NRBF2 is primarily located in the cytoplasm and colocalizes with the phosphatidylinositol 3-kinase complex, class III (PI3KC3-C1). It is involved in starvation-induced autophagy, a process essential for cellular homeostasis and survival under nutrient-deprived conditions. NRBF2 stabilizes the PI3KC3-C1 assembly and enhances ATG14-linked lipid kinase activity of PIK3C3 .
Autophagy is a cellular degradation process that involves the lysosomal breakdown of cellular components. NRBF2 plays a pivotal role in this process by modulating interactions within the PI3KC3-C1 complex. It has been proposed to negatively regulate basal and starvation-induced autophagy and inhibit PIK3C3 activity . This regulation is crucial for maintaining cellular homeostasis and preventing excessive autophagy, which can lead to cell death.
NRBF2 is also implicated in the survival of neural progenitor cells during differentiation. This function is vital for the development and maintenance of the nervous system. The protein’s role in autophagosome biogenesis further underscores its importance in cellular processes that ensure proper cell function and survival .
The study of NRBF2 has significant implications for understanding diseases such as Alzheimer’s and other neurodegenerative disorders. By elucidating the pathways and mechanisms involving NRBF2, researchers can develop potential therapeutic strategies to modulate autophagy and improve cell survival under stress conditions .