Evidence map›Paper›PMID 25122462›Full record

ArticleeLife2014

Epsin deficiency impairs endocytosis by stalling the actin-dependent invagination of endocytic clathrin-coated pits.

Mirko Messa, Rubén Fernández-Busnadiego, Elizabeth Wen Sun, Hong Chen, Heather Czapla, Kristie Wrasman, Yumei Wu, Genevieve Ko, Theodora Ross, Beverly Wendland and 1 more

Open access · goldAbstract read
In one paragraph

Article in eLife, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

69 citing papers in PubMed, 135 citations in OpenAlex.

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  11. Generation of nanoscopic membrane curvature for membrane trafficking.Nature reviews. Molecular cell biology · 2023
    Review
  12. Article
  13. Review
  14. Article
  15. Load adaptation by endocytic actin networks.Molecular biology of the cell · 2022
    Article
  16. Article
  17. Article
  18. Article
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  20. Article

9 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

11 authors at 4 institutions in 1 country.

Mirko MessaProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States.
Rubén Fernández-BusnadiegoProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States.
Elizabeth Wen SunProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States.
Hong ChenProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States.
Heather CzaplaProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States.
Kristie WrasmanDepartment of Biology, Johns Hopkins University, Baltimore, United States.
Yumei WuProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States.
Genevieve KoProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States.
Theodora RossDepartment of Internal Medicine, UT Southwestern Medical Center, Dallas, United States.
Beverly WendlandDepartment of Biology, Johns Hopkins University, Baltimore, United States.
Pietro De CamilliProgram in Cellular Neuroscience, Neurodegeneration and Repair, Department of Cell Biology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, United States pietro.decamilli@yale.edu.
Howard Hughes Medical Institute · USYale University · USJohns Hopkins University · USSouthwestern Medical Center

Funding

Yale Diabetes Research CenterP30DK045735 · NIDDK · YALE UNIVERSITY · PI Richard A Flavell · 1993 to 2026
$44.0M
Yale/NIDA Neuroproteomics Research CenterP30DA018343 · NIDA · YALE UNIVERSITY · PI Marina R Picciotto · 2004 to 2026
$37.1M
Yale University Clinical and Translational Science Award ProgramUL1TR000142 · NCATS · YALE UNIVERSITY · PI SHERWIN, ROBERT S · 2012 to 2015
$31.8M
Skill Development for Diverse Scientific Careers: A New Course Predoctoral Program in Cellular and Molecular BiologyT32GM007223 · NIGMS · YALE UNIVERSITY · PI BASERGA, SUSAN J · 1985 to 2019
$31.0M
CELLULAR AND MOLECULAR BIOLOGYT32GM007231 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI VAN DOREN, MARK B · 1985 to 2020
$18.4M
Epsin in Angiogenesis and Vascular RemodelingR01HL093242 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CHEN, HONG, WANG, DA-ZHI · 2009 to 2021
$7.3M
MOLECULAR ANALYSIS OF ENDOCYTOSIS PROTEINS IN YEASTR01GM060979 · NIGMS · JOHNS HOPKINS UNIVERSITY · PI WENDLAND, BEVERLY R · 2000 to 2013
$4.3M
Molecular Mechanisms in Synaptic Vesicle RecyclingR37NS036251 · NINDS · YALE UNIVERSITY · PI DE CAMILLI, PIETRO · 2010 to 2016
$2.7M
Huntington Interacting Protein-1(HIP1) and the Promotion of NeoplasiaR01CA098730 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI ROSS, THEODORA S · 2003 to 2012
$2.6M
OCRL and the pathogenesis of Lowe Syndrome and Dent DiseaseR01DK082700 · NIDDK · YALE UNIVERSITY · PI DE CAMILLI, PIETRO · 2009 to 2016
$2.4M
The Role of Signaling Adaptor Protein Epsin in AtherosclerosisR01HL118676 · NHLBI · OKLAHOMA MEDICAL RESEARCH FOUNDATION · PI CHEN, HONG · 2014 to 2017
$1.8M
NCATS NIH HHS UL1 TR000142NCI NIH HHS R01 CA098730NCI NIH HHS R01CA098730NHLBI NIH HHS R01 HL093242NHLBI NIH HHS R01 HL118676NIDA NIH HHS DA018343NIDA NIH HHS P30 DA018343NIDDK NIH HHS DK082700NIDDK NIH HHS DK45735NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK082700NIGMS NIH HHS 5T32GM007223-38/39NIGMS NIH HHS R01 GM060979NIGMS NIH HHS R01GM60979NIGMS NIH HHS T32 GM007223NIGMS NIH HHS T32 GM007231NINDS NIH HHS R37 NS036251NINDS NIH HHS R37NS036251PHS HHS NIGMST32007231
6 · The paper itself

Abstract

Epsin is an evolutionarily conserved endocytic clathrin adaptor whose most critical function(s) in clathrin coat dynamics remain(s) elusive. To elucidate such function(s), we generated embryonic fibroblasts from conditional epsin triple KO mice. Triple KO cells displayed a dramatic cell division defect. Additionally, a robust impairment in clathrin-mediated endocytosis was observed, with an accumulation of early and U-shaped pits. This defect correlated with a perturbation of the coupling between the clathrin coat and the actin cytoskeleton, which we confirmed in a cell-free assay of endocytosis. Our results indicate that a key evolutionary conserved function of epsin, in addition to other roles that include, as we show here, a low affinity interaction with SNAREs, is to help generate the force that leads to invagination and then fission of clathrin-coated pits.

Indexed as

Actin CytoskeletonActinsAdaptor Proteins, Vesicular TransportAnimalsClathrinCoated Pits, Cell-MembraneEmbryo, MammalianEndocytosisFibroblastsGene ExpressionMiceMice, KnockoutPrimary Cell CultureProtein BindingSignal TransductionSNARE ProteinsActinsAdaptor Proteins, Vesicular TransportClathrinepsinSNARE Proteinsactinclathrin-mediated endocytosiscytokinesisepsinHip1RSNARE

Identifiers

PMID25122462
PMCPMC4161027
OpenAlexW2070297191

What OpenQuestion holds

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Registered trials

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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.