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Ml240

Manufactured by Merck Group
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Sourced in United States, Japan

The ML240 is a high-performance laboratory equipment designed for precise liquid handling tasks. It features advanced automation capabilities and integrated digital control systems to ensure accurate and consistent results. The core function of the ML240 is to facilitate efficient and reliable liquid handling processes within laboratory environments.

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Lab products found in correlation

Nms 873, by Selleck Chemicals (3 mentions) Colchicine, by Fujifilm (2 mentions) Thapsigargin, by Fujifilm (2 mentions) Cb 5083, by Selleck Chemicals (1 mentions) Tunicamycin, by Merck Group (1 mentions) Nms 873, by Merck Group (1 mentions) Vincristine, by Cayman Chemical (1 mentions) Celltiter glo 2, by Promega (1 mentions) Substrate, by Promega (1 mentions) Vincristine, by Fujifilm (1 mentions) Pd153035, by Selleck Chemicals (1 mentions) Sb203580, by Merck Group (1 mentions) Lytic buffer, by Promega (1 mentions) Lgbit, by Promega (1 mentions) Brefeldin a, by BioLegend (1 mentions) Cb 5083, by MedChemExpress (1 mentions) Acy 1215, by MedChemExpress (1 mentions)

6 protocols using ml240

1

Preparing Stock Solutions for Cell-Based Assays

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CB-5083 (Selleckchem, Houston, TX, USA, S8101), ML240 (Sigma-Aldrich, SML1071), DBeQ (Sigma-Aldrich, SML0031), NMS-873 (Selleckchem, S7285) and UPCDC30245 (Sigma-Aldrich, SML1674) were dissolved in DMSO to make a 50 mM stock solution. Tunicamycin (Sigma-Aldrich, T7765) was dissolved in DMSO to make 10 mM stock solution. The stock solution was aliquoted and stored at −80 °C, which was further diluted before making the final concentrations of the compound in culture media.
Bastola P., Wang F., Schaich M.A., Gan T., Freudenthal B.D., Chou T.F, & Chien J. (2017). Specific mutations in the D1–D2 linker region of VCP/p97 enhance ATPase activity and confer resistance to VCP inhibitors. Cell Death Discovery, 3, 17065-.
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2

Purification and Use of Inhibitor Compounds

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Candidate inhibitor compounds DBeQ, ML240, and NMS-873 were purchased from Sigma-Aldrich (St Louis, MO) and used directly without further purification; C3 and C6 were obtained from TimTec (Newark, DE). The compounds in a powder form were dissolved in DMSO at 10 mM and used in biochemical studies after further dilutions.
Glaza P., Ranaweera C.B., Shiva S., Roy A., Geisbrecht B.V., Schoenen F.J, & Zolkiewski M. (2020). Repurposing p97 inhibitors for chemical modulation of the bacterial ClpB–DnaK bichaperone system. The Journal of Biological Chemistry, 296, 100079.
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3

Cytotoxicity Assessment of Anticancer Drugs

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Initially, 5×103 of PC9-KI, A375, and MDAMB231 cells were seeded on 96 well plates. After 24 h, 0.1 % DMSO or 10−5 μM, 10−4 μM, 10−3μM, 10−2μM, 10−1μM, 1 μM, or 10 μM of colchicine (WAKO), vincristine (Cayman), thapsigargin (WAKO), and ML-240 (Sigma Aldrich) were added. After 48h, 25 μL of Cell Titer Glo 2.0 (Promega) was added and incubated at 37°C for 30 min. Absorbance at 490 nm was measured using ARVO X3.
Uchida Y., Matsushima T., Kurimoto R., Chiba T., Inutani Y, & Asahara H. (2021). Identification of chemical compounds regulating PD-L1 by introducing HiBiT-tagged cells. FEBS letters, 595(5), 563-576.
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4

Cytotoxicity Screening of Drug Candidates

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First, 4×104 of PC9-KI cells were seeded on 96 well plates. After 24 h, 0.1 % of DMSO or 10−5μM, 10−4μM, 10−3μM, 10−2μM, 10−1μM, 1 μM, or 10 μM of SB203580 (Sigma Aldrich), brefeldin A (BioLegend, CA, USA), PD153035 (Selleck, TX, USA), colchicine (WAKO), vincristine (Cayman, Michigan, USA), thapsigargin (WAKO, Osaka, Japan), and ML-240 (Sigma Aldrich, MO, USA) were added. After 24 h, the medium was discarded, and detection mix (PBS 12.5 μL, lytic buffer (Promega) 12.5 μL, substrate (Promega) 0.25 μL, and LgBiT (Promega) 0.125 μL) was added to each well.
Uchida Y., Matsushima T., Kurimoto R., Chiba T., Inutani Y, & Asahara H. (2021). Identification of chemical compounds regulating PD-L1 by introducing HiBiT-tagged cells. FEBS letters, 595(5), 563-576.
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5

Inhibitor Treatment in Drosophila and Fibroblasts

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Powdered forms of NMS-873 (Selleckchem) and ML240 (Sigma-Aldrich) were dissolved in DMSO as stocks. Stock solution and DMSO as the vehicle control were diluted in ethanol/ddH2O and mixed with Drosophila food. Food dye was added to ensure thorough mix. Parents of desired genotypes were put in DMSO or inhibitors containing food for 3 days and removed. Thus, all growth following egg laying occurred in the presence of inhibitors. Immediately after eclosion, the progeny were transferred to newly prepared food vials containing the same concentration of DMSO or inhibitors. The progeny was assayed at the time points stated in the text. For human fibroblast treatment, stock solution of ML240, NMS-873 and DMSO vehicle control were diluted to the desired concentration and added to the culture media. Media were changed each day if the treatment was longer than 24 hr.
Zhang T., Mishra P., Hay B.A., Chan D, & Guo M. (2017). Valosin-containing protein (VCP/p97) inhibitors relieve Mitofusin-dependent mitochondrial defects due to VCP disease mutants. eLife, 6, e17834.
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6

MCL Cell Lines and De-identified Samples

Cited 2 times
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Human MCL cell lines MO2058, JeKo-1 and Z138C were cultured as described previously [4 (link)]. Rec-1 and JVM-2 cells were obtained from ATCC. All cells were screened for cyclin D1 expression and authenticated from University of Arizona Genetics Core every 6 months. All primary de-linked de-identified MCL samples were procured after informed consent through an institutionally approved protocol (HSC-5929). B cells were isolated from MCL specimens as described previously [22 (link)]. p97 inhibitors DBeQ and NMS-873 were obtained from Selleck chemicals (Houston, TX), ML240 was obtained from Sigma Aldrich (St. Louis, MO) and ACY-1215 and CB-5083 were obtained from MedChem Express (NJ.)
Vekaria P.H., Kumar A., Subramaniam D., Dunavin N., Vallurupalli A., Schoenen F., Ganguly S., Anant S., McGurik J.P., Jensen R.A, & Rao R. (2019). Functional cooperativity of p97 and histone deacetylase 6 in mediating DNA repair in mantle cell lymphoma cells.. Leukemia, 33(7), 1675-1686.
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