM gefitinib, 1μM osimertinib, 10μM JBJ-04-125-02 alone or with gefitinib/JBJ or osimertinib/JBJ drug combinations with media and drug change once a week. Cell growth was monitored and number of resistant colonies were counted and expanded.
To C., Jang J., Chen T., Park E., Mushajiang M., De Clercq D.J., Xu M., Wang S., Cameron M.D., Heppner D.E., Shin B.H., Gero T.W., Yang A., Dahlberg S.E., Wong K.K., Eck M.J., Gray N.S, & Jänne P.A. (2019). Single and dual targeting of mutant EGFR with an allosteric inhibitor. Cancer discovery, 9(7), 926-943.
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3

ENU-induced Mouse Cancer Model

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In carcinogen‐induced mouse model, N‐ethyl‐N‐nitrosourea (ENU) (759‐73‐9, Sigma–Aldrich) or PBS was administrated intraperitoneally (0.5 µmol per g of body weight) to Ripk3+/+and Ripk3−/‐ mice at postnatal day 14 (P14). After 30 days of injection, mice were injected with LB‐100 (S7537, Selleck) or SMAP (S8774, Selleck) intraperitoneally at 2 mg kg−1 on alternate days for 30 days.
Hwang S., Ha Y., Koo G., Noh H., Lee A., Kim B., Hong S.M., Morgan M.J., Eyun S., Lee D., Roe J., Lee Y, & Kim Y. (2022). LCK‐Mediated RIPK3 Activation Controls Double‐Positive Thymocyte Proliferation and Restrains Thymic Lymphoma by Regulating the PP2A‐ERK Axis. Advanced Science, 9(32), 2204522.
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4

ENU Mutagenesis in Zebrafish

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Tuebingen male fish were treated with N-ethyl-N-nitrosourea (ENU; Sigma) following an optimized protocol using clove oil (Sigma) as a sedative (Rohner et al., 2011 (link)). The surviving mutagenized founders were crossed to frntt31786 homozygous females. Progeny were screened at 2–3 months of age to identify frnt phenotypes. Mutants were maintained by out crossing to Tuebingen wild-type strain and incrossing.
Li C., Barton C., Henke K., Daane J., Treaster S., Caetano-Lopes J., Tanguay R.L, & Harris M.P. (2020). celsr1a is essential for tissue homeostasis and onset of aging phenotypes in the zebrafish. eLife, 9, e50523.
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5

Obinutuzumab-based Combination Chemotherapy

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Obinutuzumab was provided by F. Hoffmann-La Roche Ltd. Doxorubicin, vincristine, bendamustine (Selleck Chemicals LLC), 4-hydroperoxy-cyclophosphamide (4-OOH-CY), an active metabolite of cyclophosphamide (Cayman Chemical), and prednisolone (Fujifilm Wako Pure Chemical Corporation) were used as the combined chemotherapeutic agents. Each of these agents was dissolved in dimethyl sulfoxide (Sigma-Aldrich). N-ethyl-N-nitrosourea (ENU) and Z-VAD-FMK were purchased from Sigma-Aldrich and Promega Corporation, respectively. SU-DHL-4 cells, a human germinal center B cell-like diffuse large B-cell lymphoma cell line, were obtained from the ATCC at 2017, and were maintained in RPMI1640 (Sigma-Aldrich) supplemented with 10% FBS (Sigma-Aldrich), 10 mmol/L HEPES (Sigma-Aldrich), 0.45% D-glucose (Sigma-Aldrich), and 1 mmol/L sodium pyruvate (Thermo Fisher Scientific). All cells were cultured at 37 C under 5% CO 2 , tested Mycoplasma contamination, and passed less than 20 times.
Fujimura T., Yamashita-Kashima Y., Kawasaki N., Yoshiura S., Harada N, & Yoshimura Y. (2021). Obinutuzumab in Combination with Chemotherapy Enhances Direct Cell Death in CD20-Positive Obinutuzumab-resistant Non-Hodgkin Lymphoma Cells. Molecular cancer therapeutics, 20(6).
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