Abstract
Programmed cell death is governed by a set of gene networks, which define a variety of distinct molecular mechanisms essential for the maintenance of multicellular organisms. The most studied modality of programmed cell death is known as apoptosis. Caspase-2, as a member of the family of the cysteine-dependent protease, demonstrates both proapoptotic and tumor suppressive functions. This protease plays an essential role in the maintenance of genomic stability and induces apoptotic cell death in response to geno-toxic stress. Here we discuss the molecular mechanisms of caspase-2 regulation and its physiological role as a tumor suppressor and metabolic regulator.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
