ArticleNature communications2020
TBC1D9 regulates TBK1 activation through Ca
Article in Nature communications, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Sex-stratified genome-wide association study of multisite chronic pain in UK Biobank.PLoS genetics · 2021Pooled it
- Trial
- Purinergic signaling promotes gliomagenesis through nuclear calcium transients.bioRxiv : the preprint server for biology · 2026Article
- Restricting intracellularAutophagy · 2026Article
- Minding the gates: dual cell-autonomous and non-cell-autonomous mechanisms of TBK1 in ALS/FTD.Frontiers in neuroscience · 2026Review
- Autophagy is involved in the toxicity of the biocontrol agent GC16 against Tetranychus pueraricola (Acari: Tetranychidae) based on transcriptomic and proteomic analyses.BMC genomics · 2025Article
- The battle between bacterial infection and autophagy in aquatic animals.Frontiers in immunology · 2025Review
- A TBC1D9-Rab29 axis controls homeostatic NF-κB signaling and selective IL-6 production in epithelial cells.Frontiers in cellular and infection microbiology · 2025Article
- TBC1 domain-containing proteins are frequently involved in triple-negative breast cancers in connection with the induction of a glycolytic phenotype.Cell death & disease · 2024Article
- Article
- TANK Binding Kinase 1 Promotes BACH1 Degradation through Both Phosphorylation-Dependent and -Independent Mechanisms without Relying on Heme and FBXO22.International journal of molecular sciences · 2024Article
- Interplay between group AMicrobiology and molecular biology reviews : MMBR · 2024Review
- Response to Bruton's tyrosine kinase inhibitors in aggressive lymphomas linked to chronic selective autophagy.Cancer cell · 2024Article
- Pancreatic β-cell mitophagy as an adaptive response to metabolic stress and the underlying mechanism that involves lysosomal CaExperimental & molecular medicine · 2023Review
- VANGL2 inhibits antiviral IFN-I signaling by targeting TBK1 for autophagic degradation.Science advances · 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
- Article
- Mitochondria inInternational journal of molecular sciences · 2022Review
- Mitochondrial Dysfunction in Oxidative Stress-Mediated Intervertebral Disc Degeneration.Orthopaedic surgery · 2022Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Invading microbial pathogens can be eliminated selectively by xenophagy. Ubiquitin-mediated autophagy receptors are phosphorylated by TANK-binding kinase 1 (TBK1) and recruited to ubiquitinated bacteria to facilitate autophagosome formation during xenophagy, but the molecular mechanism underlying TBK1 activation in response to microbial infection is not clear. Here, we show that bacterial infection increases Ca
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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.