Evidence map›Paper›PMID 21441077›Full record

ArticleJournal of cystic fibrosis : official journal of the European Cystic Fibrosis Society2011

Curcumin and genistein additively potentiate G551D-CFTR.

Ying-Chun Yu, Haruna Miki, Yumi Nakamura, Akiko Hanyuda, Yohei Matsuzaki, Yoichiro Abe, Masato Yasui, Kazuhiko Tanaka, Tzyh-Chang Hwang, Silvia G Bompadre and 1 more

Abstract read
In one paragraph

Article in Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

26 citing papers in PubMed, 55 citations in OpenAlex.

  1. Review
  2. CFTR Modulators: From Mechanism to Targeted Therapeutics.Handbook of experimental pharmacology · 2024
    Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Mutation-specific dual potentiators maximize rescue of CFTR gating mutants.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. CFTR potentiators: from bench to bedside.Current opinion in pharmacology · 2017
    Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Neuron membrane trafficking and protein kinases involved in autism and ADHD.International journal of molecular sciences · 2015
    Review
  18. Article
  19. Article
  20. 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

11 authors at 3 institutions in 2 countries.

Ying-Chun YuDepartment of Pharmacology, Keio University School of Medicine, Shinjuku, Tokyo 160-8582, Japan.
Haruna Miki
Yumi Nakamura
Akiko Hanyuda
Yohei Matsuzaki
Yoichiro Abe
Masato Yasui
Kazuhiko Tanaka
Tzyh-Chang Hwang
Silvia G Bompadre
Yoshiro Sohma
Keio University · JPUniversity of Missouri · USOsaka University of Pharmaceutical Sciences · JP

Funding

MOLECULAR PATHOPHYSIOLOGY OF CYSTIC FIBROSISR01DK055835 · NIDDK · UNIVERSITY OF MISSOURI-COLUMBIA · PI HWANG, TZYH-CHANG · 1999 to 2022
$6.1M
MODEL OBSERVERS FOR COMPRESSION OF CORONARY ANGIOGRAMSR01HL053455 · NHLBI · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI ECKSTEIN, MIGUEL PATRICIO · 1996 to 2008
$1.7M
Molecular Physiology and Pharmacology of CFTRK01DK075408 · NIDDK · UNIVERSITY OF MISSOURI-COLUMBIA · PI BOMPADRE, SILVIA G · 2006 to 2009
$323k
NHLBI NIH HHS NIHR01HL53455NHLBI NIH HHS R01 HL053455NIDDK NIH HHS K01 DK075408NIDDK NIH HHS NIHK01DK075408NIDDK NIH HHS NIHR01DK55835NIDDK NIH HHS R01 DK055835
6 · The paper itself

Abstract

backgroundThe G551D mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) is a common cause of cystic fibrosis (CF). G551D-CFTR is characterized by an extremely low open probability despite its normal trafficking to the plasma membrane. Numerous small molecules have been shown to increase the activity of G551D-CFTR presumably by binding to the CFTR protein.

methodsWe investigated the effect of curcumin, genistein and their combined application on G551D-CFTR activity using the patch clamp technique.

resultsCurcumin increased G551D-CFTR whole-cell and single-channel currents less than genistein did at their maximally effective concentrations. However, curcumin further increased the channel activity of G551D-CFTR that had been already maximally potentiated by genistein, up to ~50% of the WT-CFTR level. In addition, the combined application of genistein and curcumin over a lower concentration range synergistically rescued the gating defect of G551D-CFTR.

conclusionsThe additive effects between curcumin and genistein not only support the hypothesis that multiple mechanisms are involved in the action of CFTR potentiators, but also pose pharmaceutical implications in the development of drugs for CF pharmacotherapy.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalCHO CellsCricetinaeCricetulusCurcuminCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorDrug SynergismGenisteinGreen Fluorescent ProteinsHumansIon Channel GatingMembrane PotentialsMutation, MissensePatch-Clamp TechniquesAnti-Inflammatory Agents, Non-SteroidalCFTR protein, humanCurcuminCystic Fibrosis Transmembrane Conductance Regulatorenhanced green fluorescent proteinGenisteinGreen Fluorescent ProteinsPhytoestrogens

Identifiers

PMID21441077
PMCPMC4939241
OpenAlexW2063028064

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.