Affinage

GBF1

Golgi-specific brefeldin A-resistance guanine nucleotide exchange factor 1 · UniProt Q92538

Length
1860 aa
Mass
206.6 kDa
Annotated
2026-04-28
90 papers in source corpus 49 papers cited in narrative 49 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

GBF1 is a large Sec7-domain ARF guanine nucleotide exchange factor (ArfGEF) that serves as a master regulator of COPI-dependent vesicle trafficking, Golgi homeostasis, lipid droplet metabolism, and cell division. GBF1 rapidly cycles on and off cis-Golgi and ERGIC membranes—stabilized by ARF-GDP and released upon catalyzing GDP-to-GTP exchange on ARF1/4/5—thereby recruiting COPI coats for retrograde and anterograde transport of transmembrane cargo, GGA adaptors for lysosomal sorting, and BIG1/2 GEFs in a sequential ARF activation cascade (PMID:15813748, PMID:18003980, PMID:17666033, PMID:23386609). Membrane targeting requires its HDS1/HDS2 domains, a proteinaceous Golgi receptor, Rab1b-dependent PI4P generation by PI4KIIIα, and lipid interactions via an HDS1 amphipathic helix that also mediates lipid droplet association; phosphorylation by CDK1–cyclin B, AMPK (at Thr1337), CK2 (triggering SCFβTrCP-mediated degradation), and Src (promoting retrograde tubule formation) dynamically regulates GBF1 membrane dissociation during mitosis, Golgi fragmentation, cytokinesis, and glycosyltransferase relocation (PMID:20530568, PMID:20175751, PMID:39575556, PMID:29898406, PMID:34870592). Pathogenic heterozygous GBF1 variants cause distal hereditary motor neuropathy/CMT2 with Golgi fragmentation in patient fibroblasts, and GBF1 haploinsufficiency in mice produces cataracts, underscoring its essential role in neuronal and lens cell secretory homeostasis (PMID:32937143, PMID:39110251).

Mechanistic history

Synthesis pass · year-by-year structured walk · 22 steps
  1. 1999 High

    Establishing GBF1 as an ARF-GEF: the foundational question of whether GBF1 possesses nucleotide exchange activity was resolved by demonstrating BFA-resistant Sec7-domain GEF activity toward ARF5, with overexpression conferring BFA resistance to COPI recruitment.

    Evidence Expression cloning, in vitro GEF assay with purified His-GBF1, immunogold EM, BFA resistance assay in mammalian cells

    PMID:10402461

    Open questions at the time
    • Substrate specificity toward other ARF isoforms (ARF1, ARF3, ARF4) not yet tested
    • No membrane recruitment mechanism defined
    • No structural data on Sec7 domain
  2. 2004 High

    Defining GBF1's dynamic membrane behavior: FRAP demonstrated that GBF1 is not a stable Golgi resident but cycles rapidly on and off membranes, with BFA trapping it in an abortive ARF-GDP–GBF1 complex—resolving how BFA inhibits GBF1 in vivo.

    Evidence YFP-GBF1 FRAP, in vivo ARF1-GTP loading assay, BFA treatment in living cells

    PMID:15616190

    Open questions at the time
    • Mechanism of initial membrane recruitment unknown
    • Whether catalytic turnover drives dissociation not yet shown
  3. 2005 High

    Establishing catalytic product release as the membrane dissociation trigger: the observation that GBF1 is stabilized on membranes by ARF-GDP (via inactive mutants) and released upon GTP loading demonstrated a single-turnover catalytic cycle per membrane association event.

    Evidence GFP-GBF1 FRAP with catalytically dead E794K mutant, ARF1-T31N dominant-negative, BFA treatment

    PMID:15813748

    Open questions at the time
    • Structural basis of ARF-GDP stabilization of GBF1 not resolved
    • Stoichiometry of the GBF1–ARF complex on membranes unknown
  4. 2003 High

    Linking GBF1 to membrane tethering: identification of p115 as a direct binding partner connected GBF1's ARF-GEF activity to the vesicle tethering machinery at VTCs and Golgi.

    Evidence Yeast two-hybrid, in vitro binding, co-immunoprecipitation, dominant-negative GBF1 pro-rich domain expression

    PMID:12634853

    Open questions at the time
    • Functional consequence of p115–GBF1 interaction on tethering efficiency not quantified
    • Whether p115 recruits GBF1 or vice versa unclear
  5. 2006 High

    Demonstrating GBF1 as the specific GEF for cis-Golgi COPI recruitment: anti-GBF1 antibody microinjection directly dissociated COPI from membranes, while GBF1 localized to cis-Golgi and VTCs distinct from ER exit sites, establishing compartmental specificity.

    Evidence Anti-GBF1 microinjection, GFP live imaging, FRAP, subcellular fractionation

    PMID:16926190

    Open questions at the time
    • How GBF1 is excluded from trans-Golgi COPI recruitment not addressed
  6. 2007 High

    Multiple discoveries resolved GBF1's upstream regulation, downstream effectors, dimerization, and cargo specificity: Rab1b was identified as an upstream activator stabilizing GBF1 on membranes; GGAs and BIG1/2 were shown as downstream effectors; the DCB–HUS dimerization architecture was mapped; and GBF1 depletion selectively blocked transmembrane (but not soluble) cargo transport.

    Evidence Rab1b co-IP and siRNA (PMID:17429068); GGA co-IP and cargo sorting assay (PMID:17666033); DCB/HUS yeast two-hybrid and co-IP (PMID:17640864); siRNA with differential cargo assays and EM (PMID:17956946); parallel GEF knockdowns with VSVGtsO45 (PMID:18003980)

    PMID:17429068 PMID:17640864 PMID:17666033 PMID:17956946 PMID:18003980

    Open questions at the time
    • Whether Rab1b directly binds GBF1 or acts through PI4P not distinguished
    • GGA recruitment mechanism (direct versus ARF-mediated) not resolved
    • Structural basis of DCB–DCB dimerization unknown
  7. 2008 High

    GBF1 depletion was shown to trigger ER stress and UPR activation (ATF6 processing) and G0/G1 arrest, revealing that GBF1 loss has consequences beyond trafficking—disrupting ER–Golgi proteostasis. Separately, class II ARFs (ARF4/5) were found to associate with ERGIC membranes independently of GBF1 in their GDP-bound state.

    Evidence Selective GEF siRNA with proteomics, ATF6 cleavage, cell-cycle analysis (PMID:18287014); live imaging of tagged ARF isoforms with BFA/Exo1 (PMID:18524849)

    PMID:18287014 PMID:18524849

    Open questions at the time
    • Whether ER stress is a direct or indirect consequence of COPI loss unclear
    • How class II ARFs are recruited to ERGIC without GBF1 not defined
  8. 2008 High

    GBF1 was established as a critical host factor for RNA virus replication, initially for MHV coronavirus: GBF1 (but not BIG1/BIG2) knockdown blocked viral RNA replication, and BFA-resistant GBF1 rescued replication, indicating that GBF1-dependent ARF1 activation controls replication complex formation.

    Evidence Selective GEF siRNA, BFA-resistant GBF1 rescue in MDCK cells, quantitative EM of replication complexes

    PMID:18551169

    Open questions at the time
    • Whether GBF1 acts at replication membranes directly or via global secretory pathway disruption not distinguished
  9. 2009 High

    GBF1's role as a host factor was extended to enteroviruses (CVB3, poliovirus) and HCV, establishing it as a broadly exploited target; separately, Drosophila garz (GBF1 ortholog) was shown to function in clathrin-independent GEEC endocytosis, expanding GBF1's role beyond secretory trafficking.

    Evidence CVB3/poliovirus replicon assays with BFA-resistant GBF1 rescue and siRNA (PMID:19740986); HCV selective GEF knockdown with rescue (PMID:19906930); Drosophila RNAi screen with TIRF imaging and GEF-dead mutant (PMID:19707569)

    PMID:19707569 PMID:19740986 PMID:19906930

    Open questions at the time
    • Precise viral replication membrane composition and GBF1 role therein unknown
    • Whether GEEC endocytic function is conserved in mammalian cells not tested
  10. 2010 High

    Two key regulatory inputs were defined: CDK1–cyclin B phosphorylates GBF1 to trigger mitotic Golgi fragmentation, and PI4KIIIα-generated PI4P (downstream of Rab1) is required for GBF1 Golgi membrane recruitment, linking lipid identity to GEF targeting. Additionally, a non-catalytic scaffolding role was uncovered for poliovirus replication.

    Evidence In vitro CDK1 kinase assay, mitotic phosphoprotein analysis, ARF-GTP measurement (PMID:20175751); PI4KIIIα siRNA, PI4P sensor, Rab1 dominant-active (PMID:20530568); N-terminal GBF1 truncation rescue of poliovirus replication (PMID:20497182)

    PMID:20175751 PMID:20497182 PMID:20530568

    Open questions at the time
    • CDK1 phosphorylation sites on GBF1 not mapped
    • Whether PI4P binding is direct or mediated by an adaptor unclear
    • The non-catalytic viral function mechanism remains obscure
  11. 2011 High

    GBF1 was linked to lipid droplet biology through direct interaction with ATGL and lipid droplet targeting via HDS1/HDS2 domains, and to pathogen lipid acquisition through Chlamydia co-option of GBF1-dependent sphingomyelin trafficking.

    Evidence ATGL–GBF1 yeast two-hybrid, co-IP, in vitro binding, domain-LD localization (PMID:21789191); selective GEF siRNA with fluorescent SM trafficking in Chlamydia-infected cells (PMID:21909260)

    PMID:21789191 PMID:21909260

    Open questions at the time
    • Whether GBF1 activates ARFs on lipid droplet surfaces not shown
    • ATGL delivery mechanism via COPI not fully reconstituted
  12. 2012 High

    GBF1 function was extended to GPCR-stimulated neutrophil chemotaxis via a novel phosphoinositide-binding module (BP3K) that redirects GBF1 from Golgi to the leading edge, and to epithelial tubulogenesis in Drosophila where Garz loss disrupts apical membrane delivery.

    Evidence GBF1 phospholipid binding assay, leading-edge live imaging, siRNA in neutrophils (PMID:22573891); Drosophila garz mutant with EM and live cargo imaging (PMID:22302994)

    PMID:22302994 PMID:22573891

    Open questions at the time
    • BP3K domain boundaries and binding specificity not fully characterized
    • Whether leading-edge ARF activation serves a distinct function from Golgi ARF activation unknown
  13. 2013 High

    The HDS1 amphipathic helix was identified as a direct lipid-binding element for both Golgi membranes and lipid droplets, auto-inhibited by the Sec7 domain in the full-length protein; a GEF cascade was defined in which GBF1-activated ARF4/5 recruit BIG1/2 to the TGN; and AMPK was identified as a second mitotic kinase phosphorylating GBF1 to promote Golgi disassembly.

    Evidence In vitro liposome/droplet binding with amphipathic helix mutagenesis (PMID:23943872); immunoEM localization with ARF isoform-specific rescue (PMID:23386609); in vitro AMPK kinase assay with mitotic cell fractionation (PMID:23418352)

    PMID:23386609 PMID:23418352 PMID:23943872

    Open questions at the time
    • Structural basis of Sec7-mediated autoinhibition of HDS1 unknown
    • Which AMPK site(s) are phosphorylated during mitosis not mapped in this study
  14. 2015 High

    GBF1 oligomerization via DCB domain was shown to be dispensable for all tested GEF functions (Golgi targeting, ARF activation, COPI recruitment, secretion) but required for protein stability; simultaneously, the GBF1–ARF1/ARF4–COPI pathway was demonstrated to transport Dengue virus capsid from ER to lipid droplets independently of COPII.

    Evidence DCB mutagenesis (K91/E130) with FRAP, ARF activation, COPI, secretion, stability assays (PMID:26718629); BFA-resistant GBF1 rescue of Dengue capsid distribution (PMID:26031340)

    PMID:26031340 PMID:26718629

    Open questions at the time
    • Whether oligomerization has a regulatory role under stress conditions untested
    • COPII-independent ER-to-LD transport mechanism not fully resolved
  15. 2016 High

    In vivo vertebrate validation came from zebrafish, where GBF1 loss-of-function (HDS2 L1246R mutation) caused intracerebral hemorrhage due to vascular breakage, and the mutant protein failed to target Golgi or activate ARF1, confirming HDS2 as essential for membrane targeting.

    Evidence ENU mutagenesis/positional cloning, morpholino and CRISPR knockout in zebrafish, mammalian cell Golgi recruitment assay

    PMID:28003365

    Open questions at the time
    • Specific vascular cargo whose mis-trafficking causes hemorrhage not identified
    • Whether endothelial or pericyte GBF1 is the critical cell type not determined
  16. 2017 High

    GBF1 was shown to form a ternary complex with rhodopsin and ARF4 at the photoreceptor Golgi for ciliary transport carrier biogenesis, with the DCB-HUS domain mediating rhodopsin/ARF4 binding and GBF1 also interacting with the ArfGAP ASAP1.

    Evidence Frog retina in vivo analysis, co-IP with recombinant human proteins, GCA inhibitor, domain mapping

    PMID:29025970

    Open questions at the time
    • Whether GBF1 functions in ciliogenesis beyond photoreceptors not tested
    • ASAP1 functional role in the complex not defined
  17. 2018 High

    Three advances refined GBF1 regulation and targeting: CK2 phosphorylation at S292/S297 targets GBF1 for SCFβTrCP-mediated degradation at the cytokinetic bridge, required for postmitotic Golgi reformation; HDS1/HDS2 domains and a proteinaceous Golgi receptor were shown essential for membrane recruitment in vitro; and GBF1–Miro interaction was found to regulate mitochondrial positioning.

    Evidence Phosphosite mutagenesis with βTrCP co-IP, non-degradable mutant cytokinesis failure (PMID:29898406); in vitro Golgi recruitment reconstitution with protease/heat sensitivity (PMID:29507113); GBF1–Miro co-IP, GCA inhibition, dynein pathway (PMID:30459446); HDS2 alanine scanning with functional replacement (PMID:29443553)

    PMID:29443553 PMID:29507113 PMID:29898406 PMID:30459446

    Open questions at the time
    • Identity of the proteinaceous Golgi receptor for GBF1 unknown
    • Miro–GBF1 interaction interface not mapped
    • How CK2 phosphorylation timing is controlled at the midbody unclear
  18. 2019 High

    Multiple studies expanded GBF1's functional network: C10orf76 was identified as a Golgi-cycling GBF1 interactor required for Golgi integrity and secretion; GBF1 was shown to be rate-limiting for VWF granule biogenesis with AMPK coupling; HCV NS3 was found to directly bind GBF1's Sec7 domain; and GBF1 catalytic activity was required for rotavirus VP7 trimerization and particle assembly.

    Evidence BioID proximity labeling with co-IP and siRNA (PMID:31519766); GBF1 over/underexpression with AMPK activation and VWF imaging (PMID:31056345); NS3–GBF1 yeast two-hybrid, co-IP, PLA, NS3 mutant replication (PMID:30567983); GBF1 pharmacological/genetic inhibition with VP7 trimerization assay (PMID:31270230)

    PMID:30567983 PMID:31056345 PMID:31270230 PMID:31519766

    Open questions at the time
    • C10orf76 molecular function in GBF1 regulation unknown
    • Whether AMPK directly modulates GBF1 at the Golgi versus indirectly through energy sensing not resolved at this point
    • NS3–GBF1 binding does not explain how GBF1 supports HCV replication mechanistically
  19. 2020 Medium

    Human genetic evidence established GBF1 as a disease gene: heterozygous pathogenic GBF1 variants were identified in families with distal hereditary motor neuropathy/CMT2, with patient fibroblasts showing marked Golgi fragmentation.

    Evidence Genomic sequencing of affected families, Golgi fragmentation assay in patient fibroblasts, GBF1 expression in mouse motor neurons

    PMID:32937143

    Open questions at the time
    • Specific GBF1 variant effects on ARF activation or COPI recruitment not tested biochemically
    • Motor neuron-specific vulnerability mechanism unknown
    • No animal model recapitulating the neuropathy phenotype
  20. 2021 High

    Src kinase phosphorylation of GBF1 (Y876/Y898 near the Sec7 C-terminus) was shown to enhance ARF1 binding and induce retrograde tubular transport carriers carrying GALNTs from Golgi to ER, defining a regulated retrograde trafficking pathway.

    Evidence Phosphoproteomics, Src kinase assay, phosphomimetic/phosphodeficient GBF1 mutants, live-cell tubule imaging, ARF1 binding assay

    PMID:34870592

    Open questions at the time
    • Whether Src phosphorylation occurs in response to specific physiological signals not determined
    • How phosphorylation alters GBF1 conformation to enhance ARF1 binding not structurally resolved
  21. 2023 High

    N-terminal GBF1 phosphorylation sites (S233, S371, Y377, Y515) were shown to differentially regulate cytokinesis versus Golgi homeostasis: phosphomimetic mutants supported normal Golgi and secretion but impaired cytokinetic bridge resolution, revealing separable phospho-regulatory modules.

    Evidence Phosphomimetic and non-phosphorylatable GBF1 mutants with Golgi morphology, secretion, and multinucleation assays

    PMID:37604968

    Open questions at the time
    • Kinases responsible for these N-terminal phosphorylations not identified
    • Mechanism by which phosphorylation impairs cytokinesis not defined
  22. 2024 High

    AMPK phosphorylation of GBF1 was pinpointed to Thr1337 using gene-edited non-phosphorylatable knock-in cells, directly demonstrating that this single site mediates AMPK-induced Golgi fragmentation and trafficking slowdown; separately, GBF1 haploinsufficiency was linked to congenital cataracts in mice.

    Evidence AMPK-α KO cells, GBF1-T1337A knock-in by gene editing, trafficking assay (PMID:39575556); Gbf1 heterozygous KO mice with cataracts, UPR/autophagy in lens cells (PMID:39110251)

    PMID:39110251 PMID:39575556

    Open questions at the time
    • Whether T1337 phosphorylation and CDK1/CK2 phosphorylation act synergistically in mitosis not tested
    • Lens-specific trafficking cargo affected by GBF1 deficiency not identified

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key open questions remain: the identity of the proteinaceous Golgi receptor for GBF1, the structural basis for Sec7-domain autoinhibition of HDS1, a full-length GBF1 structure, and the mechanism by which motor neuron-specific vulnerability arises from GBF1 mutations.
  • No high-resolution structure of full-length GBF1
  • Golgi membrane receptor identity unknown
  • Motor neuron vulnerability mechanism in CMT2 not explained
  • Relationship between multiple kinase inputs and GBF1 conformational states not integrated

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0098772 molecular function regulator activity 6 GO:0008289 lipid binding 2
Localization
GO:0005794 Golgi apparatus 6 GO:0005829 cytosol 3 GO:0005811 lipid droplet 2 GO:0031410 cytoplasmic vesicle 2
Pathway
R-HSA-5653656 Vesicle-mediated transport 5 R-HSA-1640170 Cell Cycle 4 R-HSA-9609507 Protein localization 4 R-HSA-1852241 Organelle biogenesis and maintenance 3 R-HSA-8953897 Cellular responses to stimuli 3 R-HSA-1430728 Metabolism 2
Partners
ARF1ASAP1ATGLC10ORF76COPIP115RAB1BRHOT1
Complex memberships
COPI coat (functional effector complex)GBF1 homodimer (DCB-HUS mediated)

Evidence

Reading pass · 49 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1999 GBF1 was identified as a novel Golgi-associated guanine nucleotide exchange factor (GEF) with a Sec7 domain that exhibits BFA-resistant GEF activity specific towards ARF5 at physiological Mg2+ concentration. Overexpression conferred BFA resistance to Golgi morphology and ARF activation/COPI recruitment. GBF1 localized primarily to the cytosol with a pool co-localizing with β-COPI at a perinuclear (Golgi) structure. Expression cloning, in vitro GEF assay with His-tagged GBF1, immunogold EM localization, BFA resistance functional assay The Journal of cell biology High 10402461
2004 GBF1 cycles rapidly on and off Golgi membranes (not stably associated). BFA, acting as an uncompetitive inhibitor binding to an Arf-GDP–GBF1 complex, stabilizes GBF1 on Golgi membranes. GBF1 exchange activity on Arf1 is inhibited by BFA in mammalian cells. YFP-GBF1 FRAP analysis, in vivo Arf1-GTP level assay, BFA treatment Molecular biology of the cell High 15616190
2003 GBF1 physically interacts with the membrane-tethering protein p115 through the proline-rich region of GBF1 and the head region of p115. The two proteins colocalize at the Golgi and peripheral VTCs. Expression of the p115-binding (pro-rich) region of GBF1 causes Golgi disruption, indicating functional relevance of this interaction. Yeast two-hybrid screen, in vitro binding assay, in vivo co-immunoprecipitation, mutagenesis, immunofluorescence EMBO reports High 12634853
2005 GBF1 rapidly cycles between membranes and cytosol (t1/2 ~17 s by FRAP), faster than ARF itself. GBF1 is stabilized on membranes when in complex with ARF-GDP (shown by inactive E794K mutant, ARF1-T31N mutant, and BFA treatment). GBF1 dissociation is triggered by its own catalytic activity (GDP displacement and GTP binding to ARF), implying each GBF1 membrane association catalyzes a single ARF activation event. GFP-GBF1 FRAP, dominant-negative mutant expression, BFA treatment Traffic (Copenhagen, Denmark) High 15813748
2006 GBF1 localizes to both cis-Golgi membranes and peripheral puncta (VTCs) near but separate from ER exit sites. Live-cell imaging showed rapid GFP-GBF1 exchange with a large cytosolic pool. Microinjection of anti-GBF1 antibodies specifically caused dissociation of COPI from membranes, demonstrating GBF1 regulates COPI membrane recruitment in the early secretory pathway. GFP-live imaging, FRAP, BFA treatment, anti-GBF1 microinjection, subcellular fractionation Journal of cell science High 16926190
2006 The enterovirus 3A protein inhibits Arf1 activation and COP-I coat recruitment by directly interacting with the N-terminus of GBF1 and inhibiting its GEF function. This 3A–GBF1 interaction is the mechanism by which 3A blocks ER-to-Golgi transport. Co-immunoprecipitation, dominant-negative Arf1 expression, siRNA knockdown, EM, in vivo transport assay, mouse virulence assay Developmental cell High 16890159
2007 GBF1 acts as a Rab1b effector: active GTP-locked Rab1b (Rab1bQ67L) increases GBF1 and COPI association with peripheral ER exit site structures and stabilizes Arf1 on Golgi membranes. Rab1b siRNA knockdown reduced GBF1 membrane association. The N-terminal domain of GBF1 mediates its interaction with Rab1b. Co-immunoprecipitation, siRNA knockdown, live-cell GFP imaging, FRAP, dominant-active Rab1b mutant expression Molecular biology of the cell High 17429068
2007 GBF1 dimerizes through its DCB domain; DCB–DCB homodimerization and DCB–HUS interactions define the N-terminal architecture of GBF1 (and BIG ArfGEFs). The HUS box (most conserved motif after Sec7) mediates the DCB–HUS interaction within each homodimer. Both DCB and HUS domains are necessary for GBF1 dimerization in mammalian cells. Yeast two-hybrid, biochemical interaction assays, co-immunoprecipitation in mammalian cells, mutagenesis The Journal of biological chemistry High 17640864
2007 Molecular determinants of 3A–GBF1 interaction: 3A must dimerize to bind GBF1; a conserved N-terminal region of 3A is critical for GBF1 binding but not dimerization. Within GBF1, the extreme N-terminus, the DCB (dimerization/cyclophilin binding) domain, and the HUS domain are required for interaction with 3A. 3A mutagenesis, co-immunoprecipitation, GBF1 deletion mutant analysis Journal of virology High 17329336
2007 GBF1 is required for GGA (Golgi-localized, gamma-ear-containing, ARF-binding protein) recruitment to Golgi membranes. GBF1 co-localizes and co-immunoprecipitates with GGAs. Depletion of GBF1 or expression of inactive GBF1 prevents GGA membrane recruitment and causes missorting of lysosomal cargo (mannose-6-phosphate receptor, sortilin). Co-immunoprecipitation, GBF1 siRNA knockdown, dominant-negative GBF1, cargo trafficking assay Traffic (Copenhagen, Denmark) High 17666033
2007 GBF1 depletion by siRNA causes COPI dispersal and extensive tubulation of cis-Golgi without complete Golgi collapse into ER. This causes dramatic inhibition of transmembrane protein trafficking but soluble protein secretion continues, indicating GBF1-mediated ARF activation and COPI recruitment are specifically required for transmembrane cargo but not soluble cargo transport. siRNA knockdown, immunofluorescence, live-cell trafficking assays, EM Journal of cell science High 17956946
2007 GBF1 regulates COPI recruitment specifically on cis-Golgi compartments (not TGN), whereas BIG proteins regulate adaptor proteins on trans-Golgi. GBF1/COPI knockdown does not prevent ER export but causes VSVGtsO45 accumulation in peripheral VTCs. GBF1 is required for Golgi subcompartmentalization and cargo progression to the cell surface. siRNA knockdown (GBF1, BIG1, BIG2, COPI), immunofluorescence, VSVGtsO45 trafficking assay Molecular biology of the cell High 18003980
2008 GBF1 depletion (but not BIG1 or BIG2 depletion) causes cell-cycle arrest in G0/G1, Golgi marker dispersal, ER stress (elevated calreticulin, PDI, ER chaperones), and triggers ATF6 proteolysis mimicking an unfolded protein response. GBF1 depletion causes relocalization of S2P from Golgi to ER with ATF6 cleavage and upregulation of ERSE genes. Selective siRNA depletion of each GEF, proteomic analysis, immunofluorescence, cell-cycle analysis Proceedings of the National Academy of Sciences of the United States of America High 18287014
2008 Class II ARFs (Arf4, Arf5) associate with ERGIC membranes through GBF1-independent binding sites in their GDP-bound form, whereas class I Arfs (Arf1, Arf3) rapidly dissociate from all endomembranes upon BFA treatment. Loss of Arf-GTP (not formation of Arf·GDP·BFA·GBF1 complex) causes GBF1 accumulation on membranes. Live-cell imaging of fluorescently tagged Arfs, BFA and Exo1 treatment, GDP-locked Arf4 mutant Molecular biology of the cell High 18524849
2008 GBF1 (but not BIG1 or BIG2) is critically required for mouse hepatitis coronavirus (MHV) RNA replication. ARF1, the cellular effector of GBF1, is also required. GBF1-mediated ARF1 activation controls the number of viral replication complexes formed. Individual siRNA knockdown of GBF1, BIG1, BIG2, ARF1; BFA sensitivity in MDCK cells expressing BFA-resistant GBF1; immunofluorescence and quantitative EM PLoS pathogens High 18551169
2009 GBF1 is critically required for CVB3 RNA replication. BFA-resistant GBF1-M832L rescues replication in BFA-treated cells; GBF1 knockdown by RNAi inhibits replication; only active (not inactive catalytic mutant) GBF1 rescues replication. Overexpression of ARF proteins or Rab1B did not rescue BFA-inhibited replication. siRNA knockdown, BFA-resistant GBF1 mutant rescue, overexpression of Arf proteins and Rab1B, replicon assays Journal of virology High 19740986
2009 GBF1 is a host factor critically required for HCV RNA replication. GBF1 knockdown (but not BIG1 or BIG2) inhibits HCV replication. BFA-resistant GBF1 mutant rescues HCV replication in BFA-treated cells. BFA/GBF1 inhibition does not block membranous web formation but impairs replication complex activity. siRNA knockdown of individual GEFs, BFA-resistant GBF1 rescue, pharmacological GBF1 inhibitor, immunofluorescence and EM Journal of virology High 19906930
2009 Drosophila garz (ortholog of GBF1) is a novel component of the clathrin-independent GEEC endocytic pathway, required for GPI-anchored protein and fluid-phase internalization. A catalytically inactive GBF1 GEF mutant has altered Arf1 activation at nascent pinosomes and impairs fluid-phase uptake. RNAi screen, live confocal and TIRF imaging with GBF1-GFP and Arf1 sensor, GEF-dead mutant, quantitative endocytosis assays PloS one High 19707569
2010 For poliovirus replication, the N-terminal region of GBF1 (lacking the catalytic Sec7 domain) is sufficient to rescue BFA-inhibited replication. In infected cells p115 is degraded and neither p115 nor Rab1b knockdown affects viral replication, indicating viral replication requires a non-catalytic function of GBF1 distinct from its cellular role in ARF/COPI secretory trafficking. N-terminal GBF1 truncation rescue assay, p115/Rab1b siRNA knockdown, BFA-resistant virus replicon Cellular microbiology High 20497182
2010 GBF1 is phosphorylated by CDK1-cyclin B during mitosis, causing its dissociation from Golgi membranes and reduction of membrane-associated GTP-bound ARF. A low level of GBF1 activity persists in mitosis and remains required for COPI recruitment, suggesting GBF1 phosphorylation and membrane dissociation contribute to Golgi fragmentation during mitotic entry. Phosphoprotein analysis, CDK1-cyclin B in vitro kinase assay, immunofluorescence in mitotic cells, ARF-GTP measurement The Biochemical journal High 20175751
2010 PI4KIIIα-generated phosphatidylinositol 4-phosphate [PtdIns(4)P] is required for GBF1 recruitment to Golgi membranes. Dominant-active Rab1 increases PtdIns(4)P levels at the Golgi, suggesting Rab1 contributes to GBF1 recruitment specificity by activating PI4KIIIα to produce PtdIns(4)P. PI4KIIIα siRNA knockdown, PI4P inhibitors (wortmannin, LY294002), GFP-PH PtdIns(4)P sensor, dominant-active Rab1 expression, GBF1 localization assay Journal of cell science High 20530568
2011 C. trachomatis selectively co-opts GBF1 (but not BIG1 or BIG2) for vesicle-mediated sphingomyelin (SM) acquisition. The Arf1/GBF1-dependent SM pathway is essential for inclusion membrane growth and stability but not for bacterial replication. GBF1 depletion by siRNA blocks SM delivery to the inclusion. siRNA knockdown of individual BFA targets, BFA sensitivity analysis, fluorescent SM trafficking assay, inclusion integrity measurement PLoS pathogens High 21909260
2011 GBF1 and ATGL (adipose triglyceride lipase) interact directly through multiple contact sites: ATGL C-terminus contacts GBF1 N-terminal domains including the Sec7 domain; ATGL N-terminal patatin domain interacts with GBF1 HDS1 and HDS2 domains. GBF1 HDS1 and HDS2 domains localize to lipid droplets when expressed alone. The GBF1–Arf1–COPI pathway is required for ATGL delivery to lipid droplets. Yeast two-hybrid, co-immunoprecipitation in mammalian cells, direct protein binding (in vitro), GFP domain-localization assays PloS one High 21789191
2012 ARF1 and GBF1 generate a PI4P-enriched environment at HCV replication complexes. ARF1 and GBF1 colocalize with PI4KIIIβ and are both required for HCV replication. HCV replication is inhibited by PI4P phosphatase Sac1 overexpression. Co-immunoprecipitation/colocalization, PI4P sensor, Sac1 overexpression, siRNA knockdown PloS one Medium 22359663
2012 GBF1 bears a novel phosphatidylinositol-phosphate binding module (BP3K) that links PI3Kγ activity with Arf1 activation in GPCR-stimulated neutrophil chemotaxis. Upon GPCR stimulation, GBF1 translocates from Golgi to the leading edge via PI3Kγ product binding, where it activates Arf1 and recruits p22phox and GIT2, thereby regulating directional sensing and superoxide production. Subcellular fractionation, GFP-GBF1 live imaging, phospholipid binding assay, siRNA knockdown, GPCR stimulation Molecular biology of the cell High 22573891
2013 GBF1's HDS1 domain (immediately downstream of the Sec7 domain) contains an amphipathic helix that binds lipid droplets and Golgi membranes in cells, and bilayer liposomes and artificial droplets in vitro. The Sec7 domain inhibits the HDS1 lipid-droplet binding capacity in the context of full-length GBF1. In vitro liposome binding, artificial droplet binding, GFP domain expression in cells, mutagenesis of amphipathic helix Journal of cell science High 23943872
2013 GBF1-activated ARF4 and ARF5 (but not ARF3) facilitate BIG1 and BIG2 recruitment to the TGN, establishing a functional GEF cascade. GBF1 localizes ultrastructurally to pre-Golgi, Golgi, and TGN. This defines a sequential coating pathway in which GBF1 at the TGN activates ARFs that then recruit BIG1/2. Immunoelectron microscopy, siRNA knockdown, Arf isoform-specific rescue experiments, GBF1 inhibitor treatment The Journal of biological chemistry High 23386609
2013 AMPK phosphorylates GBF1 during mitosis, causing GBF1 dissociation from the Golgi membrane and abolishing GBF1's Arf1-GEF activity, thereby promoting Golgi disassembly required for mitosis entry. In vitro AMPK kinase assay on GBF1, phospho-specific analysis, mitotic cell fractionation, dominant-negative and pharmacological approaches Journal of cell science High 23418352
2015 The Dengue virus GBF1–Arf1/Arf4–COPI pathway is required for capsid protein transport from ER membrane to lipid droplets, independently of COPII components and Golgi integrity. A BFA-resistant GBF1 mutant rescues capsid subcellular distribution in BFA-treated infected cells. BFA and GCA pharmacological inhibition, BFA-resistant GBF1 rescue, siRNA knockdown, immunofluorescence Traffic (Copenhagen, Denmark) High 26031340
2015 GBF1 oligomerization (mediated by the DCB domain residues K91 and E130) is dispensable for Golgi targeting, rapid membrane cycling, ARF activation, COPI recruitment, and cargo secretion. However, oligomerization stabilizes GBF1 protein; the non-oligomerizing 91/130 mutant is degraded faster than wild-type. GBF1 DCB domain mutagenesis, live-cell FRAP, ARF activation assay, COPI immunofluorescence, secretion assay, protein stability measurement American journal of physiology. Cell physiology High 26718629
2017 GBF1 and Arf4 form a functional complex with the sensory receptor rhodopsin at the photoreceptor Golgi/TGN during transport carrier biogenesis for ciliary targeting. Rhodopsin and Arf4 bind the regulatory N-terminal DCB-HUS domain of GBF1. GCA (GBF1 inhibitor) blocks this complex and prevents rhodopsin delivery to cilia without disrupting the Golgi. GBF1 also interacts with the Arf GAP ASAP1 in a GCA-resistant manner. Frog retina in vivo analysis, co-immunoprecipitation with recombinant human proteins, GCA inhibitor, domain binding mapping Journal of cell science High 29025970
2018 GBF1 is phosphorylated on Ser292 and Ser297 by casein kinase 2 (CK2) during mitosis, enabling recognition by the F-box protein βTrCP and recruitment to the SCFβTrCP ubiquitin ligase complex, triggering GBF1 degradation. This degradation occurs at the intercellular bridge of telophase cells and is required for Golgi membrane positioning and postmitotic Golgi reformation. A non-degradable GBF1 mutant blocks Golgi cluster transport and causes cytokinesis failure. Phosphorylation site mutagenesis, co-immunoprecipitation with βTrCP/SCF complex, proteomics, non-degradable GBF1 mutant live imaging, cytokinesis assay Cell reports High 29898406
2018 GBF1 recruitment to Golgi membranes requires the HDS1 and HDS2 domains and a heat-labile, protease-sensitive Golgi-localized protein receptor. Arf-GDP localization at the cis-Golgi (but not TGN) promotes GBF1 recruitment. ArfGAP2 and ArfGAP3 do not regulate GBF1 recruitment. In vitro GBF1 recruitment assay with Golgi fractions, heat/protease treatment of membranes, Arf-GDP targeted mutants, GBF1 HDS1/HDS2 domain mapping Journal of cell science High 29507113
2018 GBF1 and its substrate Arf1 interact with the mitochondrial membrane protein Miro, regulating mitochondrial spatial organization. GBF1 inhibition promotes dynein- and Miro-dependent retrograde mitochondrial transport along microtubules toward the centrosome, causing mitochondrial network collapse. Active GTP-bound Arf1 also physically interacts with Miro. Co-immunoprecipitation (GBF1-Miro, Arf1-GTP-Miro), GBF1 inhibition (GCA), Miro siRNA, dynein inhibitor, electron tomography, live-cell time-lapse imaging Scientific reports High 30459446
2018 Conserved residues RDR1168 and LF1266 within α-helices 2 and 6 of the HDS2 domain of GBF1 are required for GBF1 targeting to Golgi membranes. Mutations at these positions compromise Golgi homeostasis, ARF activation, secretion, and cell viability in a functional replacement assay. HDS2 alanine-scanning mutagenesis, BFA-resistant replacement assay, Golgi morphology, COPI recruitment, secretion assay American journal of physiology. Cell physiology High 29443553
2019 C10orf76 interacts with GBF1 and rapidly cycles on and off GBF1-positive Golgi structures (identified by BioID proximity labeling of Golgi-enriched fractions). C10orf76 depletion causes Golgi fragmentation, alters GBF1 recruitment, and impairs secretion. BioID proximity labeling, mass spectrometry, co-immunoprecipitation, siRNA knockdown, Golgi morphology and secretion assays Molecular & cellular proteomics : MCP High 31519766
2019 GBF1 is required for VWF (von Willebrand factor) and extracellular matrix protein trafficking from ER to Golgi secretory granules in endothelial cells. GBF1 level is a limiting factor in VWF granule biogenesis. AMPK activation (by glucose levels) couples to GBF1 function and modulates VWF trafficking, linking physiological energy status to anterograde secretory pathway regulation. GBF1 siRNA knockdown, GBF1 overexpression, AMPK pharmacological activation, fluorescence live imaging of VWF trafficking, secretion assay Developmental cell High 31056345
2019 HCV NS3 protein directly interacts with GBF1 through the Sec7 domain of GBF1 and the protease domain of NS3, as shown by yeast two-hybrid, co-immunoprecipitation, and proximity ligation assay. NS3 alters GBF1 intracellular localization. An NS3 mutant (N77D) that disrupts GBF1 binding is non-replicative despite retaining protease activity, indicating the NS3–GBF1 interaction is important for HCV genome replication. Yeast two-hybrid, co-immunoprecipitation, proximity ligation assay, NS3 mutagenesis, replication assay Journal of virology High 30567983
2019 GBF1 catalytic activity (but not Arf1 activation per se) is essential for rotavirus assembly. Inhibition of GBF1 by BFA or GCA prevents trimerization of the outer capsid protein VP7 and blocks assembly of triple-layered particles. GBF1 inhibition alters electrophoretic mobility of VP7 and NSP4. BFA and GCA pharmacological inhibition, GBF1 siRNA knockdown, viral particle characterization, VP7 trimerization assay Journal of virology High 31270230
2019 Multiple determinants in GBF1 support poliovirus replication: the Arf-activating property of the Sec7 domain is indispensable, but the primary structure of the Sec7 domain itself is not. GBF1 is recruited to replication sites via both direct 3A interaction and redundant determinants in C-terminal non-catalytic domains (HDS regions). GBF1 domain mutant rescue assay in poliovirus replication context, viral RNA replication assay, BFA-resistant rescue Journal of virology High 31375590
2021 Src kinase phosphorylates GBF1 on 10 tyrosine residues; two residues (Y876 and Y898) near the C-terminus of the Sec7 domain promote GBF1 binding to Arf1 GTPase. This phosphorylation induces formation of tubular transport carriers containing GALNTs for Golgi-to-ER retrograde transport. Phosphomimetic GBF1 mutants induce tubules, while mutants defective for Arf1 binding prevent carrier formation and GALNTs relocation. Phosphoproteomics, Src kinase assay, GBF1 phosphomimetic/phosphodeficient mutants, live-cell tubule imaging, molecular modeling, Arf1 binding assay eLife High 34870592
2024 AMPK associates with the Golgi and phosphorylates GBF1 at Thr1337 upon activation, causing Golgi fragmentation and slowing protein trafficking through the Golgi. Golgi disassembly upon AMPK activation is blocked in cells expressing non-phosphorylatable GBF1-T1337A generated by gene editing. AMPK-α knockout cells, pharmacological AMPK activators, GBF1-T1337A knock-in by gene editing, Golgi morphology assay, protein trafficking (Gaussia luciferase) assay Journal of cell science High 39575556
2016 Zebrafish gbf1 loss-of-function (L1246R mutation in HDS2 domain, morphants, knockout) causes intracerebral hemorrhage due to vascular breakage in a cell-autonomous manner. The L1246R Gbf1 mutant fails to be recruited to the Golgi and cannot activate Arf1 or recruit the COPI complex in mammalian cells, indicating HDS2 domain is essential for GBF1 membrane targeting and function. ENU mutagenesis/positional cloning in zebrafish, gbf1 morpholino knockdown and CRISPR knockout, Gbf1-L1246R expression in mammalian cells, Golgi recruitment and Arf1 activation assay The Journal of biological chemistry High 28003365
2020 Pathogenic variants in GBF1 (four distinct heterozygous variants, two de novo) cause distal hereditary motor neuropathy/Charcot-Marie-Tooth neuropathy type 2 (HMN/CMT2). Primary fibroblasts from all affected individuals show marked Golgi fragmentation consistent with GBF1's role in Golgi maintenance. GBF1 is present in mouse spinal cord/muscle and enriched at motor neurons and growth cones. Genomic sequencing, Golgi fragmentation assay in patient fibroblasts, immunofluorescence in mouse tissue American journal of human genetics Medium 32937143
2023 Phosphorylation of specific N-terminal residues of GBF1 (S233, S371, Y377, Y515) differentially regulates its role in cytokinesis versus Golgi homeostasis/secretion: phosphomimetic mutants of these residues support normal Golgi architecture and cargo secretion but cause multi-nucleation and impair cytokinetic bridge resolution, while not affecting secretory functions. GBF1 phospho-site mutagenesis (phosphomimetic and non-phosphorylatable), Golgi morphology assay, secretion assay, cytokinesis/multinucleation assay Scientific reports High 37604968
2012 GBF1-dependent secretion (via Arf1-COPI machinery) is required for Drosophila tubulogenesis. Loss of Garz (fly GBF1 ortholog) impairs Golgi integrity, cargo vesicle transport, and directed apical membrane delivery, causing failure in epithelial polarity and lumen expansion in tubular organs. Drosophila loss-of-function mutants, immunofluorescence, EM, live imaging of cargo transport Journal of cell science High 22302994
2013 In C. elegans, GBF-1 (GBF1 ortholog) localizes to the cis-Golgi and is required for secretion, Golgi integrity, and ER reticular structure. GBF-1 RNAi also impairs receptor-mediated endocytosis in oocytes without affecting recycling pathways, and alters early/late endosome dynamics. RNAi, immunofluorescence, GFP-tagged organelle markers, yolk receptor trafficking assay in C. elegans PloS one Medium 23840591
2021 GBF1 deficiency in mouse oocytes (via GBF1 inhibitor treatment) causes aberrant Golgi accumulation around the spindle, condensation of GM130 (a Golgi matrix protein co-localizing with GBF1), ER structural disruption with elevated ER stress marker GRP78, and altered mitochondrial membrane potential, impairing polar body formation. GBF1 inhibitor (GCA) in mouse oocytes, immunofluorescence, mitochondrial membrane potential assay, Western blot Microscopy and microanalysis Medium 33478608
2024 GBF1 knockdown activates XBP1s (unfolded protein response) and enhances mTOR-independent autophagy in human lens epithelium cells. A pathological GBF1 T1287I mutation reduces GBF1 protein levels. Heterozygous Gbf1 knockout mice display cataracts, establishing GBF1 as a causative gene for congenital cataracts. siRNA knockdown, UPR activation assay (XBP1 splicing), autophagy assay, Gbf1 heterozygous knockout mice, patient mutation analysis Human genetics Medium 39110251

Source papers

Stage 0 corpus · 90 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
2011 Chlamydia trachomatis co-opts GBF1 and CERT to acquire host sphingomyelin for distinct roles during intracellular development. PLoS pathogens 189 21909260
2004 Dynamics of GBF1, a Brefeldin A-sensitive Arf1 exchange factor at the Golgi. Molecular biology of the cell 187 15616190
1999 GBF1: A novel Golgi-associated BFA-resistant guanine nucleotide exchange factor that displays specificity for ADP-ribosylation factor 5. The Journal of cell biology 171 10402461
2009 GBF1, a guanine nucleotide exchange factor for Arf, is crucial for coxsackievirus B3 RNA replication. Journal of virology 153 19740986
1992 DNA binding site preferences and transcriptional activation properties of the Arabidopsis transcription factor GBF1. The EMBO journal 140 1563344
2008 Mouse hepatitis coronavirus RNA replication depends on GBF1-mediated ARF1 activation. PLoS pathogens 130 18551169
2006 A viral protein that blocks Arf1-mediated COP-I assembly by inhibiting the guanine nucleotide exchange factor GBF1. Developmental cell 129 16890159
1992 DNA binding activity of the Arabidopsis G-box binding factor GBF1 is stimulated by phosphorylation by casein kinase II from broccoli. The Plant cell 121 1525562
2007 Rab1b interacts with GBF1 and modulates both ARF1 dynamics and COPI association. Molecular biology of the cell 114 17429068
2009 Identification of GBF1 as a cellular factor required for hepatitis C virus RNA replication. Journal of virology 107 19906930
2008 Unfolded protein response and cell death after depletion of brefeldin A-inhibited guanine nucleotide-exchange protein GBF1. Proceedings of the National Academy of Sciences of the United States of America 89 18287014
2007 Dissecting the role of the ARF guanine nucleotide exchange factor GBF1 in Golgi biogenesis and protein trafficking. Journal of cell science 89 17956946
2006 GBF1, a cis-Golgi and VTCs-localized ARF-GEF, is implicated in ER-to-Golgi protein traffic. Journal of cell science 89 16926190
2007 Distinct functions for Arf guanine nucleotide exchange factors at the Golgi complex: GBF1 and BIGs are required for assembly and maintenance of the Golgi stack and trans-Golgi network, respectively. Molecular biology of the cell 86 18003980
2006 Effects of picornavirus 3A Proteins on Protein Transport and GBF1-dependent COP-I recruitment. Journal of virology 83 17005635
2012 Molecular interactions of GBF1 with HY5 and HYH proteins during light-mediated seedling development in Arabidopsis thaliana. The Journal of biological chemistry 82 22692212
2008 Characterization of class I and II ADP-ribosylation factors (Arfs) in live cells: GDP-bound class II Arfs associate with the ER-Golgi intermediate compartment independently of GBF1. Molecular biology of the cell 74 18524849
2005 Dissection of membrane dynamics of the ARF-guanine nucleotide exchange factor GBF1. Traffic (Copenhagen, Denmark) 70 15813748
1995 Reconstitution of Arabidopsis casein kinase II from recombinant subunits and phosphorylation of transcription factor GBF1. The Plant cell 69 7696877
2013 Targeting of the Arf-GEF GBF1 to lipid droplets and Golgi membranes. Journal of cell science 68 23943872
2003 The membrane-tethering protein p115 interacts with GBF1, an ARF guanine-nucleotide-exchange factor. EMBO reports 68 12634853
2015 Dengue Virus Uses a Non-Canonical Function of the Host GBF1-Arf-COPI System for Capsid Protein Accumulation on Lipid Droplets. Traffic (Copenhagen, Denmark) 66 26031340
2013 The Sec7 guanine nucleotide exchange factor GBF1 regulates membrane recruitment of BIG1 and BIG2 guanine nucleotide exchange factors to the trans-Golgi network (TGN). The Journal of biological chemistry 66 23386609
2013 Recruitment of PI4KIIIβ to coxsackievirus B3 replication organelles is independent of ACBD3, GBF1, and Arf1. Journal of virology 64 24352456
2009 Analysis of endocytic pathways in Drosophila cells reveals a conserved role for GBF1 in internalization via GEECs. PloS one 61 19707569
2007 Molecular determinants of the interaction between coxsackievirus protein 3A and guanine nucleotide exchange factor GBF1. Journal of virology 61 17329336
2012 ARF1 and GBF1 generate a PI4P-enriched environment supportive of hepatitis C virus replication. PloS one 60 22359663
2017 GBF1 differentially regulates CAT2 and PAD4 transcription to promote pathogen defense in Arabidopsis thaliana. The Plant journal : for cell and molecular biology 57 28622438
2010 Poliovirus replication requires the N-terminus but not the catalytic Sec7 domain of ArfGEF GBF1. Cellular microbiology 57 20497182
2011 Interaction between the triglyceride lipase ATGL and the Arf1 activator GBF1. PloS one 54 21789191
2011 Polarized cell growth in Arabidopsis requires endosomal recycling mediated by GBF1-related ARF exchange factors. Nature cell biology 51 22138577
2013 AMPK phosphorylates GBF1 for mitotic Golgi disassembly. Journal of cell science 49 23418352
2010 The phosphatidylinositol 4-kinase PI4KIIIalpha is required for the recruitment of GBF1 to Golgi membranes. Journal of cell science 49 20530568
2017 GBF1 and Arf1 function in vesicular trafficking, lipid homoeostasis and organelle dynamics. Biology of the cell 46 28985001
2014 Quantitative proteomic analysis of host-virus interactions reveals a role for Golgi brefeldin A resistance factor 1 (GBF1) in dengue infection. Molecular & cellular proteomics : MCP 46 24855065
2007 Interactions between conserved domains within homodimers in the BIG1, BIG2, and GBF1 Arf guanine nucleotide exchange factors. The Journal of biological chemistry 43 17640864
2010 Differential effects of the putative GBF1 inhibitors Golgicide A and AG1478 on enterovirus replication. Journal of virology 41 20504936
2012 GBF1 bears a novel phosphatidylinositol-phosphate binding module, BP3K, to link PI3Kγ activity with Arf1 activation involved in GPCR-mediated neutrophil chemotaxis and superoxide production. Molecular biology of the cell 40 22573891
2015 Interaction of MYC2 and GBF1 results in functional antagonism in blue light-mediated Arabidopsis seedling development. The Plant journal : for cell and molecular biology 39 26047210
2019 A GBF1-Dependent Mechanism for Environmentally Responsive Regulation of ER-Golgi Transport. Developmental cell 37 31056345
2010 LG186: An inhibitor of GBF1 function that causes Golgi disassembly in human and canine cells. Traffic (Copenhagen, Denmark) 37 20854417
2012 GBF1 (Gartenzwerg)-dependent secretion is required for Drosophila tubulogenesis. Journal of cell science 33 22302994
2010 Phosphorylation and membrane dissociation of the ARF exchange factor GBF1 in mitosis. The Biochemical journal 33 20175751
2008 GBF1, a transcription factor of blue light signaling in Arabidopsis, is degraded in the dark by a proteasome-mediated pathway independent of COP1 and SPA1. The Journal of biological chemistry 33 18930926
2007 The Arf GEF GBF1 is required for GGA recruitment to Golgi membranes. Traffic (Copenhagen, Denmark) 29 17666033
2018 GBF1 and Arf1 interact with Miro and regulate mitochondrial positioning within cells. Scientific reports 26 30459446
2017 Identification of GBF1 as a cellular factor required for hepatitis E virus RNA replication. Cellular microbiology 26 29112323
2017 CSFV proliferation is associated with GBF1 and Rab2. Journal of biosciences 23 28229964
2019 BioID Performed on Golgi Enriched Fractions Identify C10orf76 as a GBF1 Binding Protein Essential for Golgi Maintenance and Secretion. Molecular & cellular proteomics : MCP 22 31519766
2017 The Arf GEF GBF1 and Arf4 synergize with the sensory receptor cargo, rhodopsin, to regulate ciliary membrane trafficking. Journal of cell science 22 29025970
2014 The AtCathB3 gene, encoding a cathepsin B-like protease, is expressed during germination of Arabidopsis thaliana and transcriptionally repressed by the basic leucine zipper protein GBF1. Journal of experimental botany 22 24600022
2018 Investigation of the role of GBF1 in the replication of positive-sense single-stranded RNA viruses. The Journal of general virology 20 29923822
1998 Human GBF1 is a ubiquitously expressed gene of the sec7 domain family mapping to 10q24. Genomics 20 9828135
2016 Impairment of Cargo Transportation Caused by gbf1 Mutation Disrupts Vascular Integrity and Causes Hemorrhage in Zebrafish Embryos. The Journal of biological chemistry 18 28003365
2015 Oligomerization of the Sec7 domain Arf guanine nucleotide exchange factor GBF1 is dispensable for Golgi localization and function but regulates degradation. American journal of physiology. Cell physiology 18 26718629
2023 An interplay between bZIP16, bZIP68, and GBF1 regulates nuclear photosynthetic genes during photomorphogenesis in Arabidopsis. The New phytologist 17 37602940
2019 The Guanine Nucleotide Exchange Factor GBF1 Participates in Rotavirus Replication. Journal of virology 17 31270230
2015 Phosphorylation Affects DNA-Binding of the Senescence-Regulating bZIP Transcription Factor GBF1. Plants (Basel, Switzerland) 17 27135347
2013 The ArfGEF GBF-1 Is Required for ER Structure, Secretion and Endocytic Transport in C. elegans. PloS one 17 23840591
2020 SNPs in SNCA, MCCC1, DLG2, GBF1 and MBNL2 are associated with Parkinson's disease in southern Chinese population. Journal of cellular and molecular medicine 15 32652860
2020 De Novo and Inherited Variants in GBF1 are Associated with Axonal Neuropathy Caused by Golgi Fragmentation. American journal of human genetics 15 32937143
2019 Functional and Physical Interaction between the Arf Activator GBF1 and Hepatitis C Virus NS3 Protein. Journal of virology 14 30567983
2019 Quantitative Proteomics of Uukuniemi Virus-host Cell Interactions Reveals GBF1 as Proviral Host Factor for Phleboviruses. Molecular & cellular proteomics : MCP 14 31570497
2018 Inheritance of the Golgi Apparatus and Cytokinesis Are Controlled by Degradation of GBF1. Cell reports 14 29898406
2020 Role of the Guanine Nucleotide Exchange Factor GBF1 in the Replication of RNA Viruses. Viruses 13 32599855
2019 A Redundant Mechanism of Recruitment Underlies the Remarkable Plasticity of the Requirement of Poliovirus Replication for the Cellular ArfGEF GBF1. Journal of virology 13 31375590
2018 Highly conserved motifs within the large Sec7 ARF guanine nucleotide exchange factor GBF1 target it to the Golgi and are critical for GBF1 activity. American journal of physiology. Cell physiology 13 29443553
2003 Characterization of alternatively spliced and truncated forms of the Arf guanine nucleotide exchange factor GBF1 defines regions important for activity. Biochemical and biophysical research communications 13 12646181
2021 Src activates retrograde membrane traffic through phosphorylation of GBF1. eLife 11 34870592
2021 Rab1b-GBF1-ARF1 Secretory Pathway Axis Is Required for Birnavirus Replication. Journal of virology 11 34878889
2020 Regulating the regulators: role of phosphorylation in modulating the function of the GBF1/BIG family of Sec7 ARF-GEFs. FEBS letters 11 32333796
2020 Rab1b-GBF1-ARFs mediated intracellular trafficking is required for classical swine fever virus replication in swine umbilical vein endothelial cells. Veterinary microbiology 9 32605744
2012 HY1 genetically interacts with GBF1 and regulates the activity of the Z-box containing promoters in light signaling pathways in Arabidopsis thaliana. Mechanisms of development 9 22766018
2022 Viral protein engagement of GBF1 induces host cell vulnerability through synthetic lethality. The Journal of cell biology 8 36305789
2018 The Arf-GDP-regulated recruitment of GBF1 to Golgi membranes requires domains HDS1 and HDS2 and a Golgi-localized protein receptor. Journal of cell science 8 29507113
2024 Enterovirus 3A protein disrupts endoplasmic reticulum homeostasis through interaction with GBF1. Journal of virology 7 38904364
2022 ARF1 with Sec7 Domain-Dependent GBF1 Activates Coatomer Protein I To Support Classical Swine Fever Virus Entry. Journal of virology 6 35044210
2021 Loss of Arf Guanine Nucleotide Exchange Factor GBF1 Activity Disturbs Organelle Dynamics in Mouse Oocytes. Microscopy and microanalysis : the official journal of Microscopy Society of America, Microbeam Analysis Society, Microscopical Society of Canada 5 33478608
2019 Rab18 regulates lipolysis via Arf/GBF1 and adipose triglyceride lipase. Biochemical and biophysical research communications 4 31610914
2024 AMPK associates with and causes fragmentation of the Golgi by phosphorylating the guanine nucleotide exchange factor GBF1. Journal of cell science 3 39575556
2020 Viral protein engagement of GBF1 induces host cell vulnerability through synthetic lethality. bioRxiv : the preprint server for biology 3 33173868
2022 AG1478 Elicits a Novel Anti-Influenza Function via an EGFR-Independent, GBF1-Dependent Pathway. International journal of molecular sciences 2 35628375
2023 Site-specific phosphorylations of the Arf activator GBF1 differentially regulate GBF1 function in Golgi homeostasis and secretion versus cytokinesis. Scientific reports 1 37604968
2026 Broad-spectrum antiviral activity of antisense oligonucleotides targeting GBF1 against SARS-CoV-2 and influenza viruses. iScience 0 41743235
2026 Intracellular protein GBF1 displays significant associations with amyloid pathology in Alzheimer's disease. Alzheimer's & dementia : the journal of the Alzheimer's Association 0 41988936
2024 GBF1 deficiency causes cataracts in human and mouse. Human genetics 0 39110251
2024 A Novel GBF1 Variant in a Charcot-Marie-Tooth Type 2: Insights from Familial Analysis. Genes 0 39766823
2020 A miRNA screen procedure identifies garz as an essential factor in adult glia functions and validates Drosophila as a beneficial 3Rs model to study glial functions and GBF1 biology. F1000Research 0 32595956
2016 Correction: Phosphorylation Affects DNA-Binding of the Senescence-Regulating bZIP Transcription Factor GBF1. Plants 2015, 4, 691-709. Plants (Basel, Switzerland) 0 27598219
2005 Development of monoclonal antibodies against GBF1 and their use in studying its functions. Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research 0 16318580