Evidence map›Paper›PMID 25869668›Full record

ArticleThe Journal of cell biology2015

Sac2/INPP5F is an inositol 4-phosphatase that functions in the endocytic pathway.

Fubito Nakatsu, Mirko Messa, Ramiro Nández, Heather Czapla, Yixiao Zou, Stephen M Strittmatter, Pietro De Camilli

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing 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

46 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Review
  3. Roles in physiology and disease of the inositol phosphatase synaptojanin 1.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2026
    Review
  4. Article
  5. Regulation of yeast polarized exocytosis by phosphoinositide lipids.Cellular and molecular life sciences : CMLS · 2024
    Review
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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

7 authors at 3 institutions in 2 countries.

Fubito NakatsuDepartment of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510.
Mirko MessaDepartment of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510.
Ramiro NándezDepartment of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510.
Heather CzaplaDepartment of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510.
Yixiao ZouDepartment of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510.
Stephen M StrittmatterDepartment of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510.
Pietro De CamilliDepartment of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 Department of Cell Biology, Howard Hughes Medical Institute, Department of Neurology, and Program in Cellular Neuroscience, Neurodegeneration and Repair, Yale University School of Medicine, New Haven, CT 06510 pietro.decamilli@yale.edu.
Howard Hughes Medical Institute · USInstitute of Cell Biology · UAYale University · US

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
Molecular Mechanisms in Synaptic Vesicle RecyclingR37NS036251 · NINDS · YALE UNIVERSITY · PI DE CAMILLI, PIETRO · 2010 to 2016
$2.7M
OCRL and the pathogenesis of Lowe Syndrome and Dent DiseaseR01DK082700 · NIDDK · YALE UNIVERSITY · PI DE CAMILLI, PIETRO · 2009 to 2016
$2.4M
Howard Hughes Medical InstituteNCATS NIH HHS UL1 TR000142NIDA NIH HHS DA018343NIDA NIH HHS P30 DA018343NIDDK NIH HHS DK082700NIDDK NIH HHS DK45735NIDDK NIH HHS P30 DK045735NIDDK NIH HHS R01 DK082700NINDS NIH HHS R37 NS036251NINDS NIH HHS R37NS036251
6 · The paper itself

Abstract

The recruitment of inositol phosphatases to endocytic membranes mediates dephosphorylation of PI(4,5)P2, a phosphoinositide concentrated in the plasma membrane, and prevents its accumulation on endosomes. The importance of the conversion of PI(4,5)P2 to PtdIns during endocytosis is demonstrated by the presence of both a 5-phosphatase and a 4-phosphatase (Sac domain) module in the synaptojanins, endocytic PI(4,5)P2 phosphatases conserved from yeast to humans and the only PI(4,5)P2 phosphatases in yeast. OCRL, another 5-phosphatase that couples endocytosis to PI(4,5)P2 dephosphorylation, lacks a Sac domain. Here we show that Sac2/INPP5F is a PI4P phosphatase that colocalizes with OCRL on endocytic membranes, including vesicles formed by clathrin-mediated endocytosis, macropinosomes, and Rab5 endosomes. An OCRL-Sac2/INPP5F interaction could be demonstrated by coimmunoprecipitation and was potentiated by Rab5, whose activity is required to recruit Sac2/INPP5F to endosomes. Sac2/INPP5F and OCRL may cooperate in the sequential dephosphorylation of PI(4,5)P2 at the 5 and 4 position of inositol in a partnership that mimics that of the two phosphatase modules of synaptojanin.

Indexed as

EndocytosisAnimalsChlorocebus aethiopsCOS CellsEndosomesHEK293 CellsHumansInositol Polyphosphate 5-PhosphatasesMice, KnockoutPhosphoric Monoester HydrolasesProtein Transportrab5 GTP-Binding ProteinsInositol Polyphosphate 5-PhosphatasesINPP5F protein, humanOcrl protein, mousePhosphoric Monoester Hydrolasesrab5 GTP-Binding Proteins

Identifiers

PMID25869668
PMCPMC4395491
OpenAlexW2001773683

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.