Evidence map›Paper›PMID 24745989›Full record

ReviewCurrent topics in membranes2014

The SLC37 family of sugar-phosphate/phosphate exchangers.

Janice Y Chou, Brian C Mansfield

Open access · greenAbstract readReview
In one paragraph

Review in Current topics in membranes, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
37.0field-weighted citation impact, top 1% 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

41 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Stage-Specific H3K14 and H3K23 Succinylation Orchestrates Insect Metamorphosis and Oogenesis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  3. Exploring extended [European journal of nuclear medicine and molecular imaging · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Structural basis of glucose-6-phosphate transport by human SLC37A2.Nature structural & molecular biology · 2026
    Article
  9. Structural basis of G6P/Pi transport and inhibition in SLC37A4.Nature structural & molecular biology · 2026
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Unravelling the synergistic interaction ofFrontiers in microbiology · 2024
    Article
  17. Article
  18. Review
  19. Article
  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

2 authors at 2 institutions in 1 country.

Janice Y ChouSection on Cellular Differentiation, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA. Electronic address: chouja@mail.nih.gov.
Brian C MansfieldSection on Cellular Differentiation, Program on Developmental Endocrinology and Genetics, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, USA; Foundation Fighting Blindness, Columbia, Maryland, USA.
Foundation Fighting Blindness · USNational Institutes of Health · US

Funding

Molecular Genetics Of Heritable Human DisordersZIAHD000912 · NICHD · EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT · PI CHOU, JANICE · 2009 to 2025
$25.1M
Intramural NIH HHS ZIA HD000912
6 · The paper itself

Abstract

The SLC37 family members are endoplasmic reticulum (ER)-associated sugar-phosphate/phosphate (P(i)) exchangers. Three of the four members, SLC37A1, SLC37A2, and SLC37A4, function as Pi-linked glucose-6-phosphate (G6P) antiporters catalyzing G6P:P(i) and P(i):P(i) exchanges. The activity of SLC37A3 is unknown. SLC37A4, better known as the G6P transporter (G6PT), has been extensively characterized, functionally and structurally, and is the best characterized family member. G6PT contains 10 transmembrane helices with both N and C termini facing the cytoplasm. The primary in vivo function of the G6PT protein is to translocate G6P from the cytoplasm into the ER lumen where it couples with either the liver/kidney/intestine-restricted glucose-6-phosphatase-α (G6Pase-α or G6PC) or the ubiquitously expressed G6Pase-β (or G6PC3) to hydrolyze G6P to glucose and P(i). The G6PT/G6Pase-α complex maintains interprandial glucose homeostasis, and the G6PT/G6Pase-β complex maintains neutrophil energy homeostasis and functionality. G6PT is highly selective for G6P and is competitively inhibited by cholorogenic acid and its derivatives. Neither SLC37A1 nor SLC37A2 can couple functionally with G6Pase-α or G6Pase-β, and the antiporter activities of SLC37A1 or SLC37A2 are not inhibited by cholorogenic acid. Deficiencies in G6PT cause glycogen storage disease type Ib (GSD-Ib), a metabolic and immune disorder. To date, 91 separate SLC37A4 mutations, including 39 missense mutations, have been identified in GSD-Ib patients. Characterization of missense mutations has yielded valuable information on functionally important residues in the G6PT protein. The biological roles of the other SLC37 proteins remain to be determined and deficiencies have not yet been correlated to diseases.

Indexed as

Carbohydrate MetabolismAmino Acid SequenceAnimalsCell MembraneHumansMembrane Transport ProteinsMolecular Sequence DataPhosphatesStructure-Activity RelationshipMembrane Transport ProteinsPhosphatesChlorogenic acidEndoplasmic reticulumGlucose-6-phosphate transporterGlycogen storage disease type IbP(i)-linked G6P antiporters

Identifiers

PMID24745989
PMCPMC4180117
OpenAlexW178109460

What OpenQuestion holds

Textmetadata
LicenceTDM
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.