Evidence map›Paper›PMID 10402461›Full record

ArticleThe Journal of cell biology1999

GBF1: A novel Golgi-associated BFA-resistant guanine nucleotide exchange factor that displays specificity for ADP-ribosylation factor 5.

A Claude, B P Zhao, C E Kuziemsky, S Dahan, S J Berger, J P Yan, A D Armold, E M Sullivan, P Melançon

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
3.8field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

104 citing papers in PubMed, 211 citations in OpenAlex.

  1. Review
  2. Article
  3. Intracellular protein GBF1 displays significant associations with amyloid pathology in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  4. Article
  5. ARF GTPases Function at the Golgi.Sub-cellular biochemistry · 2026
    Review
  6. ARF GTPases Function at the Golgi.Sub-cellular biochemistry · 2026
    Review
  7. Arfs on the Golgi: four conductors, one orchestra.Frontiers in molecular biosciences · 2025
    Review
  8. Article
  9. Article
  10. Article
  11. Sec7 regulatory domains scaffold autoinhibited and active conformations.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  12. Article
  13. COPIng with senescence.Nature cell biology · 2023
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Regulation of Survival Motor Neuron Gene Expression by Calcium Signaling.International journal of molecular sciences · 2021
    Article

44 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 2 countries.

A ClaudeDepartment of Cell Biology, University of Alberta, Edmonton, Alberta, Canada, T6G 2H7.
B P Zhao
C E Kuziemsky
S Dahan
S J Berger
J P Yan
A D Armold
E M Sullivan
P Melançon
University of Alberta · CAUniversity of Colorado Boulder · USMcGill University · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Expression cloning from a cDNA library prepared from a mutant CHO cell line with Golgi-specific resistance to Brefeldin A (BFA) identified a novel 206-kD protein with a Sec7 domain termed GBF1 for Golgi BFA resistance factor 1. Overexpression of GBF1 allowed transfected cells to maintain normal Golgi morphology and grow in the presence of BFA. Golgi- enriched membrane fractions from such transfected cells displayed normal levels of ADP ribosylation factors (ARFs) activation and coat protein recruitment that were, however, BFA resistant. Hexahistidine-tagged-GBF1 exhibited BFA-resistant guanine nucleotide exchange activity that appears specific towards ARF5 at physiological Mg2+concentration. Characterization of cDNAs recovered from the mutant and wild-type parental lines established that transcripts in these cells had identical sequence and, therefore, that GBF1 was naturally BFA resistant. GBF1 was primarily cytosolic but a significant pool colocalized to a perinuclear structure with the beta-subunit of COPI. Immunogold labeling showed highest density of GBF1 over Golgi cisternae and significant labeling over pleiomorphic smooth vesiculotubular structures. The BFA-resistant nature of GBF1 suggests involvement in retrograde traffic.

Indexed as

ADP-Ribosylation FactorsAmino Acid SequenceAnimalsBiological TransportBrefeldin ACell DivisionCHO CellsCloning, MolecularCoatomer ProteinCricetinaeCytosolDrug ResistanceFungal ProteinsGene ExpressionGolgi ApparatusGTP-Binding ProteinsADP-Ribosylation FactorsArf5 protein, ratBrefeldin ACoatomer ProteinFungal ProteinsGBF1 protein, humanGTP-Binding ProteinsGuanine Nucleotide Exchange FactorsMagnesiumMembrane ProteinsProteinsSec7 guanine nucleotide exchange factors

Identifiers

PMID10402461
PMCPMC2199737
OpenAlexW2058210463

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

None linked

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.