ArticleActa histochemica et cytochemica2008
Expression and trafficking of the gamma subunit of Na,K-ATPase in hypertonically challenged IMCD3 cells.
Article in Acta histochemica et cytochemica, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Beneficial Renal and Pancreatic Phenotypes in a Mouse Deficient in FXYD2 Regulatory Subunit of Na,K-ATPase.Frontiers in physiology · 2016Review
- FXYD2c plays a potential role in modulating Na(+)/K (+)-ATPase activity in HK-2 cells upon hypertonic challenge.The Journal of membrane biology · 2014Article
- Post-transcriptional control of Na,K-ATPase activity and cell growth by a splice variant of FXYD2 protein with modified mRNA.The Journal of biological chemistry · 2011Article
- Mechanism of noradrenaline-induced stimulation of Na-K ATPase activity in the rat brain: implications on REM sleep deprivation-induced increase in brain excitability.Molecular and cellular biochemistry · 2010Review
- FXYD2 and Na,K-ATPase expression in isolated human proximal tubular cells: disturbed upregulation on renal hypomagnesemia?The Journal of membrane biology · 2009Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The gamma subunit (FXYD2) of Na,K-ATPase is an important regulator of the sodium pump. In this investigation we have analysed the trafficking of gamma to the plasma membrane in cultures of inner medullary collecting duct cells (IMCD3) following acute hypertonic challenge and brefeldin A (BFA) treatment. Following hypertonic challenging for 24 hr immunofluorescence labeling revealed initial co-localization of the gamma subunit and 58K Golgi protein in the cytoplasm, but no co-localization of alpha1 and Golgi protein. Exposure of the challenged cells to BFA prevented the subsequent incorporation of gamma into the basolateral plasma membrane. The gamma subunit instead remained in cytoplasmic vesicles while cell proliferation and cell viability decreased simultaneously. Following removal of BFA from the hypertonic medium the IMCD3 cells recovered with distinct expression of gamma in the basolateral membrane. The alpha1 subunit was only marginally influenced by BFA. The results demonstrate that the gamma subunit trafficks to the plasma membrane via the Golgi apparatus, despite the absence of a signal sequence. The results also suggest that the gamma and alpha subunits do not traffic together to the plasma membrane, and that the gamma and alpha subunit have different turnover rates during these experimental conditions.
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