Evidence map›Paper›PMID 9722606›Full record

ArticleThe Journal of cell biology1998

An endocytosed TGN38 chimeric protein is delivered to the TGN after trafficking through the endocytic recycling compartment in CHO cells.

R N Ghosh, W G Mallet, T T Soe, T E McGraw, F R Maxfield

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of cell biology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
6.9field-weighted citation impact, top 2% 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

91 citing papers in PubMed, 242 citations in OpenAlex.

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  10. SNX-1 and RME-8 oppose the assembly of HGRS-1/ESCRT-0 degradative microdomains on endosomes.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
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  12. A TOCA/CDC-42/PAR/WAVE functional module required for retrograde endocytic recycling.Proceedings of the National Academy of Sciences of the United States of America · 2015
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  13. Article
  14. Golgi and plasma membrane pools of PI(4)P contribute to plasma membrane PI(4,5)P2 and maintenance of KCNQ2/3 ion channel current.Proceedings of the National Academy of Sciences of the United States of America · 2014
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31 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

5 authors at 1 institution in 1 country.

R N GhoshDepartment of Biochemistry, Cornell University Medical College, New York, New York 10021, USA.
W G Mallet
T T Soe
T E McGraw
F R Maxfield
Cornell University · US

Funding

RECEPTOR-MEDIATED ENDOCYTOSIS: MECHANISM AND FUNCTIONR37DK027083 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI MAXFIELD, FREDERICK R. · 1993 to 2014
$6.5M
RECEPTOR-MEDIATED ENDOCYTOSIS: MECHANISM AND FUNCTIONR01DK027083 · NIDDK · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI MAXFIELD, FREDERICK R. · 1986 to 2004
$2.0M
NIDDK NIH HHS DK27083NIDDK NIH HHS R01 DK027083NIDDK NIH HHS R37 DK027083
6 · The paper itself

Abstract

To examine TGN38 trafficking from the cell surface to the TGN, CHO cells were stably transfected with a chimeric transmembrane protein, TacTGN38. We used fluorescent and 125I-labeled anti-Tac IgG and Fab fragments to follow TacTGN38's postendocytic trafficking. At steady-state, anti-Tac was mainly in the TGN, but shortly after endocytosis it was predominantly in early endosomes. 11% of cellular TacTGN38 is on the plasma membrane. Kinetic analysis of trafficking of antibodies bound to TacTGN38 showed that after short endocytic pulses, 80% of internalized anti-Tac returned to the cell surface (t1/2 = 9 min), and the remainder trafficked to the TGN. When longer filling pulses and chases were used to load anti-Tac into the TGN, it returned to the cell surface with a t1/2 of 46 min. Quantitative confocal microscopy analysis also showed that fluorescent anti-Tac fills the TGN with a 46-min t1/2. Using the measured rate constants in a simple kinetic model, we predict that 82% of TacTGN38 is in the TGN, and 7% is in endosomes. TacTGN38 leaves the TGN slowly, which accounts for its steady-state distribution despite the inefficient targeting from the cell surface to the TGN.

Indexed as

GlycoproteinsAnimalsAntibodies, MonoclonalCHO CellsCricetinaeEndocytosisEndosomesGolgi ApparatusKineticsMembrane GlycoproteinsMembrane ProteinsMicroscopy, FluorescenceReceptors, Interleukin-2Recombinant Fusion ProteinsTransfectionTransferrinAntibodies, MonoclonalGlycoproteinsMembrane GlycoproteinsMembrane ProteinsReceptors, Interleukin-2Recombinant Fusion ProteinsTransferrin

Identifiers

PMID9722606
PMCPMC2132871
OpenAlexW2143487345

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.