2014 Volume 64 Issue 2 Pages 117-139
The 17-kDa N-terminal region (NTR) of rat histone H10 (Thr 2 - Phe107 ) was generated during TAM-induced apoptosis and acted as a DNase, for which two histidine residues at 25 and 57 were essential. The 17-kDa H10NTR was generated by the restricted cleavage of H10 with the Ca2+-dependent protease calpain-2, which was activated by TAM-induced Ca2+ influx ([Ca2+]i). The forced expression of the 17-kDa H10NTR stimulated, while its downregulation suppressed TAM-induced apoptosis. These results imply the involvement of the 17-kDa H10NTR DNase downstream of the TAM-triggered cell death signaling pathway, suggest that TAM could be a promising chemoprevention and anticancer drug for AFB1 hepatocarcinogenesis, and also provide a new insight into the biological functions of H10.