Normally, when a cell senses it’s becoming cancerous, it can press the self-destruct button to protect the body. However, mutations in this mechanism can keep a cancer cell alive.
Cells use messaging pathways that transmit signals from one protein to another in a cascade to activate cellular processes. In these pathways, there is a “signal protein” and its “receiver” that recognizes it. One example is CD154, a signal protein which activates its receiver CD40. When this happens, the immune system can “turn on” and help kill tumours!
This study investigated how CD40 causes cell death even though the “receiver” proteins that trigger self-destruction do not directly recognize it. To identify the middleman, researchers followed the trail of a protein already known to recognize CD40, TRAF2.
The scientists isolated TRAF2 and discovered its interaction with RIP1, a protein that initiates cell death. This suggests that: when CD40 is activated, it’s recognized by TRAF2, TRAF2 then signals RIP-1, and RIP-1 triggers the cell to die,
This work identifies key players that regulate cell death in cancer cells and highlights potential protein targets that could be leveraged to promote tumor cell death.
CD40 -> TRAF2-> RIP1-> SELF-DESTRUCT ACTIVATED.
Sci Scribes 