Complementary signaling pathways regulate the unfolded protein response and are required for C. elegans development.

By Xiaohua Shen, R. Ellis, Kyungho Lee, Chuan-Yin Liu, Kun Yang, A. Solomon, Hiderou Yoshida, Rick Morimoto, D. Kurnit, K. Mori and 1 more. Cell, 2001

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Endoplasmic Reticulum Stress and Oxidative Stress: A Vicious Cycle or a Double-Edged Sword? (2007, positive): “Several groups demonstrated that XBP1 mRNA is a substrate for the endoribonuclease activity of metazoan IRE1 (13, 70, 126, 159).”
Integrating the mechanisms of apoptosis induced by endoplasmic reticulum stress (2011, background): “Molecular mechanisms of apoptosis triggered by IRE1α signalling In organisms such as yeast and worms, the IRE1 branch of the UPR has an essential role in defending cells and tissues against the lethal consequences of ER stres”
Plasma cell differentiation and the unfolded protein response intersect at the transcription factor XBP-1 (2003, background): “Three independent groups working in both mammalian and Caenorhabditis elegans model systems have shown that XBP1 mRNA undergoes IRE1-dependent splicing in response to ER stres”
Regulation of apoptosis by endoplasmic reticulum pathways (2003, background): “…endonuclease domain that excises a short sequence from the mRNA of the X-Box binding protein (XBP-1), generating an active bZIP transcription factor that stimulates transcription of ER chaperone genes (Ma and Hendershot, 2001; Shen et al., 2001; Yoshida et al., 2001; Calfon et al., 2002).”