ReviewThe EMBO journal2025
Mechanism of autophagy initiation by transmembrane selective autophagy receptors.
Review in The EMBO journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- FAM134B Restricts African Swine Fever Virus Capsid Assembly via Reticulophagy and Its Antiviral Activity is Antagonized by the Viral Virulence-Associated Factor pMGF300-2R.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The role of E3 ubiquitin ligases in selective types of macroautophagy.EMBO reports · 2026Review
- Regulation and roles of mammalian mitophagy.Nature reviews. Molecular cell biology · 2026Review
- Exercise as a Programmable Regulator of Mitophagy Sensitivity in Aging Muscle and Age-Related Disease.IUBMB life · 2026Review
- Small bites for big problems: stepwise aggregate degradation by autophagy.Biochemical Society transactions · 2026Review
- Cutting edge: ESCRT-mediated phagophore closure in mammals.The Biochemical journal · 2026Review
- The multifaceted functions of selective autophagy in cancer: molecular basis, consequences, and clinical prospects.Molecular cancer · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selective autophagy ensures the targeted degradation of damaged or surplus cellular components, including organelles, thereby safeguarding cellular homeostasis. This process relies on selective autophagy receptors (SARs) that link specific cargo to the autophagy machinery. These receptors exist in two distinct forms: soluble SARs that are recruited to the cargo on demand, and transmembrane SARs that are stably embedded in the membranes of organelles they target. While both receptor types converge on the same autophagy core machinery, they differ in how they recognize cargo, are regulated, and recruit this machinery to the site of degradation. In this review, we explore the unique challenges and strategies associated with transmembrane SARs, including how their activity is suppressed under basal conditions and activated in response to stress. We compare their mode of action with that of soluble SARs, highlight key differences in kinase regulation, including the roles of TBK1, ULK1, CK2, and Src, and discuss emerging models of autophagy initiation. We further highlight fundamental principles of organelle-selective autophagy and identify open questions that will guide future research.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.