ArticleCell reports2015
Central role of ULK1 in type I interferon signaling.
Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
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
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Activating protein kinases to treat diseases: Current understanding and future challenges.Acta pharmaceutica Sinica. B · 2026Review
- ULK1 knockout suppresses pancreatic cancer progression by inhibiting autophagy and enhancing antitumor immunity.Experimental & molecular medicine · 2025Article
- The Dual Role of Interferon Signaling in Myeloproliferative Neoplasms: Pathogenesis and Targeted Therapeutics.Cancers · 2025Review
- Interferon-driven Metabolic Reprogramming and Tumor Microenvironment Remodeling.Immune network · 2025Review
- Article
- Loss of Function Mouse Models Reveal a Novel Regulatory Function for ULK1 in Myeloproliferative Neoplasms.Molecular and cellular biology · 2025Article
- Physiological functions of ULK1/2.Journal of molecular biology · 2024Review
- The nonautophagic functions of autophagy-related proteins.Autophagy · 2024Review
- Targeting CHAF1B Enhances IFN Activity against Myeloproliferative Neoplasm Cells.Cancer research communications · 2023Article
- Targeting ULK1 Decreases IFNγ-Mediated Resistance to Immune Checkpoint Inhibitors.Molecular cancer research : MCR · 2023Article
- Autophagy and Its Lineage-Specific Roles in the Hematopoietic System.Oxidative medicine and cellular longevity · 2023Review
- ULK1 Depletion Protects Mice from Diethylnitrosamine-Induced Hepatocarcinogenesis by Promoting Apoptosis and Inhibiting Autophagy.Journal of hepatocellular carcinoma · 2023Article
- Stress signaling boosts interferon-induced gene transcription in macrophages.Science signaling · 2022Article
- Protein kinase Cλ/ι in cancer: a contextual balance of time and signals.Trends in cell biology · 2022Review
- MYC promotes immune-suppression in triple-negative breast cancer via inhibition of interferon signaling.Nature communications · 2022Article
- Autophagy and beyond: Unraveling the complexity of UNC-51-like kinase 1 (ULK1) from biological functions to therapeutic implications.Acta pharmaceutica Sinica. B · 2022Review
- Regulation of IFNα-induced expression of the short ACE2 isoform by ULK1.Molecular immunology · 2022Article
- Discovery of a signaling feedback circuit that defines interferon responses in myeloproliferative neoplasms.Nature communications · 2022Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 6 institutions in 4 countries.
Funding
Abstract
We provide evidence that the Unc-51-like kinase 1 (ULK1) is activated during engagement of the type I interferon (IFN) receptor (IFNR). Our studies demonstrate that the function of ULK1 is required for gene transcription mediated via IFN-stimulated response elements (ISRE) and IFNγ activation site (GAS) elements and controls expression of key IFN-stimulated genes (ISGs). We identify ULK1 as an upstream regulator of p38α mitogen-activated protein kinase (MAPK) and establish that the regulatory effects of ULK1 on ISG expression are mediated possibly by engagement of the p38 MAPK pathway. Importantly, we demonstrate that ULK1 is essential for antiproliferative responses and type I IFN-induced antineoplastic effects against malignant erythroid precursors from patients with myeloproliferative neoplasms. Together, these data reveal a role for ULK1 as a key mediator of type I IFNR-generated signals that control gene transcription and induction of antineoplastic responses.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.