ReviewCytokine & growth factor reviews2016
Beyond autophagy: New roles for ULK1 in immune signaling and interferon responses.
Review in Cytokine & growth factor reviews, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 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
14 citing papers in PubMed, 23 citations in OpenAlex.
- 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 beyond: Unraveling the complexity of UNC-51-like kinase 1 (ULK1) from biological functions to therapeutic implications.Acta pharmaceutica Sinica. B · 2022Review
- Discovery of a signaling feedback circuit that defines interferon responses in myeloproliferative neoplasms.Nature communications · 2022Article
- Genome-wide association study of disease resilience traits from a natural polymicrobial disease challenge model in pigs identifies the importance of the major histocompatibility complex region.G3 (Bethesda, Md.) · 2022Article
- ULK1 Signaling in the Liver: Autophagy Dependent and Independent Actions.Frontiers in cell and developmental biology · 2022Review
- ULK1 Inhibition as a Targeted Therapeutic Strategy for Psoriasis by Regulating Keratinocytes and Their Crosstalk With Neutrophils.Frontiers in immunology · 2021Article
- Aging induces B cell defects and decreased antibody responses to influenza infection and vaccination.Immunity & ageing : I & A · 2020Review
- Deleting key autophagy elongation proteins induces acquirement of tumor-associated phenotypes via ISG15.Cell death and differentiation · 2020Article
- Interferon signaling in cancer. Non-canonical pathways and control of intracellular immune checkpoints.Seminars in immunology · 2019Review
- Functional analysis and clinical significance of sodium iodide symporter expression in gastric cancer.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2019Article
- IFN-γ-inducible antiviral responses require ULK1-mediated activation of MLK3 and ERK5.Science signaling · 2018Article
- Slfn2 Regulates Type I Interferon Responses by Modulating the NF-κB Pathway.Molecular and cellular biology · 2018Article
- Central Regulatory Role for SIN1 in Interferon γ (IFNγ) Signaling and Generation of Biological Responses.The Journal of biological chemistry · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The human serine/threonine kinase ULK1 is the human homolog of the Caenorhabditis elegans Unc-51 kinase and of the Saccharomyces cerevisiae autophagy-related protein kinase Atg1. As Unc-51 and Atg1, ULK1 regulates both axon growth and autophagy, respectively, in mammalian cells. However, a novel immunoregulatory role of ULK1 has been recently described. This kinase was shown to be required for regulation of both type I interferon (IFN) production and induction of type I IFN signaling. Optimal regulation of IFN production is crucial for generation of effective IFN-immune responses, and defects in such networks can be detrimental for the host leading to uncontrolled pathogen infection, tumor growth, or autoimmune diseases. Thus, ULK1 plays a central role in IFN-dependent immunity. Here we review the diverse roles of ULK1, with special focus on its importance to type I IFN signaling, and highlight important future study questions.
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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.