Spns1 is an iron transporter essential for megalin-dependent endocytosis

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Abstract
Spns1 mediates a novel iron conductance essential during embryogenesis. Spns1 knockout leads to endocytic and lysosomal defects, accompanied by iron overload in the kidney. Reversal of iron overload by restricting dietary iron or by concurrent knockout of the iron transporter, DMT1 rescued the endocytic and organellar defects and reverted markers of iron overload. These data suggest feedback between iron and proximal tubule endocytosis.
Funding Information
  • National Institute of Diabetes and Digestive and Kidney Diseases (K25DK128563)
  • National Institute of Diabetes and Digestive and Kidney Diseases (DK124667)
  • National Institute of Diabetes and Digestive and Kidney Diseases (U54DK104309)
  • Tongji University (Alpha Institute of Natural Medicine)
  • American Heart Association (18840098)
  • National Cancer Institute (P30CA013696)
  • National Center for Research Resources (1S10RR027990)
  • National Institute of Diabetes and Digestive and Kidney Diseases (K08DK132511)

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