Na+/H+ exchanger isoform 6 (NHE6/SLC9A6) is involved in clathrin-dependent endocytosis of transferrin.

Am J Physiol Cell Physiol

Department of Biological Sciences, Graduate School of Science, Osaka University, Machikaneyama-cho 1-1, Toyonaka City, Osaka, Japan.

Published: December 2011

In mammalian cells, nine conserved isoforms of the Na(+)/H(+) exchanger (NHE) are known to be important for pH regulation of the cytoplasm and organellar lumens. NHE1-5 are localized to the plasma membrane, whereas NHE6-9 are localized to distinct organelles. NHE6 is localized predominantly in endosomal compartments but is also found in the plasma membrane. To investigate the role of NHE6 in endocytosis, we established NHE6-knockdown HeLa cells and analyzed the effect of this knockdown on endocytotic events. The expression level of NHE6 in knockdown cells was decreased to ∼15% of the level seen in control cells. Uptake of transferrin was also decreased. No effect was found on the endocytosis of epidermal growth factor or on the cholera toxin B subunit. Moreover, in the NHE6-knockdown cells, transferrin uptake was found to be affected in the early stages of endocytosis. Microscopic analysis revealed that, at 2 min after the onset of endocytosis, colocalization of NHE6, clathrin, and transferrin was observed, which suggests that NHE6 was localized to endocytotic, clathrin-coated vesicles. In addition, in knockdown cells, transferrin-positive endosomes were acidified, but no effect was found on cytoplasmic pH. In cells overexpressing wild-type NHE6, increased transferrin uptake was observed, but no such increase was seen in cells overexpressing mutant NHE6 deficient in ion transport. The luminal pH in transferrin-positive endosomes was alkalized in cells overexpressing wild-type NHE6 but normal in cells overexpressing mutant NHE6. These observations suggest that NHE6 regulates clathrin-dependent endocytosis of transferrin via pH regulation.

Download full-text PDF

Source
http://dx.doi.org/10.1152/ajpcell.00154.2011DOI Listing

Publication Analysis

Top Keywords

cells overexpressing
16
cells
10
nhe6
10
na+/h+ exchanger
8
clathrin-dependent endocytosis
8
endocytosis transferrin
8
plasma membrane
8
nhe6 localized
8
knockdown cells
8
transferrin uptake
8

Similar Publications

The L-type Ca channel (Ca1.2) is essential for cardiac excitation-contraction coupling. To contribute to the inward Ca flux that drives Ca-induced-Ca-release, Ca1.

View Article and Find Full Text PDF

Modulation of stomatal development and movement is a promising approach for creating water-conserving plants. Here, we identified and characterized the PagHCF106 gene of poplar (Populus alba × Populus glandulosa). The PagHCF106 protein localized predominantly to the chloroplast, and the PagHCF106 gene exhibited tissue-specific expression pattern.

View Article and Find Full Text PDF

Objective: Myocardial ischemia-reperfusion injury (MIRI) is a highly complex disease with high morbidity and mortality. Studying the molecular mechanism of MIRI and discovering new targets are crucial for the future treatment of MIRI.

Methods: We constructed the MIRI rat model and hypoxia/reoxygenation (H/R) injury cardiomyocytes model.

View Article and Find Full Text PDF

In gastric cancer, the relationship between human epidermal growth factor receptor 2 (HER2), the cyclic GMP-AMP synthase-stimulator of the interferon genes (cGAS-STING) pathway, and autophagy remains unclear. This study examines whether HER2 regulates autophagy in gastric cancer cells via the cGAS-STING signaling pathway, influencing key processes such as cell proliferation and migration. Understanding this relationship could uncover new molecular targets for diagnosis and treatment.

View Article and Find Full Text PDF

Background: Clear cell renal cell carcinoma (ccRCC) is the most common subtype of kidney cancer with a high metastatic rate and high mortality rate. The molecular mechanism of ccRCC development, however, needs further study. Aurora kinase B (AURKB) functions as an important oncogene in various tumors; therefore, in the present study, we aimed to explore the mechanism by which AURKB affects ccRCC development.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!