Evidence map›Paper›PMID 19892921›Full record

ArticleThe Journal of pharmacology and experimental therapeutics2010

Putative transmembrane domain 12 of the human organic anion transporter hOAT1 determines transporter stability and maturation efficiency.

Mei Hong, Shanshan Li, Fanfan Zhou, Paul E Thomas, Guofeng You

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.1field-weighted citation impact, top 44% 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

6 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Drug metabolism and disposition: the biological fate of chemicals · 2021
    Article
  3. Review
  4. Article
  5. Article
  6. 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

5 authors at 1 institution in 1 country.

Mei HongDepartment of Pharmaceutics, Rutgers, The State University of New Jersey, Piscataway, NJ 08854, USA.
Shanshan Li
Fanfan Zhou
Paul E Thomas
Guofeng You
Rutgers, The State University of New Jersey · US

Funding

Regulation of CYP2B6 in Human LIverR01DK061652 · NIDDK · UNIVERSITY OF NORTH CAROLINA CHAPEL HILL · PI WANG, HONGBING · 2003 to 2015
$3.7M
MOLECULAR MECHANISMS OF DRUG/XENOBIOTIC ELIMINATIONR01DK060034 · NIDDK · RUTGERS THE ST UNIV OF NJ NEW BRUNSWICK · PI YOU, GUOFENG · 2001 to 2009
$2.5M
Trafficking and Regulation of Drug/Xenobiotic Transporter OATR01GM079123 · NIGMS · RUTGERS, THE STATE UNIV OF N.J. · PI YOU, GUOFENG · 2008 to 2017
$2.2M
NIDDK NIH HHS R01 DK060034NIDDK NIH HHS R01 DK061652NIDDK NIH HHS R01-DK061652NIGMS NIH HHS R01 GM079123NIGMS NIH HHS R01-GM079123
6 · The paper itself

Abstract

Human organic anion transporter hOAT1 plays a critical role in the body disposition of clinically important drugs. In transmembrane segment (TM) 12, residues Tyr-490 and dileucine Leu-503/Leu-504 were identified to be critical for hOAT1 function. Substitution of Tyr-490 with alanine led to a dramatic reduction in protein expression of hOAT1 and its transport activity. The contribution of the side chain of Tyr-490 to transport activity was then evaluated by replacing this residue with Trp or Phe. Substitution of Tyr-490 with Trp or Phe partially or fully recovered the protein expression of hOAT1 and its transport activity, respectively, that were lost by substitution of Tyr-490 with alanine, suggesting that the aromatic ring and the size of the side chain of Tyr-490 are critical for hOAT1 expression and function. Studies with protease inhibitors and pulse-chase labeling further showed that the loss of expression of hOAT1 and its transport activity by replacing Tyr-490 with alanine resulted from accelerated degradation of the transporter, whereas its maturation efficiency was not affected. In contrast to Tyr-490, substitution of Leu-503/Leu-504 with alanine also resulted in complete loss of protein expression of hOAT1 and its transport activity. However, such loss of protein expression could not be prevented by treating mutant-expressing cells with protease inhibitors. Pulse-chase experiments showed that the mutant transporter (L503/L504A) was trapped in the endoplasmic reticulum without conversion into mature form of the transporter. Our results are the first to highlight the central role of TM 12 in maintaining the stability and in promoting the maturation efficiency of hOAT1.

Indexed as

Amino Acid SequenceAmino Acid SubstitutionAnimalsChlorocebus aethiopsCOS CellsHumansLLC-PK1 CellsMutagenesis, Site-DirectedMutant ProteinsOrganic Anion Transport Protein 1SwineTransfectionMutant ProteinsOrganic Anion Transport Protein 1

Identifiers

PMID19892921
PMCPMC2812107
OpenAlexW2093615666

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.