Apoptosis is a form of programmed cell death that results in the orderly and efficient removal of damaged cells. Cell morphology changes resulting from apoptosis include blebbing, cell shrinkage, nuclear fragmentation, chromatin condensation, chromosomal DNA fragmentation, and global mRNA decay. Apoptosis is a highly regulated process and cannot stop once it has begun. Approximately 50 to 70 billion cells die each day in an average adult human due to apoptosis.
Fig.1 Pathways of cell death, apoptosis, autophagy, oncosis and pyroptosis.
The machinery of apoptosis is complex and involves many signaling pathways. It can be triggered through one of two pathways, death receptor-dependent extrinsic apoptotic pathway or mitochondria-dependent intrinsic apoptotic pathway. In the extrinsic pathway the cell kills itself because of signals from other cells, while in the intrinsic pathway the cell kills itself because it senses cell stress. Both pathways induce cell death by activating caspases, or enzymes that degrade proteins. The two pathways both activate initiator caspases. Deregulation in apoptotic cell death machinery is a hallmark of cancer. The apoptosis alteration is responsible for tumor development, progression and tumor resistance to therapies.
Fig.2 Apoptosis is mediated by complicated and delicate network.
Research on apoptosis has increased substantially. Creative Biolabs curates a variety of recombinant antibodies involved in apoptosis and cell viability. The antibodies provided herein focused on some regulators of apoptosis and cell viability, including anti-apoptotic factors (i.e., Bcl-2 family), pro-apoptotic factors (i.e., p53 pathway), and intracellular caspases. These antibodies will contribute to your research on apoptosis signal pathways and apoptosis-associated diseases.
Fig.3 Representative immunohistochemical sections stained on active caspase-3 (brown) at end point.
Search apoptosis and cell viability antibodies on this page. For more detailed information about our antibodies, please feel free to contact us.