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Merck

Oncogenic PIK3CA induces centrosome amplification and tolerance to genome doubling.

Nature communications (2017-11-25)
Inma M Berenjeno, Roberto Piñeiro, Sandra D Castillo, Wayne Pearce, Nicholas McGranahan, Sally M Dewhurst, Valerie Meniel, Nicolai J Birkbak, Evelyn Lau, Laurent Sansregret, Daniele Morelli, Nnennaya Kanu, Shankar Srinivas, Mariona Graupera, Victoria E R Parker, Karen G Montgomery, Larissa S Moniz, Cheryl L Scudamore, Wayne A Phillips, Robert K Semple, Alan Clarke, Charles Swanton, Bart Vanhaesebroeck
RESUMO

Mutations in PIK3CA are very frequent in cancer and lead to sustained PI3K pathway activation. The impact of acute expression of mutant PIK3CA during early stages of malignancy is unknown. Using a mouse model to activate the Pik3ca

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Poli-L-lisina, 0.1 % (w/v) in H2O
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Soro de cabra
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Soro asinino
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(Z)-4-Hidroxitamoxifeno, ≥98% Z isomer
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Triton X-100, laboratory grade
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Albumina sérica bovina, heat shock fraction, pH 7, ≥98%
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Anticorpo anti-fosfohistona H2A.X (Ser139), clone JBW301, clone JBW301, Upstate®, from mouse
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Anticorpo anti-β-actina, monoclonal de camundongo, clone AC-15, purified from hybridoma cell culture
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Nocodazole, ≥99% (TLC), powder
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Senescence Cells Histochemical Staining Kit, sufficient for 100 tests
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Anti-α-tubulina monoclonal, clone B-5-1-2, purified from hybridoma cell culture
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Ribonuclease A, Type I-AS, 50-100 Kunitz units/mg protein
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Trypsin solution from porcine pancreas, 1 ×, sterile-filtered, BioReagent, suitable for cell culture, 2.5 g porcine trypsin per liter in Hanks′ Balanced Salt Solution with phenol red
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Monoclonal Anti-α-Actinin antibody produced in mouse, clone BM-75.2, ascites fluid
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Dihydrocytochalasin B