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Monoclonal mouse hsp90ab1

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Monoclonal mouse HSP90AB1 is a laboratory reagent for the detection of the HSP90AB1 protein in biological samples. It is a mouse-derived monoclonal antibody that specifically binds to the HSP90AB1 protein. The core function of this product is to serve as a tool for the identification and analysis of the HSP90AB1 protein in research applications.

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Lab products found in correlation

Polyclonal rabbit hsf1, by Cell Signaling Technology (2 mentions) Monoclonal rabbit ps326 hsf1, by Abcam (2 mentions) Monoclonal rabbit hspa8, by Cell Signaling Technology (2 mentions) Monoclonal rabbit notch1, by Cell Signaling Technology (2 mentions) Monoclonal mouse actin, by Merck Group (2 mentions) Polyclonal goat lamin a, by Santa Cruz Biotechnology (2 mentions)

2 protocols using monoclonal mouse hsp90ab1

1

Evaluating HSF1 Regulatory Targets in T-ALL

Check if the same lab product or an alternative is used in the 5 most similar protocols
Antibodies against the following proteins were used: polyclonal rabbit HSF1 (Cell Signaling, 4356), monoclonal rabbit pS326 HSF1 (Abcam, 76076), monoclonal mouse HSP90AB1 (GeneTex, 84342), monoclonal rabbit HSPA8 (Cell signaling, 8444), monoclonal rabbit NOTCH1 (Cell Signaling, 4147), monoclonal mouse Actin (Millipore, MAB1501) and polyclonal goat Lamin A (Santa Cruz biotechnology, sc-6214). The shRNAs used against HSF1 and HSF1 positively regulated targets are described in Supplementary Table 3. To generate virus, we transfected HEK293T cells with a plasmid (pLKO.1) expressing the shRNA of interest and lentiviral packaging plasmids. Viral supernatant was collected over a period of 72 h and used for the transduction of T-ALL cells. For survival assays, the cells were infected twice and selected with puromycin starting 2 days after viral infection. For RNA-seq experiments and to avoid the effects of apoptosis due to HSF1 knockdown, infection conditions were optimized to reach ~90% transduction efficiency and RNA was collected 48 h after infection.
Kourtis N., Lazaris C., Hockemeyer K., Balandrán J.C., Jimenez A.R., Mullenders J., Gong Y., Trimarchi T., Bhatt K., Hu H., Shrestha L., Ambesi-Impiombato A., Kelliher M., Paietta E., Chiosis G., Guzman M.L., Ferrando A.A., Tsirigos A, & Aifantis I. (2018). Oncogenic hijacking of the stress response machinery in T cell acute lymphoblastic leukemia. Nature medicine, 24(8), 1157-1166.
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2

Evaluating HSF1 Regulatory Targets in T-ALL

Check if the same lab product or an alternative is used in the 5 most similar protocols
Antibodies against the following proteins were used: polyclonal rabbit HSF1 (Cell Signaling, 4356), monoclonal rabbit pS326 HSF1 (Abcam, 76076), monoclonal mouse HSP90AB1 (GeneTex, 84342), monoclonal rabbit HSPA8 (Cell signaling, 8444), monoclonal rabbit NOTCH1 (Cell Signaling, 4147), monoclonal mouse Actin (Millipore, MAB1501) and polyclonal goat Lamin A (Santa Cruz biotechnology, sc-6214). The shRNAs used against HSF1 and HSF1 positively regulated targets are described in Supplementary Table 3. To generate virus, we transfected HEK293T cells with a plasmid (pLKO.1) expressing the shRNA of interest and lentiviral packaging plasmids. Viral supernatant was collected over a period of 72 h and used for the transduction of T-ALL cells. For survival assays, the cells were infected twice and selected with puromycin starting 2 days after viral infection. For RNA-seq experiments and to avoid the effects of apoptosis due to HSF1 knockdown, infection conditions were optimized to reach ~90% transduction efficiency and RNA was collected 48 h after infection.
Kourtis N., Lazaris C., Hockemeyer K., Balandrán J.C., Jimenez A.R., Mullenders J., Gong Y., Trimarchi T., Bhatt K., Hu H., Shrestha L., Ambesi-Impiombato A., Kelliher M., Paietta E., Chiosis G., Guzman M.L., Ferrando A.A., Tsirigos A, & Aifantis I. (2018). Oncogenic hijacking of the stress response machinery in T cell acute lymphoblastic leukemia. Nature medicine, 24(8), 1157-1166.
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