Evidence map›Paper›PMID 10508850›Full record

ArticleThe Journal of cell biology1999

ADP-ribosylation factor 6 and endocytosis at the apical surface of Madin-Darby canine kidney cells.

Y Altschuler, S Liu, L Katz, K Tang, S Hardy, F Brodsky, G Apodaca, K Mostov

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 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 147 citations in OpenAlex.

  1. Iron triggersmBio · 2025
    Article
  2. Roles for ELMOD2 and Rootletin in ciliogenesis.Molecular biology of the cell · 2021
    Article
  3. Novel function for AP-1B during cell migration.Molecular biology of the cell · 2020
    Article
  4. Article
  5. Review
  6. ELMOD1 Stimulates ARF6-GTP Hydrolysis to Stabilize Apical Structures in Developing Vestibular Hair Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  7. Article
  8. Article
  9. Article
  10. Arf6 exchange factor EFA6 and endophilin directly interact at the plasma membrane to control clathrin-mediated endocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2014
    Article
  11. Review
  12. Arf6 regulation of Gyrating-clathrin.Traffic (Copenhagen, Denmark) · 2013
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
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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

8 authors at 2 institutions in 1 country.

Y AltschulerDepartment of Anatomy, University of California, San Francisco, California 94143-0452, USA. yoram@itsa.ucsf.edu
S Liu
L Katz
K Tang
S Hardy
F Brodsky
G Apodaca
K Mostov
University of California, San Francisco · USUniversity of Pittsburgh · US

Funding

THE MOLECULAR MECHANISM OF CLATHRIN ASSEMBLYR01GM038093 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BRODSKY, FRANCES M. · 1988 to 2014
$5.0M
REGULATION OF ENDOCYTIC TRAFFIC IN KIDNEY CELLSR01DK051970 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI APODACA, GERARD L · 1997 to 2005
$1.4M
NIDDK NIH HHS DK51970-01NIDDK NIH HHS R01 DK051970NIGMS NIH HHS GM38093NIGMS NIH HHS R01 GM038093
6 · The paper itself

Abstract

We report that the small GTPase, ADP-ribosylation factor 6 (ARF6), is present only on the apical surface of polarized MDCK epithelial cells. Overexpression of a mutant of ARF6, ARF6-Q67L, which is predicted to be in the GTP-bound form, stimulates endocytosis exclusively at this surface. Surprisingly, overexpression of the mutant ARF6-T27N, which is predicted to be in the GDP-bound form, also stimulated apical endocytosis, though to a lesser extent. ARF6-stimulated endocytosis is inhibited by a dominant-negative form of dynamin, or a dominant-negative hub fragment of clathrin heavy chain, indicating that it is mediated by clathrin. Correspondingly, overexpression of either mutant of ARF6 leads to an increase in the number of clathrin-coated pits at the apical plasma membrane. When ARF6-Q67L is overexpressed in the presence of the dominant-negative dynamin, the ARF6-Q67L colocalizes with clathrin and with IgA bound to its receptor. We conclude that ARF6 is an important modulator of clathrin-mediated endocytosis at the apical surface of epithelial cells.

Indexed as

Cell PolarityEndocytosisADP-Ribosylation Factor 6ADP-Ribosylation FactorsAnimalsCell LineClathrinClathrin Heavy ChainsCoated Pits, Cell-MembraneDogsDynaminsEpithelial CellsGenes, DominantGTP PhosphohydrolasesGuanosine DiphosphateGuanosine TriphosphateADP-Ribosylation Factor 6ADP-Ribosylation FactorsClathrinClathrin Heavy ChainsDynaminsGTP PhosphohydrolasesGuanosine DiphosphateGuanosine TriphosphateImmunoglobulin APeptide FragmentsRecombinant Proteins

Identifiers

PMID10508850
PMCPMC2164974
OpenAlexW2163751558

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.