ArticleFEBS letters2021
Generation of fully functional fluorescent fusion proteins to gain insights into ABCC6 biology.
Article in FEBS letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Fluorescence labeling strategies for cell surface expression of TRPV1.The Journal of general physiology · 2024Article
- Fluorescence labeling strategies for the study of ion channel and receptor cell surface expression: A comprehensive toolkit for extracellular labeling of TRPV1.bioRxiv : the preprint server for biology · 2024Article
- Article
- The Mineralization Regulator ANKH Mediates Cellular Efflux of ATP, Not Pyrophosphate.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2022Article
- RAB10 Interacts with ABCB4 and Regulates Its Intracellular Traffic.International journal of molecular sciences · 2021Article
- Mutagenic Analysis of the Putative ABCC6 Substrate-Binding Cavity Using a New Homology Model.International journal of molecular sciences · 2021Article
- Detailed Phenotype Supports Pathogenicity of Hypomorphic Variant inCase reports in ophthalmologyArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
ABCC6 mediates release of ATP from hepatocytes into the blood. Extracellularly, ATP is converted into the mineralization inhibitor pyrophosphate. Consequently, inactivating mutations in ABCC6 give low plasma pyrophosphate and underlie the ectopic mineralization disorder pseudoxanthoma elasticum. How ABCC6 mediates cellular ATP release is still unknown. Fluorescent ABCC6 fusion proteins would allow mechanistic studies, but fluorophores attached to the ABCC6 N- or C-terminus result in intracellular retention and degradation. Here we describe that intramolecular introduction of fluorophores yields fully functional ABCC6 fusion proteins. A corresponding ABCC6 variant in which the catalytic glutamate of the second nucleotide binding domain was mutated, correctly routed to the plasma membrane but was inactive. Finally, N-terminal His
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Registered trials
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