Caspase 6, also known as Apoptotic protease Mch-2, belongs to the peptidase C14A family. It functions as a downstream enzyme in the caspase activation cascade and is responsible for the execution of apoptosis. Its overexpression promotes programmed cell death.
Diseases associated with CASP6 include thoracic cancer and myocardial infarction. Among its related super-pathways are DR3 Signaling and Apoptosis and the survival FAS signaling cascade.
A clinically relevant model of transient global brain ischemia involving cardiac arrest followed by resuscitation in dogs was utilized to study the expression and proteolytic processing of apoptosis-regulatory proteins. Immunohistochemical analysis using antibodies, which recognize processed caspase-3, -6, -8, and -10, provided evidence of time-dependent activation of these proteases in both neurons and glia in ischemia-sensitive regions of the brain. Extremely rapid, cell-selective processing of apoptosis-regulatory proteins occurs in a clinically relevant model of ischemic brain injury caused by cardiac arrest and resuscitation. (1)
Immunohistochemistry: Caspase 6 Antibody
Caspases play an essential role during apoptotic cell death, and their alterations are known to contribute to human cancer development. The results of a study indicated that caspase-2, -6 and -7 expression in gastric cancer cells is decreased compared to in normal gastric mucosal cells, and suggest that loss of caspase-2, -6 and -7 expression might be involved in the mechanisms of gastric cancer development. (2)
Little is known about how a cell's apoptotic threshold is controlled after exposure to chemotherapy, although the p53 tumor suppressor has been implicated. A study identified executioner caspase-6 as a transcriptional target of p53. The mechanism involves DNA binding by p53 to the third intron of the caspase-6 gene and transactivation. The induction of caspase-6 expression lowers the cell death threshold in response to apoptotic signals that activate caspase-6. (3)
Streptococcus pneumoniae is the major pathogen of community-acquired pneumonia and one of the most common causes of death due to infectious diseases in industrialized countries. A study showed that pneumococci induced apoptosis of human alveolar and bronchial epithelial cells. Programmed cell death was executed by caspase 6 and non-caspase proteases, and could be blocked by overexpression of Bcl2. (4)
Novus Biologicals offers Caspase 6 reagents for your research needs including:
