ArticleNature cell biology2013
A CREB3-ARF4 signalling pathway mediates the response to Golgi stress and susceptibility to pathogens.
Article in Nature cell biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.
What it found
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Who cites it
115 citing papers in PubMed, 173 citations in OpenAlex.
- Metabolic stress remodels the Golgi-sphingolipid-lipid droplet axis in INS-1E β-cells: an integrated molecular signature of early β-cell vulnerability.Molecular biology reports · 2026Article
- The diverse functions of viral microproteins.bioRxiv : the preprint server for biology · 2026Article
- A coordinated transcriptional program controls de novo Golgi biogenesis.The EMBO journal · 2026Article
- Characterization of Novel Decenoic Acid Derivatives Exhibiting Cytotoxic Activity Against T98G Glioma Cells Under a Serum- and Glucose-deprived Condition.Cell biochemistry and biophysics · 2026Article
- Endoplasmic reticulum and Golgi stress signaling-mediated regulation of protein secretion.Cellular & molecular biology letters · 2026Review
- Activation of unfolded protein response pathways promotes keratinocyte differentiation and ameliorates psoriasis phenotypes.Cell stress & chaperones · 2026Article
- Stress-induced proteome remodeling at the Golgi-endosome interface.Journal of cell science · 2026Article
- Organelle homeostasis disruption: A driving force in the progression of cardiomyopathy (Review).Experimental and therapeutic medicine · 2026Review
- Dynamic Shifts in ER-Plasma Membrane Junctions Signaling Define Pro-Metastatic N-Glycosylation and Predict Prostate Cancer Progression.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- CrebA regulation of secretory capacity: genome-wide transcription profiling coupled with in vivo DNA binding studies.Genetics · 2025Article
- Perinuclear organelle trauma at the nexus of cardiomyopathy pathogenesis arising from loss of functionNucleus (Austin, Tex.) · 2025Review
- Perturbation of multiprotein complexes in skeletal muscle induces protective proteases in the CNS that degrade pathogenic proteins.npj aging · 2025Article
- A long-term ketogenic diet causes hyperlipidemia, liver dysfunction, and glucose intolerance from impaired insulin secretion in mice.Science advances · 2025Article
- Endothelial NMMHC IIA dissociation from PAR1 activates the CREB3/ARF4 signaling in thrombin-mediated intracerebral hemorrhage.Journal of advanced research · 2025Article
- A receptor-kinase cascade confers cold-induced root growth inhibition in Arabidopsis.Nature plants · 2025Article
- CrebA regulation of secretory capacity: Genome-wide transcription profiling coupled with in vivo DNA binding studies.bioRxiv : the preprint server for biology · 2025Article
- Nanomedicine in Cancer Therapeutics: Current Perspectives from Bench to Bedside.Molecular cancer · 2025Review
- Interpretable AI for inference of causal molecular relationships from omics data.Science advances · 2025Article
- Noncanonical UPR factor CREB3L2 drives immune evasion of triple-negative breast cancer through Hedgehog pathway modulation in T cells.Science advances · 2025Article
- Arfs on the Golgi: four conductors, one orchestra.Frontiers in molecular biosciences · 2025Review
55 more citing papers are in PubMed but not listed here.
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 4 institutions in 1 country.
Funding
Abstract
Treatment of cells with brefeldin A (BFA) blocks secretory vesicle transport and causes a collapse of the Golgi apparatus. To gain more insight into the cellular mechanisms mediating BFA toxicity, we conducted a genome-wide haploid genetic screen that led to the identification of the small G protein ADP-ribosylation factor 4 (ARF4). ARF4 depletion preserves viability, Golgi integrity and cargo trafficking in the presence of BFA, and these effects depend on the guanine nucleotide exchange factor GBF1 and other ARF isoforms including ARF1 and ARF5. ARF4 knockdown cells show increased resistance to several human pathogens including Chlamydia trachomatis and Shigella flexneri. Furthermore, ARF4 expression is induced when cells are exposed to several Golgi-disturbing agents and requires the CREB3 (also known as Luman or LZIP) transcription factor, whose downregulation mimics ARF4 loss. Thus, we have uncovered a CREB3-ARF4 signalling cascade that may be part of a Golgi stress response set in motion by stimuli compromising Golgi capacity.
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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.