Phospho erαser167

Manufactured by Cell Signaling Technology

Phospho-ERαSer167 is a lab equipment product from Cell Signaling Technology. It is an antibody that specifically recognizes the serine 167 phosphorylated form of the estrogen receptor alpha (ERα) protein.

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Lab products found in correlation

2 protocols using phospho erαser167

Molecular Response to Taselisib and Letrozole

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Taselisib, also called GDC-0032, was generated at Genentech, Inc. (South San Francisco, CA). Letrozole was obtained from US Biological. Antibodies used include phospho-AKT^Ser473, AKT, phospho-PRAS40^Thr246, phospho-S6^Ser235/236, phospho-S6^Ser240/242, S6, phospho-ERK^{Thr202/Tyr204}, ERK, phospho-ERα^Ser118, phospho-ERα^Ser167, cleaved PARP, p110α, phospho-p70S6K^Thr389, PR, cyclin E, phospho-mTOR^Ser2448, IGF1R, BRCA1, c-Myc, CAV1, HER2 and cyclin D1 obtained from Cell Signaling (Danvers, MA). Antibodies for ERα and ERβ were obtained from Santa Cruz biotechnology (Santa Cruz, CA) and a βActin antibody was obtained from Sigma (St. Louis, MO).

Hoeflich K.P., Guan J., Edgar K.A., O'Brien C., Savage H., Wilson T.R., Neve R.M., Friedman L.S, & Wallin J.J. (2016). The PI3K inhibitor taselisib overcomes letrozole resistance in a breast cancer model expressing aromatase. Genes & Cancer, 7(3-4), 73-85.

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Characterization of Cell Line Models

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The 293T, MCF7, T47D, ZR-75-30 (ZR), BT549, 231, 468, and derived cell lines were from ATCC. The 2FTGH, U1A, U4A, and γ2A cells were described by Watling et al. (25 (link)). All cells were maintained in Dulbecco’s modified Eagle’s medium supplemented with 10% fetal calf serum (Gibco), 100 U/mL penicillin, and 100 mg/mL streptomycin (Sangon Biotech). Antibodies against phospho-JAK2 (Tyr1007/1008), JAK2, phosphor-STAT3 (Tyr705), STAT3, phospho-STAT1 (Tyr-701), STAT1, phospho-STAT5 (Tyr-694), STAT5, phospho-AKT (Tyr-473), AKT, pmTOR, PTEN, p-HER2, HER2, pFGFR, pSRC, pERK, pPKA, pP65, pIKK, IKK, pIκB, IκB, phospho-ERα (Ser167), and ERα were from Cell Signaling Technology. Hygromycin, puromycin, and anti-FLAG were from Sigma-Aldrich. Anti-ZIP was from Abgent. Antibody against mouse IgG was from Santa Cruz. Antibodies against actin and GAPDH were from Goodhere. AZD1480 and ruxolitinib were from SelleckChem. Tamoxifen citrate was from Merck. Transfection reagents were from Qiagen or Invitrogen. The luciferase assay substrate was from Promega. General biochemical reagents were from Sangon Biotech. Restriction, ligation, and PCR enzymes were from Thermo Fisher. The EGFR inhibitor (C3327), the HER2 inhibitor, AG879, the AKT inhibitor, AZD5363, and the NFκB inhibitor, QNZ, were from APExBio.

Zhu N., Zhang J., Du Y., Qin X., Miao R., Nan J., Chen X., Sun J., Zhao R., Zhang X., Shi L., Li X., Lin Y., Wei W., Mao A., Zhang Z., Stark G.R., Wang Y, & Yang J. (2020). Loss of ZIP facilitates JAK2-STAT3 activation in tamoxifen-resistant breast cancer. Proceedings of the National Academy of Sciences of the United States of America, 117(26), 15047-15054.

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