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Modulation of renal type IIa Na+/Pi cotransporter kinetics by the arginine modifier phenylglyoxal.

作者信息

Forster I C, Köhler K, Stange G, Biber J, Murer H

机构信息

Physiologisches Institut, Universität Zürich-Irchel, Winterthurerstr. 190, CH-8057, Switzerland.

出版信息

J Membr Biol. 2002 May 15;187(2):85-96. doi: 10.1007/s00232-001-0154-6.

DOI:10.1007/s00232-001-0154-6
PMID:12029367
Abstract

The effects of the arginine-modifying reagent phenylglyoxal on the kinetics of the type IIa Na + /Pi cotransporter expressed in Xenopus, oocytes were studied by means of 32Pi uptake and electrophysiology. Phenylglyoxal incubation induced up to 60% loss of cotransport function but only marginally altered the Na+-leak. Substrate activation and pH dependency remained essentially unaltered, whereas the voltage dependency of Pi-induced change in electrogenic response was significantly reduced. Presteady-state charge movements were suppressed and the equilibrium charge distribution was shifted slightly towards hyperpolarizing potentials. Charge movements in the absence of external Na+ were also suppressed, which indicated that the empty-carrier kinetics were modified. These effects were incorporated into an ordered alternating access model for NaPi-IIa, whereby the arginine modification by phenylglyoxal was modeled as altered apparent electrical distances moved by mobile charges, together with a slower rate of translocation of the electroneutral, fully loaded carrier.

摘要

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