Key result
Ionizing radiation induced caspase-dependent cleavage of Sam68 in immune cells undergoing apoptosis, and knockdown of Sam68 attenuated radiation-induced cell death.
The cleavage of Sam68 by caspases serves as a novel indicator for the cellular damaging effects of ionizing radiation.
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Sam68 may modulate radiation-induced immune apoptosis; leaves open its value as radioprotective target pending in vivo studies.
The RNA-binding protein Sam68, a mitotic substrate of tyrosine kinases, has been reported to participate in the cell cycle, apoptosis, and signaling. In particular, overexpression of Sam68 protein is known to suppress cell growth and cell cycle progression in NIH3T3 cells. Although Sam68 is involved in many cellular activities, the function of Sam68, especially in response to apoptotic stimulation, is not well understood. In this study, we found that Sam68 protein is cleaved in immune cells undergoing apoptosis induced by γ-radiation. Moreover, we found that Sam68 cleavage was induced by apoptotic stimuli containing γ-radiation in a caspase-dependent manner. In particular, we showed that activated casepase-3, 7, 8 and 9 can directly cleave Sam68 protein through in vitro protease cleavage assay. Finally, we found that the knockdown of Sam68 attenuated γ-radiation-induced cell death and growth suppression. Conclusively, the cleavage of Sam68 is a new indicator for the cell damaging effects of ionizing radiation.
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Cho et al. (2015) studied Apoptotic cell death induced by ionizing radiation. Ionizing radiation (γ-radiation) was evaluated on Sam68 cleavage and cell death. Ionizing radiation induced caspase-dependent cleavage of Sam68 in immune cells undergoing apoptosis, and knockdown of Sam68 attenuated radiation-induced cell death.
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