Curcumin, a major constituent of turmeric, corrects cystic fibrosis defects
| Autor: | Scott A. Weiner, Gergely L. Lukacs, Vanathy Rajendran, Daniel Rubin, Susan Canny, Marie E. Egan, Michael J. Caplan, Marilyn Pearson, Kai Du, Judith Glöckner-Pagel |
|---|---|
| Rok vydání: | 2004 |
| Předmět: |
congenital
hereditary and neonatal diseases and abnormalities medicine.medical_specialty Protein Folding Pancreatic disease Curcumin Glycosylation Cystic Fibrosis Calnexin Cystic Fibrosis Transmembrane Conductance Regulator Pharmacology Endoplasmic Reticulum Transfection Cystic fibrosis Cell Line Membrane Potentials Polyethylene Glycols chemistry.chemical_compound Electrolytes Mice Internal medicine Cricetinae medicine Baby hamster kidney cell Animals Humans Intestinal Mucosa Mice Knockout Multidisciplinary biology Endoplasmic reticulum Cell Membrane Isoproterenol Rectum Gene targeting respiratory system medicine.disease Cystic fibrosis transmembrane conductance regulator Nasal Mucosa Endocrinology chemistry Gene Targeting Mutation biology.protein Triphosphatase Calcium Intestinal Obstruction |
| Zdroj: | Science (New York, N.Y.). 304(5670) |
| ISSN: | 1095-9203 |
| Popis: | Cystic fibrosis is caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR). The most common mutation, ΔF508, results in the production of a misfolded CFTR protein that is retained in the endoplasmic reticulum and targeted for degradation. Curcumin is a nontoxic Ca–adenosine triphosphatase pump inhibitor that can be administered to humans safely. Oral administration of curcumin to homozygous ΔF508 CFTR mice in doses comparable, on a weight-per-weight basis, to those well tolerated by humans corrected these animals' characteristic nasal potential difference defect. These effects were not observed in mice homozygous for a complete knockout of the CFTR gene. Curcumin also induced the functional appearance of ΔF508 CFTR protein in the plasma membranes of transfected baby hamster kidney cells. Thus, curcumin treatment may be able to correct defects associated with the homozygous expression of ΔF508 CFTR. |
| Databáze: | OpenAIRE |
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