Apoptosis and Cell Death

Cell death can occur through 3 mechanisms: apoptosis, autophagy, and necrosis. Apoptosis, or programmed cell death, results in controlled cell shrinkage and nuclear fragmentation via the action of caspases, as well as an anti-inflammatory cytokine release. In contrast, necrosis signals via RIPK1 (RIP1), leading to cell swelling, lysis, and a pro-inflammatory cytokine release. Autophagy destroys the cell's damaged proteins and organelles via an intracellular catabolic process in the lysosome. Multiple physiological processes require the removal of specific cells by a controlled cell-death program. For example, tissue remodeling activates apoptosis, whereas energy metabolism and growth regulation responses rely on autophagy. Developmental processes often activate apoptosis, while bodily injuries or infection more commonly induce necrosis. The molecular mechanisms behind these cell death pathways overlap, and can be co-activated during some cellular functions. Apoptosis and necrosis both signal through the death domain receptors FAS, TNFRSF1A (TNFR1), and TNFRSF10A (TRAIL-R), while autophagy and apoptosis share BCL2 family members as key players.

QIAGEN provides a broad range of assay technologies for cell death research that enable analysis of gene expression and regulation, epigenetic modification, genotyping, and signal transduction pathway activation. Solutions optimized for cell death studies include PCR array, miRNA, siRNA, mutation analysis, pathway reporter, chromatin IP, DNA methylation, and protein expression products.