ArticleMolecular cell2016
The Noncanonical Role of ULK/ATG1 in ER-to-Golgi Trafficking Is Essential for Cellular Homeostasis.
Article in Molecular cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 97 papers, 1 of them a synthesis that pooled it.
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
97 citing papers in PubMed, 1 synthesis or guideline pooled it, 184 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Remaking an exit: dynamic regulation of ER exit sites by post-translational modifications.Trends in cell biology · 2026Review
- Divergent Role of ULK1 to Balance Mitochondrial Homeostasis and Bioenergetics in Ovarian Cancer Spheroids.Cancers · 2026Article
- Autophagy-Independent Function of ATG-18 Is Essential for Gonadal Longevity in Caenorhabditis elegans.Aging cell · 2026Article
- Construction of pathogenic Sec16a mutation mouse model using CRISPR/Cas9.Animal models and experimental medicine · 2026Article
- The role of autophagy in protozoan infections.Frontiers in cellular and infection microbiology · 2026Review
- The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025Review
- Knockdown of Atg1 Impairs Brain Regeneration and Downregulates ECM-Related Genes in the Planarian Dugesia japonica.Molecular neurobiology · 2025Article
- Genetic and clinical spectrum of steroid-resistant nephrotic syndrome with nuclear pore gene mutation.Pediatric nephrology (Berlin, Germany) · 2025Article
- Targeting secretory autophagy in solid cancers: mechanisms, immune regulation and clinical insights.Experimental hematology & oncology · 2025Review
- α-Synuclein disrupts microglial autophagy through STAT1-dependent suppression of Ulk1 transcription.Journal of neuroinflammation · 2024Article
- TFG regulates inner COPII coat recruitment to facilitate anterograde secretory protein transport.Molecular biology of the cell · 2024Article
- Physiological functions of ULK1/2.Journal of molecular biology · 2024Review
- ULK/Atg1: phasing in and out of autophagy.Trends in biochemical sciences · 2024Review
- The nonautophagic functions of autophagy-related proteins.Autophagy · 2024Review
- Knockdown of Sec16 causes early lethality and defective deposition of the protein Rp30 in the eggshell of the vectorFrontiers in cell and developmental biology · 2024Article
- To eat or not to eat: a critical review on the role of autophagy in prostate carcinogenesis and prostate cancer therapeutics.Frontiers in pharmacology · 2024Review
- Implications of endoplasmic reticulum stress and autophagy in aging and cardiovascular diseases.Frontiers in pharmacology · 2024Review
- Epigenetic regulation ofAutophagy · 2024Review
- Nutrient deprivation alters the rate of COPII subunit recruitment at ER subdomains to tune secretory protein transport.Nature communications · 2023Article
37 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
- Erratum issued
Authors and funding
17 authors at 6 institutions in 1 country.
Funding
Abstract
ULK1 and ULK2 are thought to be essential for initiating autophagy, and Ulk1/2-deficient mice die perinatally of autophagy-related defects. Therefore, we used a conditional knockout approach to investigate the roles of ULK1/2 in the brain. Although the mice showed neuronal degeneration, the neurons showed no accumulation of P62(+)/ubiquitin(+) inclusions or abnormal membranous structures, which are observed in mice lacking other autophagy genes. Rather, neuronal death was associated with activation of the unfolded protein response (UPR) pathway. An unbiased proteomics approach identified SEC16A as an ULK1/2 interaction partner. ULK-mediated phosphorylation of SEC16A regulated the assembly of endoplasmic reticulum (ER) exit sites and ER-to-Golgi trafficking of specific cargo, and did not require other autophagy proteins (e.g., ATG13). The defect in ER-to-Golgi trafficking activated the UPR pathway in ULK-deficient cells; both processes were reversed upon expression of SEC16A with a phosphomimetic substitution. Thus, the regulation of ER-to-Golgi trafficking by ULK1/2 is essential for cellular homeostasis.
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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.