Evidence map›Paper›PMID 32893190›Full record

ArticleThe Journal of biological chemistry2020

A proton-coupled folate transporter mutation causing hereditary folate malabsorption locks the protein in an inward-open conformation.

He-Qin Zhan, Mitra Najmi, Kai Lin, Srinivas Aluri, Andras Fiser, I David Goldman, Rongbao Zhao

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Biology and therapeutic applications of the proton-coupled folate transporter.Expert opinion on drug metabolism & toxicology · 2022
    Article
  3. The evolving biology of the proton-coupled folate transporter: New insights into regulation, structure, and mechanism.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Review
  4. Metabolic Therapy of Heart Failure: Is There a Future for B Vitamins?International journal of molecular sciences · 2021
    Review
  5. 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

7 authors at 3 institutions in 2 countries.

He-Qin ZhanDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA; Department of Pathology, School of Basic Medical Sciences, Anhui Medical University, Hefei, China.
Mitra NajmiDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA.
Kai LinDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA; Air Force Medical Center, People's Liberation Army, Beijing, China.
Srinivas AluriDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA.
Andras FiserDepartment of Systems and Computational Biology, Albert Einstein College of Medicine, Bronx, New York, USA; Department of Biochemistry, Albert Einstein College of Medicine, Bronx, New York, USA.
I David GoldmanDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, USA. Electronic address: i.david.goldman@einsteinmed.org.
Rongbao ZhaoDepartment of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, New York, USA; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York, USA.
Albert Einstein College of Medicine · USAir Force General Hospital PLA · CNAnhui Medical University · CN

Funding

Proton-coupled folate/antifolate transportR01CA082621 · NCI · YESHIVA UNIVERSITY · PI GOLDMAN, ISRAEL DAVID · 1999 to 2017
$9.0M
NCI NIH HHS R01 CA082621
6 · The paper itself

Abstract

The proton-coupled folate transporter (PCFT, SLC46A1) is required for folate intestinal absorption and transport across the choroid plexus. Recent work has identified a F392V mutation causing hereditary folate malabsorption. However, the residue properties responsible for this loss of function remains unknown. Using site-directed mutagenesis, we observed complete loss of function with charged (Lys, Asp, and Glu) and polar (Thr, Ser, and Gln) Phe-392 substitutions and minimal function with some neutral substitutions; however, F392M retained full function. Using the substituted-cysteine accessibility method (with

Indexed as

Amino Acid SequenceAnimalsBiological TransportCysteineFolic Acid DeficiencyHeLa CellsHumansKineticsMalabsorption SyndromesMethotrexateMutagenesis, Site-DirectedProtein Structure, TertiaryProton-Coupled Folate TransporterCysteineMethotrexateProton-Coupled Folate TransporterSLC46A1 protein, humanfacilitative transportersfolatehereditary folate malabsorption (HFM)homology modelingmethotrexatemutantmutually compensatory mutationsPCFTproton-coupled folate transporterproton transportreduced folate carrierSLC46A1suppressor mutationstransporter

Identifiers

PMID32893190
PMCPMC7667981
OpenAlexW3083579035

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.