ArticleThe Journal of biological chemistry2009
Curcumin cross-links cystic fibrosis transmembrane conductance regulator (CFTR) polypeptides and potentiates CFTR channel activity by distinct mechanisms.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 38 citations in OpenAlex.
- Exploring the Mechanism of Activation of CFTR by Curcuminoids: An Ensemble Docking Study.International journal of molecular sciences · 2023Article
- Sensitivity of Acute Myelocytic Leukemia Cells to the Dienone Compound VLX1570 Is Associated with Inhibition of the Ubiquitin-Proteasome System.Biomolecules · 2021Article
- The Diarylheptanoid Curcumin Induces MYC Inhibition and Cross-Links This Oncoprotein to the Coactivator TRRAP.Frontiers in oncology · 2021Article
- Dienone Compounds: Targets and Pharmacological Responses.Journal of medicinal chemistry · 2020Article
- Mutation-specific dual potentiators maximize rescue of CFTR gating mutants.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2020Article
- Cystic Fibrosis Transmembrane Conductance Regulator: A Possible New Target for Photodynamic Therapy Enhances Wound Healing.Advances in wound care · 2019Article
- ER residency of the ceramide phosphoethanolamine synthase SMSr relies on homotypic oligomerization mediated by its SAM domain.Scientific reports · 2017Article
- Monitoring Changes in the Oligomeric State of a Candidate Endoplasmic Reticulum (ER) Ceramide Sensor by Single-molecule Photobleaching.The Journal of biological chemistry · 2016Article
- CFTR-regulated MAPK/NF-κB signaling in pulmonary inflammation in thermal inhalation injury.Scientific reports · 2015Article
- Effects of curcumin on ion channels and transporters.Frontiers in physiology · 2014Review
- Curcumin and genistein: the combined effects on disease-associated CFTR mutants and their clinical implications.Current pharmaceutical design · 2013Review
- Erythrocytic stage-dependent regulation of oligomerization of Plasmodium ribosomal protein P2.The Journal of biological chemistry · 2012Article
- Cystic fibrosis transmembrane conductance regulator (CFTR) potentiator VX-770 (ivacaftor) opens the defective channel gate of mutant CFTR in a phosphorylation-dependent but ATP-independent manner.The Journal of biological chemistry · 2012Article
- Anaphase-promoting complex/cyclosome protein Cdc27 is a target for curcumin-induced cell cycle arrest and apoptosis.BMC cancer · 2012Article
- Encapsulation of curcumin in self-assembling peptide hydrogels as injectable drug delivery vehicles.Biomaterials · 2011Article
- Curcumin and genistein additively potentiate G551D-CFTR.Journal of cystic fibrosis : official journal of the European Cystic Fibrosis Society · 2011Article
- Therapeutic potential of curcumin in gastrointestinal diseases.World journal of gastrointestinal pathophysiology · 2011Article
- Autoxidative and cyclooxygenase-2 catalyzed transformation of the dietary chemopreventive agent curcumin.The Journal of biological chemistry · 2011Article
- Cross-linking of ΔF508-CFTR promotes its trafficking to the plasma membrane.Channels (Austin, Tex.)Article
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Cystic fibrosis (CF) is caused by loss-of-function mutations in the CFTR chloride channel. Wild type and mutant CFTR channels can be activated by curcumin, a well tolerated dietary compound with some appeal as a prospective CF therapeutic. However, we show here that curcumin has the unexpected effect of cross-linking CFTR polypeptides into SDS-resistant oligomers. This effect occurred for CFTR channels in microsomes as well as in intact cells and at the same concentrations that are effective for promoting CFTR channel activity (5-50 mum). Both mature CFTR polypeptides at the cell surface and immature CFTR protein in the endoplasmic reticulum were cross-linked by curcumin, although the latter pool was more susceptible to this modification. Curcumin cross-linked two CF mutant channels (Delta F508 and G551D) as well as a variety of deletion constructs that lack the major cytoplasmic domains. In vitro cross-linking could be prevented by high concentrations of oxidant scavengers (i.e. reduced glutathione and sodium azide) indicating a possible oxidation reaction with the CFTR polypeptide. Importantly, cyclic derivatives of curcumin that lack the reactive beta diketone moiety had no cross-linking activity. One of these cyclic derivatives stimulated the activities of wild type CFTR channels, Delta 1198-CFTR channels, and G551D-CFTR channels in excised membrane patches. Like the parent compound, the cyclic derivative irreversibly activated CFTR channels in excised patches during prolonged exposure (>5 min). Our results raise a note of caution about secondary biochemical effects of reactive compounds like curcumin in the treatment of CF. Cyclic curcumin derivatives may have better therapeutic potential in this regard.
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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.