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Updated: Jun 23, 2026

Evaluation of LC3-II Release via Extracellular Vesicles in Relation to the Accumulation of Intracellular LC3-positive Vesicles
Published on: October 18, 2024
Ubiquilins accelerate autophagosome maturation and promote cell survival during nutrient starvation
Elsa-Noah N'Diaye1, Jayanta Debnath, Eric J Brown
1Macrophage Biology Laboratory, Northern California Institute for Research and Education, San Francisco, CA, USA.
Abstract:
Ubiquilins (UBQLN), a family of adaptor proteins with partial homology with ubiquitin, are proposed to facilitate proteasomal degradation of ubiquitinated substrates. We now demonstrate a novel role for UBQLN in promoting autophagosome maturation during nutrient deprivation. Ectopic expression of UBQLN protects cells against starvation-induced cell death, while depletion renders cells more susceptible. This protective function requires the essential autophagy regulators, Atg5 and Atg7. The ubiquitin-associated (UBA) domain of UBQLN is required for its association with autophagosomes as well as for its prosurvival functions.Remarkably, during starvation-induced autophagy, UBQLN promotes the fusion of early autophagosomes with lysosomes.Overall, this work illustrates an important function for UBQLN in cell survival during nutrient starvation, which requires a newly recognized function for UBQLN in autophagosome maturation.
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