Caspase 2

Caspase-2 is a conserved caspase that links apoptosis, inflammation, cell-cycle control, and protection from genomic instability^[1][2]. Mechanistically, caspase-2 can act upstream of mitochondria by processing BID, promoting BAX/BAK-dependent mitochondrial outer membrane permeabilization, and engaging p53-dependent proapoptotic responses^[3]. In tumor models, loss of caspase-2 increases proliferation, accelerates tumorigenesis, weakens apoptosis after DNA damage, and supports malignant transformation^[4]. Compared with related caspase isoforms, caspase-2 remains distinct because it combines apoptotic activity with non-apoptotic roles in genomic stability, metabolism, autophagy, aging, and tumor suppression^[1][5]. In infection models, caspase-2 mediates a hybrid cell death with apoptosis and pyroptosis features, regulating caspase-3, caspase-8, mitochondrial cytochrome c release, TNFα, caspase-1, and IL-1β production^[6]. For experimental applications, DNAzyme 13 provides an oligonucleotide-based caspase-2 activator that evokes tumor-cell apoptosis and helps evaluate caspase-2 biology^[7].