Skip to main content
. 2014 Sep 3;71(24):4815–4830. doi: 10.1007/s00018-014-1707-z

Fig. 6.

Fig. 6

Mechanism underlying the effects of protein 4.1B/DAL-1 on tumor cell growth arrest and apoptosis. In the process of cell growth arrest, 4.1B/DAL-1 can suppress cell growth by sequentially activating Src, Rac1, MLK3, and JNK, resulting in reduced cyclinA levels and decreased retinoblastoma (Rb) protein hyperphosphorylation. 4.1B can also inhibit erbB2 phosphorylation, causing cell cycle arrest in the G1 phase. Furthermore, 4.1B/DAL-1 can bind to PRMT5, thereby inhibiting cyclinE1 transcription. In the process of cell apoptosis, 4.1B/DAL-1 can enhance Caspase-8 activation levels to induce cell apoptosis. Alternatively, 4.1B/DAL-1 can activate successively activate TLR4/gab1, JNK, and Caspase-1 signaling to induce apoptosis