Evidence map›Paper›PMID 26755743›Full record

ArticleEMBO reports2016

NgBR is essential for endothelial cell glycosylation and vascular development.

Eon Joo Park, Kariona A Grabińska, Ziqiang Guan, William C Sessa

Open access · greenAbstract read
In one paragraph

Article in EMBO reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.0field-weighted citation impact, top 9% 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

28 citing papers in PubMed, 42 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Review
  5. Identifying and quantifying membrane interactions of the protein human cis-prenyltransferase.Protein science : a publication of the Protein Society · 2025
    Article
  6. Review
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  10. Review
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  13. Lysosomal cholesterol accumulation contributes to the movement phenotypes associated with NUS1 haploinsufficiency.Genetics in medicine : official journal of the American College of Medical Genetics · 2021
    Article
  14. Article
  15. Research advances on neurite outgrowth inhibitor B receptor.Journal of cellular and molecular medicine · 2020
    Review
  16. 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

4 authors at 2 institutions in 1 country.

Eon Joo ParkDepartment of Pharmacology and Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA.
Kariona A GrabińskaDepartment of Pharmacology and Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA.
Ziqiang GuanDepartment of Biochemistry, Duke University Medical Center, Durham, NC, USA.
William C SessaDepartment of Pharmacology and Vascular Biology and Therapeutics Program, Yale University School of Medicine, New Haven, CT, USA william.sessa@yale.edu.
Yale University · USDuke University Hospital · US

Funding

PHOSPHORYLATION AND ENDOTHELIAL NITRIC OXIDE PRODUCTIONR01HL064793 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2000 to 2016
$6.3M
Regulation of vascular remodeling &angiogenesis by NogoR01HL081190 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2005 to 2014
$4.1M
Endothelial NOS by Protein-Protein IntractionsR01HL061371 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 1999 to 2008
$3.6M
NgBR as a regulator of endothelial functionR01HL133018 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2016 to 2017
$995k
NHLBI NIH HHS R01 HL061371NHLBI NIH HHS R01 HL064793NHLBI NIH HHS R01 HL081190NHLBI NIH HHS R01 HL133018NHLBI NIH HHS R01 HL61371NHLBI NIH HHS R01 HL64793
6 · The paper itself

Abstract

NgBR is a transmembrane protein identified as a Nogo-B-interacting protein and recently has been shown to be a subunit required for cis-prenyltransferase (cisPTase) activity. To investigate the integrated role of NgBR in vascular development, we have characterized endothelial-specific NgBR knockout embryos. Here, we show that endothelial-specific NgBR knockout results in embryonic lethality due to vascular development defects in yolk sac and embryo proper. Loss of NgBR in endothelial cells reduces proliferation and promotes apoptosis of the cells largely through defects in the glycosylation of key endothelial proteins including VEGFR2, VE-cadherin, and CD31, and defective glycosylation can be rescued by treatment with the end product of cisPTase activity, dolichol phosphate. Moreover, NgBR functions in endothelial cells during embryogenesis are Nogo-B independent. These data uniquely show the importance of NgBR and protein glycosylation during vascular development.

Indexed as

Protein Processing, Post-TranslationalAnimalsApoptosisCadherinsCell ProliferationCells, CulturedEndothelium, VascularGlycosylationMicePlatelet Endothelial Cell Adhesion Molecule-1Receptors, Cell SurfaceVascular Endothelial Growth Factor Receptor-2CadherinsNogo-B receptor, mousePlatelet Endothelial Cell Adhesion Molecule-1Receptors, Cell SurfaceVascular Endothelial Growth Factor Receptor-2cis‐prenyltransferasedolicholglycosylationNgBRvascular development

Identifiers

PMID26755743
PMCPMC5290814
OpenAlexW2239434434

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.