ArticleThe Biochemical journal1999
Inhibition of ATPase, GTPase and adenylate kinase activities of the second nucleotide-binding fold of the cystic fibrosis transmembrane conductance regulator by genistein.
Article in The Biochemical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
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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.
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Who cites it
15 citing papers in PubMed, 62 citations in OpenAlex.
- Genetic and Dietary Regulation of Glyburide Efflux by the Human Placental Breast Cancer Resistance Protein Transporter.The Journal of pharmacology and experimental therapeutics · 2016Article
- Interaction of Isoflavones with the BCRP/ABCG2 Drug Transporter.Current drug metabolism · 2015Review
- Amphiphysin I but not dynamin I nor synaptojanin mRNA expression increased after repeated methamphetamine administration in the rat cerebrum and cerebellum.Journal of neural transmission (Vienna, Austria : 1996) · 2013Article
- Molecular modeling of the heterodimer of human CFTR's nucleotide-binding domains using a protein-protein docking approach.Journal of molecular graphics & modelling · 2009Article
- Prolonged treatment of cells with genistein modulates the expression and function of the cystic fibrosis transmembrane conductance regulator.British journal of pharmacology · 2008Article
- Characterization of a 7,8-benzoflavone double effect on CFTR Cl(-) channel activity.The Journal of membrane biology · 2007Article
- Role of CFTR's intrinsic adenylate kinase activity in gating of the Cl(-) channel.Journal of bioenergetics and biomembranes · 2007Review
- Cystic fibrosis transmembrane regulator protein mutations: 'class' opportunity for novel drug innovation.Paediatric drugs · 2007Review
- The glycine residues G551 and G1349 within the ATP-binding cassette signature motifs play critical roles in the activation and inhibition of cystic fibrosis transmembrane conductance regulator channels by phloxine B.The Journal of membrane biology · 2005Article
- ADP inhibits function of the ABC transporter cystic fibrosis transmembrane conductance regulator via its adenylate kinase activity.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Correction of G551D-CFTR transport defect in epithelial monolayers by genistein but not by CPX or MPB-07.British journal of pharmacology · 2002Article
- The flavonol quercetin activates basolateral K(+) channels in rat distal colon epithelium.British journal of pharmacology · 2002Article
- High-affinity binding of silybin derivatives to the nucleotide-binding domain of a Leishmania tropica P-glycoprotein-like transporter and chemosensitization of a multidrug-resistant parasite to daunomycin.Antimicrobial agents and chemotherapy · 2001Article
- Effect of genistein on native epithelial tissue from normal individuals and CF patients and on ion channels expressed in Xenopus oocytes.British journal of pharmacology · 2000Article
- Two mechanisms of genistein inhibition of cystic fibrosis transmembrane conductance regulator Cl- channels expressed in murine cell line.The Journal of physiology · 2000Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the presence of ATP, genistein, like the ATP analogue adenosine 5'-[beta,gamma-imido]triphosphate (pp[NH]pA), increases cystic fibrosis transmembrane conductance regulator (CFTR) chloride currents by prolonging open times. As pp[NH]pA is thought to increase CFTR currents by interfering with ATP hydrolysis at the second nucleotide-binding fold (NBF-2), the present study was undertaken to investigate the effects of genistein on a fusion protein comprising maltose-binding protein (MBP) and NBF-2 (MBP-NBF-2). MBP-NBF-2 exhibited ATPase, GTPase and adenylate kinase activities that were inhibited by genistein in a partial non-competitive manner with respect to ATP or GTP. Ki values for competitive and uncompetitive inhibition were respectively 20 microM and 63 microM for ATPase, 15 microM and 54 microM for GTPase, and 46 microM and 142 microM for adenylate kinase. For ATPase activity, genistein reduced Vmax by 29% and Vmax/Km by 77%. Additional evidence for complex-formation between genistein and MBP-NBF-2 was obtained by the detection of genistein-dependent alterations in the CD spectrum of MBP-NBF-2 that were consistent with the formation of a higher-ordered state. Addition of MBP-NBF-2 increased the fluorescence intensity of genistein, consistent with a change to a less polar environment. pp[NH]pA partially eliminated this enhanced fluorescence of genistein. These observations provide the first direct biochemical evidence that genistein interacts with CFTR, thus inhibiting NBF-2 activity, and suggest a similar mechanism for genistein-dependent stimulation of CFTR chloride currents.
Indexed as
Identifiers
10229679PMC1220242W2047863160What Socratic holds
Registered trials
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 Socratic graph.