ArticleNature communications2018
Autophagy differentially regulates TNF receptor Fn14 by distinct mammalian Atg8 proteins.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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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.
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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.
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Who cites it
11 citing papers in PubMed, 34 citations in OpenAlex.
- Macrophage autophagy protects against acute kidney injury by inhibiting renal inflammation through the degradation of TARM1.Autophagy · 2025Article
- Proteolytically generated soluble Tweak Receptor Fn14 is a blood biomarker for γ-secretase activity.EMBO molecular medicine · 2022Article
- Endosomal LC3C-pathway selectively targets plasma membrane cargo for autophagic degradation.Nature communications · 2022Article
- Unlocking the gate to GABARAPL2.Biologia futura · 2022Review
- Single-cell transcriptomic analysis reveals a novel cell state and switching genes during hepatic stellate cell activation in vitro.Journal of translational medicine · 2022Article
- Review
- Autophagy in Viral Development and Progression of Cancer.Frontiers in oncology · 2021Review
- Controversies in TWEAK-Fn14 signaling in skeletal muscle atrophy and regeneration.Cellular and molecular life sciences : CMLS · 2020Review
- Deficiency of GABARAP but not its Paralogs Causes Enhanced EGF-induced EGFR Degradation.Cells · 2020Article
- N-terminal β-strand underpins biochemical specialization of an ATG8 isoform.PLoS biology · 2019Article
- Supramolecular Complexes in Cell Death and Inflammation and Their Regulation by Autophagy.Frontiers in cell and developmental biology · 2019Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Autophagy, a conserved membrane trafficking process, sequesters cytoplasmic components into autophagosomes and targets them for lysosomal degradation. The TNF receptor Fn14 participates in multiple intracellular signaling pathways and is strongly induced upon tissue injury and solid tumorigenesis. While Fn14 is a short-lived protein, the regulation of its levels is largely obscure. Here we uncover a role for autophagy in Fn14 turnover, wherein specific core autophagy Atg8 proteins play distinct roles: Fn14 accumulates in the ERGIC in absence of GABARAP but within endosomes in the vicinity of autophagic membranes in absence of GATE-16. Moreover, GABARAP regulates overall cellular levels of Fn14, whereas GATE-16 regulates TWEAK signaling by Fn14 and thereby NF-κB activity. These findings not only implicate different Atg8 proteins in distinct roles within the mechanism of selective autophagic regulation of Fn14, but may also provide a more general view of their role in mediating autophagosome biogenesis from different membrane sources.
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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.