English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Macroautophagy, hereafter referred to as autophagy, is a process that delivers cytoplasmic material to lysosomes for degradation. When nutrients are scarce, autophagy sustains cellular renovation by recycling cellular constituents (amino acids and fatty acids) for anabolic processes. In nutrient-replete conditions, autophagy maintains cellular homeostasis by selectively degrading disease-related ‘cargoes’ (pathogenic aggregateprone proteins, damaged organelles, invasive bacteria). The first morphologically recognizable precursor of the autophagic process is a sac-like structure (phagophore) that first expands as a flat double-membrane sheet and then bends and closes into a spherical doublemembrane organelle (autophagosome). Nucleation, elongation and closure are governed by the conserved ATG (AuTophaGy-related) proteins, many of which are recruited at the autophagosome formation site [1]. During autophagosome formation, the ATG8 ubiquitin-like proteins (LC3/GABARAP) are conjugated to the lipid phosphatidylethanolamine (PE) and associate tightly with autophagosomal membranes. The site of LC3 conjugation is specified by the ATG16L1 complex, which is recruited Editorial

Coincidence detection of RAB11A and PI(3)P by WIPI2 directs autophagosome formation