AI Article Synopsis
- - Sam68 is an RNA-binding protein that plays roles in the cell cycle, apoptosis, and signaling, notably suppressing cell growth in certain cells when overexpressed.
- - The study reveals that Sam68 is cleaved in immune cells undergoing apoptosis triggered by γ-radiation, and this cleavage occurs in a caspase-dependent way.
- - Additionally, knocking down Sam68 reduces cell death and growth inhibition from γ-radiation, suggesting that its cleavage could serve as an indicator of ionizing radiation's damaging effects.
Article Abstract
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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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4380058 | PMC |
| http://dx.doi.org/10.1093/jrr/rru113 | DOI Listing |
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