ArticleProceedings of the National Academy of Sciences of the United States of America2016
Innate immunity kinase TAK1 phosphorylates Rab1 on a hotspot for posttranslational modifications by host and pathogen.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 48 citations in OpenAlex.
- Blockade of Tumor TAK1 Induces DNA Damage and Immunogenic cGAS-STING Pathway Activation in Pancreatic Cancer.Gastroenterology · 2026Article
- Pharmacological Inhibition of Small Extracellular Vesicle Secretion by ALK5i SD-208 via Lysosomal Rerouting of CD63+ Compartments.Journal of extracellular vesicles · 2026Article
- DYRK1A and Parkinson's disease, facts and hypotheses.Neurobiology of disease · 2026Review
- Singapore grouper iridovirus utilizes Rab1 to facilitate viral trafficking and evade the immune response by targeting the STING-IRF3 pathway.Cell communication and signaling : CCS · 2025Article
- Targeting tumor-intrinsic TAK1 triggers anti-tumor immunity and sensitizes pancreatic cancer to checkpoint blockade.bioRxiv : the preprint server for biology · 2025Article
- Selectivity profiles and substrate recognition of Rab-phosphorylating kinases.The Biochemical journal · 2025Article
- Regulation of HNRNP family by post-translational modifications in cancer.Cell death discovery · 2024Review
- Lung endothelium, tau, and amyloids in health and disease.Physiological reviews · 2024Review
- Cross-family small GTPase ubiquitination by the intracellular pathogenMolecular biology of the cell · 2024Article
- Interaction of PINK1 with nucleotides and kinetin.Science advances · 2024Article
- Glycosylating Effectors ofBiomolecules · 2022Review
- Chronic Activation of AMPK Induces Mitochondrial Biogenesis through Differential Phosphorylation and Abundance of Mitochondrial Proteins inInternational journal of molecular sciences · 2021Article
- Development of a multiplexed targeted mass spectrometry assay for LRRK2-phosphorylated Rabs and Ser910/Ser935 biomarker sites.The Biochemical journal · 2021Article
- Proteolysis of Rab32 byiScience · 2021Article
- Rab family of small GTPases: an updated view on their regulation and functions.The FEBS journal · 2021Review
- Article
- Phosphorylation of Rab GTPases in the regulation of membrane trafficking.Traffic (Copenhagen, Denmark) · 2020Article
- Extensive GTPase crosstalk regulates Golgi trafficking and maturation.Current opinion in cell biology · 2020Review
- Unbiased Proteomic Profiling Uncovers a Targetable GNAS/PKA/PP2A Axis in Small Cell Lung Cancer Stem Cells.Cancer cell · 2020Article
- PINK1-dependent phosphorylation of Serine111 within the SF3 motif of Rab GTPases impairs effector interactions and LRRK2-mediated phosphorylation at Threonine72.The Biochemical journal · 2020Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
TGF-β activated kinase 1 (TAK1) is a critical signaling hub responsible for translating antigen binding signals to immune receptors for the activation of the AP-1 and NF-κB master transcriptional programs. Despite its importance, known substrates of TAK1 are limited to kinases of the MAPK and IKK families and include no direct effectors of biochemical processes. Here, we identify over 200 substrates of TAK1 using a chemical genetic kinase strategy. We validate phosphorylation of the dynamic switch II region of GTPase Rab1, a mediator of endoplasmic reticulum to Golgi vesicular transport, at T75 to be regulated by TAK1 in vivo. TAK1 preferentially phosphorylates the inactive (GDP-bound) state of Rab1. Phosphorylation of Rab1 disrupts interaction with GDP dissociation inhibitor 1 (GDI1), but not guanine exchange factor (GEF) or GTPase-activating protein (GAP) enzymes, and is exclusive to membrane-localized Rab1, suggesting phosphorylation may stimulate Rab1 membrane association. Furthermore, we found phosphorylation of Rab1 at T75 to be essential for Rab1 function. Previous studies established that the pathogen Legionella pneumophila is capable of hijacking Rab1 function through posttranslational modifications of the switch II region. Here, we present evidence that Rab1 is regulated by the host in a similar fashion, and that the innate immunity kinase TAK1 and Legionella effectors compete to regulate Rab1 by switch II modifications during infection.
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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.