TRAIL promotes a pro-survival signal in erythropoietin-deprived human erythroblasts through the activation of an NF-kB/IkBalpha pathway.

0393-974X (2011) Copyright © by BIOLIFE, s.a.s. This publication and/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties 375 commonly known as death receptors, although they have also been recently linked to anti-apoptotic functions (2-4). TRAIL-R3 (DcR1) and TRAIL-R4 (DcR2) do not contain death domains and represent a mechanism through which TRAIL-mediated apoptosis is inhibited in normal cells and tissues (2). In particular, TRAIL-R4 contains a truncated death domain and inhibits TRAIL-induced apoptosis through the activation of NF-κB and expression Tumour necrosis factor (TNF)-related apoptosisinducing ligand (TRAIL), also called Apo-2L, is a member of the TNF family of cytokines which influences different functions including cell activation and death (1). TRAIL interacts with 4 high affinity transmembrane receptors belonging to the apoptosis-inducing TNF-receptor (R) family. TRAIL-R1 (DR4) and TRAIL-R2 (DR5) transduce apoptotic signals on binding of TRAIL and are TRAIL PROMOTES A PRO-SURVIVAL SIGNAL IN ERYTHROPOIETIN-DEPRIVED HUMAN ERYTHROBLASTS THROUGH THE ACTIVATION OF AN NF-κB/IκBα PATHWAY