ArticleNature communications2024
TBC1D23 mediates Golgi-specific LKB1 signaling.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Targeting non-small cell lung cancer: Molecular mechanisms and clinical studies (Review).Oncology letters · 2026Review
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- TBC1 domain family member 23 is essential for STING-mediated anti-melanoma effect.Molecular biomedicine · 2026Article
- The functional landscape of alternative splicing in hematopoietic lineage commitment.Nature communications · 2026Article
- The Functions of the Golgin Family of Coiled-Coil Proteins.Sub-cellular biochemistry · 2026Review
- AMPK at the interface of nutrient sensing, metabolic flux and energy homeostasis.Nature metabolism · 2026Review
- The Protective Effect of Phenolic Acids on Liver Disease: A Review of Possible Mechanisms.Antioxidants (Basel, Switzerland) · 2025Review
- The AMPK Pathway: Molecular Rejuvenation of Metabolism and Mitochondria.Annual review of cell and developmental biology · 2025Review
- A CRISPR/Cas9 screen reveals proteins at the endosome-Golgi interface that modulate cellular anti-sense oligonucleotide activity.Nature communications · 2025Article
- Rootstock-Scion Exchanging mRNAs Participate in Watermelon Fruit Quality Improvement.International journal of molecular sciences · 2025Article
- Cryo-EM structure of the BLOC-3 complex provides insights into the pathogenesis of Hermansky-Pudlak syndrome.Nature communications · 2025Article
- Trans-Golgi network tethering factors regulate TBK1 trafficking and promote the STING-IFN-I pathway.Cell discovery · 2025Article
- Irisin's Dual Role in Malignant Tumors and Its Potential as a Biomarker and Therapeutic Target.Drug design, development and therapy · 2025Review
- 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
- Ketogenic diet reshapes cancer metabolism through lysine β-hydroxybutyrylation.Nature metabolism · 2024Article
- TRIM25 predominately associates with anti-viral stress granules.Nature communications · 2024Article
Corrections and comments
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Authors and funding
16 authors at 5 institutions in 1 country.
Funding
Abstract
Liver kinase B1 (LKB1), an evolutionarily conserved serine/threonine kinase, is a master regulator of the AMPK subfamily and controls cellular events such as polarity, proliferation, and energy homeostasis. Functions and mechanisms of the LKB1-AMPK axis at specific subcellular compartments, such as lysosome and mitochondria, have been established. AMPK is known to be activated at the Golgi; however, functions and regulatory mechanisms of the LKB1-AMPK axis at the Golgi apparatus remain elusive. Here, we show that TBC1D23, a Golgi-localized protein that is frequently mutated in the neurodevelopment disorder pontocerebellar hypoplasia (PCH), is specifically required for the LKB1 signaling at the Golgi. TBC1D23 directly interacts with LKB1 and recruits LKB1 to Golgi, promoting Golgi-specific activation of AMPK upon energy stress. Notably, Golgi-targeted expression of LKB1 rescues TBC1D23 deficiency in zebrafish models. Furthermore, the loss of LKB1 causes neurodevelopmental abnormalities in zebrafish, which partially recapitulates defects in TBC1D23-deficient zebrafish, and LKB1 sustains normal neuronal development via TBC1D23 interaction. Our study uncovers a regulatory mechanism of the LKB1 signaling, and reveals that a disrupted Golgi-LKB1 signaling underlies the pathogenesis of PCH.
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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.