Na(+)-coupled phosphate cotransporters of the SLC34 gene family catalyze the movement of inorganic phosphate (P(i)) across epithelia by using the free energy of the downhill electrochemical Na(+) gradient across the luminal membrane. Electrogenic (NaPi-IIa/b) and electroneutral (NaPi-IIc) isoforms prefer divalent P(i) and show strict Na(+):P(i) stoichiometries of 3:1 and 2:1, respectively. For electrogenic cotransport, one charge is translocated per transport cycle. When NaPi-IIa or NaPi-IIb are expressed in Xenopus oocytes, application of the P(i) transport inhibitor phosphonoformic acid (PFA) blocks a leak current that is not detectable in the electroneutral isoform. In this review, we present the experimental evidence that this transport-independent leak originates from a Na(+)-dependent uniport carrier mode intrinsic to NaPi-IIa/b isoforms. Our findings, based on the characteristics of the PFA-inhibitable leak measured from wild-type and mutant constructs, can be incorporated into an alternating access class model in which the leak and cotransport modes are mutually exclusive and share common kinetic partial reactions.

中文翻译：

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II型Na（+）-P（i）共转运体的泄漏模式。

通过使用下腔电化学Na（+）梯度穿过腔膜的自由能，SLC34基因家族的Na（+）偶联的磷酸盐共转运蛋白催化无机磷酸盐（P（i））穿过上皮细胞的运动。电源（NaPi-IIa / b）和电子中性（NaPi-IIc）同工型更喜欢二价P（i），并且分别显示出严格的Na（+）：P（i）化学计量比为3：1和2：1。对于电共运输，每个运输周期转移一个电荷。当非洲爪蟾卵母细胞中表达NaPi-IIa或NaPi-IIb时，P（i）转运抑制剂膦甲酸甲酸（PFA）的施加会阻止在电子中性同工型中无法检测到的泄漏电流。在这篇综述中，我们提供了实验证据，表明这种与运输无关的泄漏源于NaPi-IIa / b异构体固有的Na（+）依赖性单端口载体模式。