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High salt diet-induced proximal tubular phenotypic changes and sodium-glucose cotransporter-2 expression are coordinated by cold shock Y-box binding protein-1

FASEB J. 2021-10; 
Anja Bernhardt, Saskia H?berer, JingJing Xu, Hannah Damerau, Johannes Steffen, Charlotte Reichardt, Katharina Wolters, Hannes Steffen, Berend Isermann, Katrin Borucki, Nadine Artelt, Nicole Endlich, Renata Kozyraki, Sabine Brandt, Jonathan A Lindquist, Peter R Mertens
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Proteins, Expression, Isolation and Analysis Flag-YB-1 was purified with anti-DYKDDDDK G1 affinity resin (L00432, Genscript) following the manufacturer’s instructions? Get A Quote

摘要

High salt diet (HSD) is a hallmark of blood pressure elevations, weight gain and diabetes onset in the metabolic syndrome. In kidney, compensatory mechanisms are activated to balance salt turnover and maintain homeostasis. Data on the long-term effects of HSD with respect to tubular cell functions and kidney architecture that exclude confounding indirect blood pressure effects are scarce. Additionally we focus on cold shock Y-box binding protein-1 as a tubular cell protective factor. A HSD model (4% NaCl in chow; 1% NaCl in water) was compared to normal salt diet (NSD, standard chow) over 16 months using wild type mice and an inducible conditional whole body knockout for cold shock Y-box binding protein-1 (BL6J... More

關鍵詞

cold shock protein, high salt diet, sodium glucose transporter, tubular damage
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