Evidence map›Paper›PMID 7512501›Full record

ArticleThe EMBO journal1994

Release of GPI-anchored membrane proteins by a cell-associated GPI-specific phospholipase D.

C N Metz, G Brunner, N H Choi-Muira, H Nguyen, J Gabrilove, I W Caras, N Altszuler, D B Rifkin, E L Wilson, M A Davitz

Open access · bronzeAbstract read
In one paragraph

Article in The EMBO journal, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.7field-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

36 citing papers in PubMed, 142 citations in OpenAlex.

  1. Article
  2. Review
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  8. Review
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  10. Article
  11. Article
  12. Review
  13. Roles of CD48 in regulating immunity and tolerance.Clinical immunology (Orlando, Fla.) · 2016
    Review
  14. Article
  15. Effect of the GPI anchor of human Thy-1 on antibody recognition and function.Laboratory investigation; a journal of technical methods and pathology · 2013
    Article
  16. Cancer immunotherapy using a membrane-bound interleukin-12 with B7-1 transmembrane and cytoplasmic domains.Molecular therapy : the journal of the American Society of Gene Therapy · 2012
    Article
  17. Article
  18. Article
  19. Article
  20. Article
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

10 authors at 2 institutions in 1 country.

C N MetzDepartment of Pathology, New York University Medical Center, NY 10016.
G Brunner
N H Choi-Muira
H Nguyen
J Gabrilove
I W Caras
N Altszuler
D B Rifkin
E L Wilson
M A Davitz
Columbia University Irving Medical Center · USNew York University · US

Funding

Regulation of TGF-Beta Activity in the Lung by LTBP-4R01CA034282 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI RIFKIN, DANIEL B · 1985 to 2016
$5.8M
THE ROLE OF PLASMINOGEN ACTIVATORS IN MYELOPOIESISR01CA049419 · NCI · NEW YORK UNIVERSITY · PI WILSON, E LYNETTE · 1989 to 1991
–
NCI NIH HHS CA 34282NCI NIH HHS CA 49419
6 · The paper itself

Abstract

Although many glycosylphosphatidylinositol (GPI)-anchored proteins have been observed as soluble forms, the mechanisms by which they are released from the cell surface have not been demonstrated. We show here that a cell-associated GPI-specific phospholipase D (GPI-PLD) releases the GPI-anchored, complement regulatory protein decay-accelerating factor (DAF) from HeLa cells, as well as the basic fibroblast growth factor-binding heparan sulfate proteoglycan from bone marrow stromal cells. DAF found in the HeLa cell culture supernatants contained both [3H]ethanolamine and [3H]inositol, but not [3H]palmitic acid, whereas the soluble heparan sulfate proteoglycan present in bone marrow stromal cell culture supernatants contained [3H]ethanolamine. 125I-labeled GPI-DAF incorporated into the plasma membranes of these two cell types was released in a soluble form lacking the fatty acid GPI-anchor component. GPI-PLD activity was detected in lysates of both HeLa and bone marrow stromal cells. Treatment of HeLa cells with 1,10-phenanthroline, an inhibitor of GPI-PLD, reduced the release of [3H]ethanolamine-DAF by 70%. The hydrolysis of these GPI-anchored molecules is likely to be mediated by an endogenous GPI-PLD because [3H]ethanolamine DAF is constitutively released from HeLa cells maintained in serum-free medium. Furthermore, using PCR, a GPI-PLD mRNA has been identified in cDNA libraries prepared from both cell types. These studies are the first demonstration of the physiologically relevant release of GPI-anchored proteins from cells by a GPI-PLD.

Indexed as

Antigens, CDBone MarrowBone Marrow CellsCD55 AntigensDNA, ComplementaryEthanolamineEthanolaminesGene LibraryGlycosylphosphatidylinositolsHeLa CellsHeparan SulfateHeparan Sulfate ProteoglycansHumansInositolMembrane GlycoproteinsPhenanthrolines1,10-phenanthrolineAntigens, CDCD55 AntigensDNA, ComplementaryEthanolamineEthanolaminesglycoprotein phospholipase DGlycosylphosphatidylinositolsHeparan SulfateHeparan Sulfate ProteoglycansInositolMembrane GlycoproteinsPhenanthrolinesPhospholipase DProteoglycansRNA, Messenger

Identifiers

PMID7512501
PMCPMC395007
OpenAlexW46783220

What OpenQuestion holds

Textmetadata
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.