Evidence map›Paper›PMID 24019517›Full record

ArticleThe Journal of biological chemistry2013

Identification of cysteine residues in human cationic amino acid transporter hCAT-2A that are targets for inhibition by N-ethylmaleimide.

Sarah R Beyer, Robert T Mallmann, Isabel Jaenecke, Alice Habermeier, Jean-Paul Boissel, Ellen I Closs

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.7field-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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Amino Acid Metabolism in Lupus.Frontiers in immunology · 2021
    Review
  6. Review
  7. Article
  8. Review
  9. European journal of nuclear medicine and molecular imaging · 2017
    Article
  10. 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

6 authors at 2 institutions in 1 country.

Sarah R BeyerFrom the Department of Pharmacology, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany.
Robert T MallmannFrom the Department of Pharmacology, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany.
Isabel JaeneckeFrom the Department of Pharmacology, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany.
Alice HabermeierFrom the Department of Pharmacology, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany.
Jean-Paul BoisselFrom the Department of Pharmacology, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany.
Ellen I ClossFrom the Department of Pharmacology, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany. Electronic address: closs@uni-mainz.de.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In most cells, cationic amino acids such as l-arginine, l-lysine, and l-ornithine are transported by cationic (CAT) and y(+)L (y(+)LAT) amino acid transporters. In human erythrocytes, the cysteine-modifying agent N-ethylmaleimide (NEM) has been shown to inhibit system y(+) (most likely CAT-1), but not system y(+)L (Devés, R., Angelo, S., and Chávez, P. (1993) J. Physiol. 468, 753-766). We thus wondered if sensitivity to NEM distinguishes generally all CAT and y(+)LAT isoforms. Transport assays in Xenopus laevis oocytes established that indeed all human CATs (including the low affinity hCAT-2A), but neither y(+)LAT isoform, are inhibited by NEM. hCAT-2A inhibition was not due to reduced transporter expression in the plasma membrane, indicating that NEM reduces the intrinsic transporter activity. Individual mutation of each of the seven cysteine residues conserved in all CAT isoforms did not lead to NEM insensitivity of hCAT-2A. However, a cysteine-less mutant was no longer inhibited by NEM, suggesting that inhibition occurs through modification of more than one cysteine in hCAT-2A. Indeed, also the double mutant C33A/C273A was insensitive to NEM inhibition, whereas reintroduction of a cysteine at either position 33 or 273 in the cysteine-less mutant led to NEM sensitivity. We thus identified Cys-33 and Cys-273 in hCAT-2A as the targets of NEM inhibition. In addition, all proteins with Cys-33 mutations showed a pronounced reduction in transport activity, suggesting that, surprisingly, this residue, located in the cytoplasmic N terminus, is important for transporter function.

Indexed as

Amino Acid SubstitutionAmino Acid Transport Systems, BasicAnimalsCysteineEnzyme InhibitorsEthylmaleimideHumansMutation, MissenseOocytesProtein Structure, TertiaryXenopus laevisAmino Acid Transport Systems, BasicCysteineEnzyme InhibitorsEthylmaleimideSLC7A2 protein, humanAmino Acid Transportl-Arginine TransportMutagenesis Site-specificN-Ethylmaleimide (NEM)Plasma MembraneSolute Carrier Family 7SulfhydrylSystem y+System y+LXenopus

Identifiers

PMID24019517
PMCPMC3798505
OpenAlexW2076644904

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.