Evidence map›Paper›PMID 24338480›Full record

ArticleThe Journal of biological chemistry2014

The endoplasmic reticulum coat protein II transport machinery coordinates cellular lipid secretion and cholesterol biosynthesis.

Lee G D Fryer, Bethan Jones, Emma J Duncan, Claire E Hutchison, Tozen Ozkan, Paul A Williams, Olivia Alder, Max Nieuwdorp, Anna K Townley, Arjen R Mensenkamp and 3 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.6field-weighted citation impact, top 19% 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

25 citing papers in PubMed, 47 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Sar1 Affects the Localization of Perilipin 2 to Lipid Droplets.International journal of molecular sciences · 2022
    Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. COPII-mediated trafficking at the ER/ERGIC interface.Traffic (Copenhagen, Denmark) · 2019
    Review
  18. Article
  19. Review
  20. Review
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

13 authors at 7 institutions in 2 countries.

Lee G D FryerFrom the Endocrinology Centre, William Harvey Research Institute, Queen Mary University of London and Barts and The London School of Medicine and Dentistry, Charterhouse Square, London EC1M 6BQ, United Kingdom.
Bethan Jones
Emma J Duncan
Claire E Hutchison
Tozen Ozkan
Paul A Williams
Olivia Alder
Max Nieuwdorp
Anna K Townley
Arjen R Mensenkamp
David J Stephens
Geesje M Dallinga-Thie
Carol C Shoulders
Medical Research Council · GBAcademic Medical Center · NLImperial College London · GBUniversity of Bristol · GBWilliam Harvey Research Institute · GBGeneral Medical Council · GBQueen Mary University of London · GB

Funding

British Heart Foundation FS/12/25/29569British Heart Foundation PG/04/010/16596Medical Research Council G117/554Medical Research Council MC_U120074258
6 · The paper itself

Abstract

Triglycerides and cholesterol are essential for life in most organisms. Triglycerides serve as the principal energy storage depot and, where vascular systems exist, as a means of energy transport. Cholesterol is essential for the functional integrity of all cellular membrane systems. The endoplasmic reticulum is the site of secretory lipoprotein production and de novo cholesterol synthesis, yet little is known about how these activities are coordinated with each other or with the activity of the COPII machinery, which transports endoplasmic reticulum cargo to the Golgi. The Sar1B component of this machinery is mutated in chylomicron retention disorder, indicating that this Sar1 isoform secures delivery of dietary lipids into the circulation. However, it is not known why some patients with chylomicron retention disorder develop hepatic steatosis, despite impaired intestinal fat malabsorption, and why very severe hypocholesterolemia develops in this condition. Here, we show that Sar1B also promotes hepatic apolipoprotein (apo) B lipoprotein secretion and that this promoting activity is coordinated with the processes regulating apoB expression and the transfer of triglycerides/cholesterol moieties onto this large lipid transport protein. We also show that although Sar1A antagonizes the lipoprotein secretion-promoting activity of Sar1B, both isoforms modulate the expression of genes encoding cholesterol biosynthetic enzymes and the synthesis of cholesterol de novo. These results not only establish that Sar1B promotes the secretion of hepatic lipids but also adds regulation of cholesterol synthesis to Sar1B's repertoire of transport functions.

Indexed as

Lipid MetabolismApolipoproteins BCell LineCholesterolCOP-Coated VesiclesEndoplasmic ReticulumGolgi ApparatusHumansHypobetalipoproteinemiasLipidsLiverMalabsorption SyndromesMonomeric GTP-Binding ProteinsVesicular Transport ProteinsApolipoproteins BCholesterolLipidsMonomeric GTP-Binding ProteinsSAR1A protein, humanSAR1B protein, humanVesicular Transport ProteinsApolipoproteinsCholesterol RegulationEndoplasmic Reticulum (ER)Lipoprotein SecretionTranscriptomics

Identifiers

PMID24338480
PMCPMC3924288
OpenAlexW1975526639

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.