Thymocyte apoptosis induced by p53-dependent and independent pathways

摘要: Death by apoptosis is characteristic of cells undergoing deletion during embryonic development, T- and B-cell maturation endocrine-induced atrophy. Apoptosis can be initiated various agents may a result expression the oncosuppressor gene p53 (refs 6-8). Here we study dependence on in from thymus cortex. Short-term thymocyte cultures were prepared mice constitutively heterozygous or homozygous for introduced into germ line after targeting. Wild-type thymocytes readily undergo treatment with ionizing radiation, glucocorticoid methylprednisolone, etoposide (an inhibitor topoisomerase II), Ca(2+)-dependent activation phorbol ester calcium ionophore. In contrast, null are resistant to induction radiation etoposide, but retain normal sensitivity calcium. The time-dependent that occurs untreated unaffected status. Cells partially etoposide. Our results show exerts significant dose-dependent effect initiation apoptosis, only when it induced cause DNA-strand breakage.