Recombinant Human BNIP3L

Background

BCL2 Interacting Protein 3 Like (BNIP3L), also known as NIX, is a member of the BCL2 family of proteins and plays a critical role in programmed cell death and mitochondrial quality control. BNIP3L is known to interact with BCL2 and other apoptotic regulators, promoting mitochondrial autophagy (mitophagy), a selective process that removes damaged or dysfunctional mitochondria to maintain cellular homeostasis. Its function is particularly crucial under conditions of hypoxia, where BNIP3L is upregulated, contributing to cell survival by mitigating oxidative stress and preventing the accumulation of damaged mitochondria. In the context of erythroid maturation, BNIP3L is essential for mitophagy-mediated clearance of mitochondria, a necessary step in the development of red blood cells. Dysregulation of BNIP3L has been implicated in various pathologies, including cancer, where its role can vary between promoting cell death in some contexts and contributing to tumor survival and resistance in others. Additionally, alterations in BNIP3L function are associated with neurodegenerative diseases due to impaired mitochondrial dynamics and clearance. This duality highlights the importance of BNIP3L as a potential therapeutic target for addressing diseases linked to apoptosis and mitochondrial dysfunction.