Human Bcl2 Antagonist/Killer 1 (BAK1) Protein

Background

BCL2 antagonist/killer 1 (BAK1) is a pro-apoptotic member of the Bcl-2 family of proteins, which regulate cell death pathways and cellular survival BAK1 plays a critical role in mitochondrial-mediated apoptosis, where it promotes the release of cytochrome c from the mitochondria, triggering the activation of caspase enzymes that lead to programmed cell death It functions as a key mediator of apoptosis in response to cellular stress, DNA damage, and oncogenic signaling, making it essential for maintaining cellular homeostasis and preventing the accumulation of damaged cells BAK1's activation is tightly regulated by anti-apoptotic proteins like Bcl-2, and its dysregulation is commonly associated with cancer, where loss of BAK1 function allows tumor cells to evade apoptosis, promoting tumor growth and resistance to chemotherapy Studies have also linked BAK1 to neurodegenerative diseases, where its dysregulation may contribute to neuronal loss and dysfunction Additionally, BAK1 has been implicated in immune responses, where it regulates T-cell homeostasis and immune cell survival, underscoring its broader role in cellular death and immune regulation