Transcriptional regulation of tumour necrosis factor-related apoptosis-inducing ligand

Abstract

Tumour necrosis factor-related apoptosis-inducing ligand (TRAIL) has dual functions mediating both apoptosis and survival of cells. This review focusses on the current regulatory factors that control TRAIL transcription. Here, we also highlight the role of distinct transcription factors that co-operate and regulate TRAIL in different pathological states. A better understanding of the molecular signalling pathways of TRAIL-induced cell death and survival in disease may lead to more sophisticated technologies for novel therapeutic targets.

Fig. 1

TRAIL-receptor signalling. TRAIL initiates cell death by binding to its death receptors. This results in activation of caspases via either the intrisic (mitochondria) or extrinsic pathway, resulting in cell death. By binding its receptors, TRAIL can also activate the JNK, MAPK, PI3K and NFκB pathways to induce expression of survival genes resulting in increased proliferation and migration of cells and inhibition of apoptosis

Fig. 2

Genomic structure of human TRAIL isoforms. Patterned boxes depict novel exons and sequences recently identified