ENDOG Activators

ENDOG activators are chemically diverse molecules that can indirectly promote the apoptotic function of ENDOG by inducing mitochondrial stress or initiating apoptosis through various signaling pathways. These activators work at different levels of the apoptotic cascade. For instance, kinase inhibitors like staurosporine nonspecifically activate multiple kinases that signal for apoptosis, leading to the release of mitochondrial factors, including ENDOG. DNA-damaging agents such as camptothecin can lead to the activation of p53 and other pro-apoptotic factors that promote mitochondrial membrane permeabilization and the release of ENDOG. Similarly, compounds like arsenic trioxide act on mitochondrial integrity, directly leading to the release of ENDOG.

On the other hand, agents that induce ER stress, such as tunicamycin and thapsigargin, initiate apoptotic signaling that eventually culminates in the mitochondrial release of apoptotic factors, including ENDOG. In addition, some compounds can influence apoptosis through the generation of reactive oxygen species (ROS) or the disruption of cellular metabolism, which, in a cascade-like fashion, activate the mitochondrial pathway of apoptosis and thus lead to the activation of ENDOG. Sphingolipids like ceramide can activate mitochondrial pathways involved in apoptotic signaling, causing the release of ENDOG from mitochondria.