Cell Death, Apoptosis, Autophagy

Enzo Life Sciences offers a wide range of novel products for researching and analyzing cell death. Our catalog includes over 1,000 different antibodies, assay kits, and small molecule activators and inhibitors spanning the 3 major classes of programmed cell death (PCD) highlighted by the Nomenclature Committee on Cell Death (NCCD): Apoptosis, Autophagy, and Necrosis.

Apoptosis (PCD Type 1) is the best-characterized type of programmed cell death because of its importance in development and homeostasis, and in the pathogenesis of different diseases such as cancer. Apoptotic cells die in a controlled fashion in response to a variety of extrinsic or intrinsic signals (e.g., activation of TNF receptors, DNA damage, mitochondrial pathways). The hallmarks of apoptotic cell death include exposure of phosphatidylserine on the extracellular face of the plasma membrane, activation of caspases, disruption of mitochondrial membrane potential, cell shrinkage, DNA fragmentation and DNA condensation.

Autophagy (PCD Type 2) is selective degradation of intracellular targets, such as misfolded proteins and damaged organelles, and is an important homeostatic function. Autophagy performs in concert with the Ubiquitin-Proteasome System (UPS) to degrade aggregated/misfolded proteins that are ubiquitinated, targeting them for degradation by autophagy. The ubiquitinated cargo is carried to the phagophore and surrounds its cargo forming a double membrane vesicle, the autophagosome. The lyososome fuses to the autophagosome and the cargo is degraded inside the autolysosome.

Necrosis (PCD Type 3) is an uncontrolled cell death characterized by cell swelling, as well as destruction of the plasma membrane and subcellular organelles, without nuclear fragmentation and condensation. Necrotic cell death is considered a heterogeneous phenomenon including both programmed and accidental cell death. Necrosis is often defined in a negative manner, as a type of cell death that involves rupture of the plasma membrane without the hallmarks of apoptosis and without massive autophagic vacuolization.