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  • p53 deficiency triggers dysregulation of diverse cellular processes in physiological oxygen.

p53 deficiency triggers dysregulation of diverse cellular processes in physiological oxygen.

The Journal of cell biology (2020-09-05)
Liz J Valente, Amy Tarangelo, Albert Mao Li, Marwan Naciri, Nitin Raj, Anthony M Boutelle, Yang Li, Stephano Spano Mello, Kathryn Bieging-Rolett, Ralph J DeBerardinis, Jiangbin Ye, Scott J Dixon, Laura D Attardi
要旨

The mechanisms by which TP53, the most frequently mutated gene in human cancer, suppresses tumorigenesis remain unclear. p53 modulates various cellular processes, such as apoptosis and proliferation, which has led to distinct cellular mechanisms being proposed for p53-mediated tumor suppression in different contexts. Here, we asked whether during tumor suppression p53 might instead regulate a wide range of cellular processes. Analysis of mouse and human oncogene-expressing wild-type and p53-deficient cells in physiological oxygen conditions revealed that p53 loss concurrently impacts numerous distinct cellular processes, including apoptosis, genome stabilization, DNA repair, metabolism, migration, and invasion. Notably, some phenotypes were uncovered only in physiological oxygen. Transcriptomic analysis in this setting highlighted underappreciated functions modulated by p53, including actin dynamics. Collectively, these results suggest that p53 simultaneously governs diverse cellular processes during transformation suppression, an aspect of p53 function that would provide a clear rationale for its frequent inactivation in human cancer.

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モノクローナル抗FLAG® M2抗体 マウス宿主抗体, 1 mg/mL, clone M2, affinity isolated antibody, buffered aqueous solution (50% glycerol, 10 mM sodium phosphate, and 150 mM NaCl, pH 7.4)
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ギムザ染色, 改良溶液, (for the staining (of cellular blood components and blood parasites))