A6185

Manufactured by Merck Group

A6185 is a laboratory equipment product. It serves as a centrifuge, which is a machine used to separate components of a liquid mixture based on their relative density. The centrifuge spins the sample at high speed, causing the denser components to move outward and separate from the less dense components.

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Lab products found in correlation

Doxorubicin, by Merck Group (1 mentions) Nu7026, by Merck Group (1 mentions) Ly2157299, by Selleck Chemicals (1 mentions) S2619, by Selleck Chemicals (1 mentions) 5 aza dc, by Merck Group (1 mentions) Tunicamycin, by Merck Group (1 mentions)

2 protocols using a6185

Cell Line Culture and Manipulation

Cited 5 times

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LNCaP, LNCaP-LN3, C4, C4–2, C4–2B, PC-3M, PC-3M-LN4, PC-3M-Pro4, and MDA-MB453 cells were grown as previously described [30 (link), 67 (link)]. The HEK293T, PC3, and C4–2 cells were cultured in DMEM supplemented with 10% fetal calf serum, 1% penicillin, and 1% streptomycin. The DNA methylase inhibitor 5-Aza-dC (10 μM) (#A3656, Sigma), the 26S proteasome inhibitors MG132 (20 μM) (#S2619, Selleckchem), or N-acetyl-L-leucyl-L-leucyl-L-nor leucinal (LLNL) (25 μM) (#A6185, Sigma), Doxorubicin (Sigma), Talazoparib (SeleckChem), NU7026 (Sigma) were used as described in the text. TGF-β receptor type I (TGF-βRI) kinase inhibitors LY2157299 and LY363947 were bought from Selleckchem.
The expression vectors encoding DACH1 [69 (link)], Ku70 (RFP-Ku70) and Ku80 (RFP-Ku80) [70 (link)], shDACH1[71 (link)] were previously described. The EGFP-DACH1 expression plasmid was made by inserting the human DACH1 cDNA into the HindIII and BamHI sites of the pEGFP-C1 vector.

Li Z., Jiao X., Robertson A.G., Sante G.D., Ashton A.W., DiRocco A., Wang M., Zhao J., Addya S., Wang C., McCue P.A., South A.P., Cordon-Cardo C., Liu R., Patel K., Hamid R., Parmar J., DuHadaway J.B., Jones S.J., Casimiro M.C., Schultz N., Kossenkov A., Phoon L.Y., Chen H., Lan L., Sun Y., Iczkowski K.A., Rui H, & Pestell R.G. (2023). The DACH1 gene is frequently deleted in prostate cancer, restrains prostatic intraepithelial neoplasia, decreases DNA damage repair, and predicts therapy responses. Research Square.

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Pharmacological Induction of ER Stress

Cited 1 time

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Pharmacological induction of ER stress and activation of the UPR was performed according to previously described methods^{21 (link),22 (link)}. Briefly, cells were treated with ALLN (calpain inhibitor I; 100 μM, Sigma-Aldrich, A6185) or tunicamycin (2.5 μg/ml, Sigma-Aldrich, T7765) for the time periods specified.

Gebert M., Bartoszewska S., Janaszak-Jasiecka A., Moszyńska A., Cabaj A., Króliczewski J., Madanecki P., Ochocka R.J., Crossman D.K., Collawn J.F, & Bartoszewski R. (2018). PIWI proteins contribute to apoptosis during the UPR in human airway epithelial cells. Scientific Reports, 8, 16431.

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