Necrosis is a form of cell death that is detrimental to the affected tissue because the cell
ruptures and releases its content (reactive oxygen species among others) into the
extracellular space. Clusterin (CLU), a cytoprotective extracellular chaperone has been
shown to be upregulated in the face of necrosis. We here show that in addition to CLU
upregulation, necrotic cell lysates induce JNK/SAPK signaling, the IRE1α branch of the
unfolded protein response (UPR), the MAPK/ERK1/2, and the mTOR signaling pathways …