FXYD5 (dysadherin) may mediate metastatic progression through regulation of the β-Na+-K+-ATPase subunit in the 4T1 mouse breast cancer model
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چکیده
منابع مشابه
FXYD5 (dysadherin) may mediate metastatic progression through regulation of the β-Na+-K+-ATPase subunit in the 4T1 mouse breast cancer model.
FXYD5 is a Na+-K+-ATPase regulator, expressed in a variety of normal epithelia. In parallel, it has been found to be associated with several types of cancer and effect lethal outcome by promoting metastasis. However, the molecular mechanism underlying FXYD5 mediated invasion has not yet been identified. In this study, using in vivo 4T1 murine breast cancer model, we found that FXYD5-specific sh...
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FXYD5 (dysadherin or also called a related to ion channel, RIC) is a transmembrane auxiliary subunit of the Na(+)-K(+)-ATPase shown to increase its maximal velocity (Vmax). FXYD5 has also been identified as a cancer-associated protein whose expression in tumor-derived cell lines impairs cytoskeletal organization and increases cell motility. Previously, we have demonstrated that the expression o...
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FXYD5 (Dysadherin, RIC) is a single span type I membrane protein that plays multiple roles in regulation of cellular functions. It is expressed in a variety of epithelial tissues and acts as an auxiliary subunit of the Na(+)/K(+)-ATPase. During the past decade, a correlation between enhanced expression of FXYD5 and tumor progression has been established for various tumor types. In this review, ...
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15 صفحه اولThe β Subunit of the Na+/K+-ATPase Follows the Conformational State of the Holoenzyme
The Na+/K+-ATPase is a ubiquitous plasma membrane ion pump that utilizes ATP hydrolysis to regulate the intracellular concentration of Na+ and K+. It is comprised of at least two subunits, a large catalytic alpha subunit that mediates ATP hydrolysis and ion transport, and an ancillary beta subunit that is required for proper trafficking of the holoenzyme. Although processes mediated by the alph...
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ژورنال
عنوان ژورنال: American Journal of Physiology-Cell Physiology
سال: 2017
ISSN: 0363-6143,1522-1563
DOI: 10.1152/ajpcell.00206.2016