ArticleThe Journal of membrane biology2009
FXYD2 and Na,K-ATPase expression in isolated human proximal tubular cells: disturbed upregulation on renal hypomagnesemia?
Article in The Journal of membrane biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- The functions of FXYD family members in human health and disease.Genes & diseases · 2026Review
- Molecular Basis of Na, K-ATPase Regulation of Diseases: Hormone and FXYD2 Interactions.International journal of molecular sciences · 2024Review
- Navigating the multifaceted intricacies of the NaPhysiological reviews · 2024Review
- Maternal High Fat Diet and in-Utero Metformin Exposure Significantly Impact upon the Fetal Renal Proteome of Male Mice.Journal of clinical medicine · 2019Article
- Renal Mg handling, FXYD2 and the central role of the Na,K-ATPase.Physiological reports · 2018Review
- PharmGKB summary: Diuretics pathway, pharmacodynamics.Pharmacogenetics and genomics · 2013Article
- FXYD proteins stabilize Na,K-ATPase: amplification of specific phosphatidylserine-protein interactions.The Journal of biological chemistry · 2011Article
- Getting beta all the time: discovery of reliable markers of beta cell mass.Diabetologia · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autosomal dominant renal hypomagnesemia (OMIM 154020), associated with hypocalciuria, has been linked to a 121G to A mutation in the FXYD2 gene. To gain insight into the molecular mechanisms linking this mutation to the clinical phenotype, we studied isolated proximal tubular cells from urine of a patient and a healthy subject. Cells were immortalized and used to assess the effects of hypertonicity-induced overexpression of FXYD2 on amount, activity and apparent affinities for Na(+), K(+) and ATP of Na,K-ATPase. Both cell lines expressed mRNA for FXYD2a and FXYD2b, and patient cells contained both the wild-type and mutated codons. FXYD2 protein expression was lower in patient cells and could be increased in both cell lines upon culturing in hyperosmotic medium but to a lesser extent in patient cells. Similarly, hyperosmotic culturing increased Na,K-ATPase protein expression and ATP hydrolyzing activity but, again, to a lesser extent in patient cells. Apparent affinities of Na,K-ATPase for Na(+), K(+) and ATP did not differ between patient and control cells or after hyperosmotic induction. We conclude that human proximal tubular cells respond to a hyperosmotic challenge with an increase in FXYD2 and Na,K-ATPase protein expression, though to a smaller absolute extent in patient cells.
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