ArticleThe Journal of clinical investigation2000
Inhibition of cystic fibrosis transmembrane conductance regulator by novel interaction with the metabolic sensor AMP-activated protein kinase.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.
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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.
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Who cites it
96 citing papers in PubMed, 220 citations in OpenAlex.
- Metformin Therapy in Autosomal Dominant Polycystic Kidney Disease: A Feasibility Study.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2022Trial
- Primary results of the randomized trial of metformin administration in polycystic kidney disease (TAME PKD).Kidney international · 2021Trial
- Baseline Characteristics and Patient-Reported Outcomes of ADPKD Patients in the Multicenter TAME-PKD Clinical Trial.Kidney360 · 2020Trial
- Metformin Use and Clinical Outcomes in Autosomal Dominant Polycystic Kidney Disease: A Nationwide Cohort Study.Biomedicines · 2025Article
- Mechanism of Atractylenolide Ⅲ alleviating pyrotinib-induced diarrhea by regulating AMPK/CFTR pathway through metabolite of gut microbiota.Journal of traditional and complementary medicine · 2025Article
- Functional Consequences of CFTR Interactions in Cystic Fibrosis.International journal of molecular sciences · 2024Review
- PHLPP1 regulates CFTR activity and lumen expansion through AMPK.Development (Cambridge, England) · 2022Article
- PF-06409577 inhibits renal cyst progression by concurrently inhibiting the mTOR pathway and CFTR channel activity.FEBS open bio · 2022Article
- Review
- Mechanistic analysis and significance of sphingomyelinase-mediated decreases in transepithelial CFTR currents in nHBEs.Physiological reports · 2021Article
- Overweight and Obesity and Progression of ADPKD.Clinical journal of the American Society of Nephrology : CJASN · 2021Article
- Oral delivery of metformin by chitosan nanoparticles for polycystic kidney disease.Journal of controlled release : official journal of the Controlled Release Society · 2021Article
- Cystic Fibrosis Lung Disease in the Aging Population.Frontiers in pharmacology · 2021Review
- Review
- Transient Receptor Potential Melastatin 8 (TRPM8) Channel Regulates Proliferation and Migration of Breast Cancer Cells by Activating the AMPK-ULK1 Pathway to Enhance Basal Autophagy.Frontiers in oncology · 2020Article
- AMPK mediates inhibition of electrolyte transport and NKCC1 activity by reactive oxygen species.American journal of physiology. Gastrointestinal and liver physiology · 2019Article
- AMP-Activated Protein Kinase (AMPK)-Dependent Regulation of Renal Transport.International journal of molecular sciences · 2018Review
- Metabolism and mitochondria in polycystic kidney disease research and therapy.Nature reviews. Nephrology · 2018Review
- Metformin in autosomal dominant polycystic kidney disease: experimental hypothesis or clinical fact?BMC nephrology · 2018Article
- CFTR/ENaC-dependent regulation of membrane potential during human sperm capacitation is initiated by bicarbonate uptake through NBC.The Journal of biological chemistry · 2018Article
36 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The cystic fibrosis transmembrane conductance regulator (CFTR) is an ATP-gated Cl(-) channel that regulates other epithelial transport proteins by uncharacterized mechanisms. We employed a yeast two-hybrid screen using the COOH-terminal 70 residues of CFTR to identify proteins that might be involved in such interactions. The alpha1 (catalytic) subunit of AMP-activated protein kinase (AMPK) was identified as a dominant and novel interacting protein. The interaction is mediated by residues 1420-1457 in CFTR and by the COOH-terminal regulatory domain of alpha1-AMPK. Mutations of two protein trafficking motifs within the 38-amino acid region in CFTR each disrupted the interaction. GST-fusion protein pull-down assays in vitro and in transfected cells confirmed the CFTR-alpha1-AMPK interaction and also identified alpha2-AMPK as an interactor with CFTR. AMPK is coexpressed in CFTR-expressing cell lines and shares an apical distribution with CFTR in rat nasal epithelium. AMPK phosphorylated full-length CFTR in vitro, and AMPK coexpression with CFTR in Xenopus oocytes inhibited cAMP-activated CFTR whole-cell Cl(-) conductance by approximately 35-50%. Because AMPK is a metabolic sensor in cells and responds to changes in cellular ATP, regulation of CFTR by AMPK may be important in inhibiting CFTR under conditions of metabolic stress, thereby linking transepithelial transport to cell metabolic state.
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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 OpenQuestion graph.