ArticleCell reports2018
The NF-κB Factor Relish Regulates Atg1 Expression and Controls Autophagy.
Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 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.
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.
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Who cites it
30 citing papers in PubMed, 44 citations in OpenAlex.
- Polygonatum sibiricum polysaccharides regulate chondrocyte inflammation and metabolism via S100A9 inhibition-mediated autophagy promotion to ameliorate osteoarthritis.BMC complementary medicine and therapies · 2026Article
- Atg8 orchestrates stress-responsive chromatin programs across immunity and metabolism.bioRxiv : the preprint server for biology · 2026Article
- Autophagy-Apoptosis Crosstalk in Cancer: Mechanisms, Signaling Pathways, and Therapeutic Targeting.Cancers · 2026Review
- Cell wall components of gut commensal bacteria stimulate peritrophic matrix formation in malaria vector mosquitoes through activation of the IMD pathway.PLoS biology · 2025Article
- Pathogen-specific social immunity is associated with erosion of individual immune function in an ant.Nature communications · 2024Article
- The NF-κB Factor Relish maintains blood progenitor homeostasis in the developing Drosophila lymph gland.PLoS genetics · 2024Article
- Chrysin Inhibits TAMs-Mediated Autophagy Activation via CDK1/ULK1 Pathway and Reverses TAMs-Mediated Growth-Promoting Effects in Non-Small Cell Lung Cancer.Pharmaceuticals (Basel, Switzerland) · 2024Article
- Evolution of innate immunity: lessons from mammalian models shaping our current view of insect immunity.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2024Review
- Autophagic dysfunction and gut microbiota dysbiosis cause chronic immune activation in a Drosophila model of Gaucher disease.PLoS genetics · 2023Article
- Evaluation of the therapeutic potential of cerebrolysin and/or lithium in the male Wistar rat model of Parkinson's disease induced by reserpine.Metabolic brain disease · 2023Article
- Review
- Antimicrobial peptides do not directly contribute to aging in Drosophila, but improve lifespan by preventing dysbiosis.Disease models & mechanisms · 2023Article
- Tea Tree Oil Mediates Antioxidant Factors Relish and Nrf2-Autophagy Axis Regulating the Lipid Metabolism ofAntioxidants (Basel, Switzerland) · 2022Article
- A circular RNA Edis-Relish-castor axis regulates neuronal development in Drosophila.PLoS genetics · 2022Article
- Autophagy: An important target for natural products in the treatment of bone metabolic diseases.Frontiers in pharmacology · 2022Review
- Toll-like receptor 4 mutation protects the kidney from Ang-II-induced hypertensive injury.Pharmacological research · 2022Article
- Transcription and Post-translational Regulation of Autophagy in Insects.Frontiers in physiology · 2022Article
- Article
- Article
- Role of Herbal Teas in Regulating Cellular Homeostasis and Autophagy and Their Implications in Regulating Overall Health.Nutrients · 2021Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Macroautophagy and cell death both contribute to innate immunity, but little is known about how these processes integrate. Drosophila larval salivary glands require autophagy for developmentally programmed cell death, and innate immune signaling factors increase in these dying cells. Here, we show that the nuclear factor κB (NF-κB) factor Relish, a component of the immune deficiency (Imd) pathway, is required for salivary gland degradation. Surprisingly, of the classic Imd pathway components, only Relish and the PGRP receptors were involved in salivary gland degradation. Significantly, Relish controls salivary gland degradation by regulating autophagy but not caspases. In addition, expression of either Relish or PGRP-LC causes premature autophagy induction and subsequent gland degradation. Relish controls autophagy by regulating the expression of Atg1, a core component and activator of the autophagy pathway. Together these findings demonstrate that a NF-κB pathway regulates autophagy during developmentally programmed cell death.
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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 OpenQuestion graph.