In vitro experiment demonstrates that FAM134B knockdown accelerates mammalian cell proliferation and elevates STIM1 levels, suggesting that selective ER-phagy limits cell growth.
Autophagy is classified as nonselective or selective depending on the types of degrading substrates. Endoplasmic reticulum (ER)-phagy is a form of selective autophagy for transporting the ER-resident proteins to autolysosomes. FAM134B, a member of the family with sequence similarity 134, is a well-known ER-phagy receptor. Dysfunction of FAM134B results in several diseases including viral infection, inflammation, neurodegenerative disorder, and cancer, indicating that FAM134B has crucial roles in various kinds of intracellular functions. However, how FAM134B-mediated ER-phagy regulates intracellular functions is not well understood. In this study, we found that FAM134B knockdown in mammalian cells accelerated cell proliferation. FAM134B knockdown increased the protein amount of stromal interaction molecule 1 (STIM1), an ER Ca
No takes yet. Share an insight, caveat, or question.
Kajiho et al. (2024) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: