Based on the study of the RB51 - macrophage interaction model,
endoplasmic reticulum stress activates the inflammasome via NLRP3 - and caspase -2-driven mitochondrial damage (Bronner et al, 2015).
Not exact matches
Without CPEB4, the
endoplasmic reticulum is unable to
activate the
stress response, thus causing hepatocytes to accumulate the lipids produced by the fatty liver.
Endoplasmic reticulum stress and trophic factor withdrawal
activate distinct signaling cascades that induce glycogen synthase kinase - 3β and a caspase -9-dependent apoptosis in cerebellar granule neurons.