The Opossum Kidney Cell Type IIa Na/Pi Cotransporter Is a Phosphoprotein

M Jankowski, H Hilfiker, J Biber, H Murer - Kidney and Blood Pressure …, 2001 - karger.com
M Jankowski, H Hilfiker, J Biber, H Murer
Kidney and Blood Pressure Research, 2001karger.com
Abstract Background/Aim: Parathyroid hormone (PTH)-dependent inhibition of proximal
tubular Pi reabsorption is mediated by protein kinase A and/or C and is associated with
reduced border membrane expression of the type IIa Na/Pi cotransporter. The aim of this
study was to analyze phosphorylation of the type IIa cotransporter protein. Methods:
Opossum kidney cells were used as a 'proximal tubular'cell model. Protein phosphorylation
was determined by immunoprecipitation of the type IIa Na/Pi cotransporter, followed by …
Abstract
Background/Aim: Parathyroid hormone (PTH)-dependent inhibition of proximal tubular Pi reabsorption is mediated by protein kinase A and/or C and is associated with reduced border membrane expression of the type IIa Na/Pi cotransporter. The aim of this study was to analyze phosphorylation of the type IIa cotransporter protein. Methods: Opossum kidney cells were used as a ‘proximal tubular’ cell model. Protein phosphorylation was determined by immunoprecipitation of the type IIa Na/Pi cotransporter, followed by autoradiography. The transporter protein content was evaluated by Western blotting and transport activity by tracer Pi uptake. Results: Under control conditions (no PTH) the transporter was phosphorylated; upon treatment with PTH, a decrease in phosphorylation was observed. A protein phosphatase inhibitor (okadaic acid) was unable to prevent PTH-induced Na/Pi cotransporter inhibition but reduced transporter degradation. Conclusion: The type IIa Na/Pi cotransporter is a phosphoprotein, but alterations in its phosphorylation seem not to be involved in Pi transport inhibition.
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