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首页> 外文期刊>Eukaryotic cell >Ability of Sit4p To Promote K+ Efflux via Nha1p Is Modulated by Sap155p and Sap185p
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Ability of Sit4p To Promote K+ Efflux via Nha1p Is Modulated by Sap155p and Sap185p

机译:Sit4p通过Nha1p促进K +外排的能力由Sap155p和Sap185p调节

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We demonstrate here that SAP155 encodes a negative modulator of K+ efflux in the yeast Saccharomyces cerevisiae. Overexpression of SAP155 decreases efflux, whereas deletion increases efflux. In contrast, a homolog of SAP155, called SAP185, encodes a positive modulator of K+ efflux: overexpression of SAP185 increases efflux, whereas deletion decreases efflux. Two other homologs, SAP4 and SAP190, are without effect on K+ homeostasis. Both SAP155 and SAP185 require the presence of SIT4 for function, which encodes a PP2A-like phosphatase important for the G1-S transition through the cell cycle. Overexpression of either the outwardly rectifying K+ channel, Tok1p, or the putative plasma membrane K+/H+ antiporter, Kha1p, increases efflux in both wild-type and sit4Δ strains. However, overexpression of the Na+-K+/H+ antiporter, Nha1p, is without effect in a sit4Δ strain, suggesting that Sit4p signals to Nha1p. In summary, the combined activities of Sap155p and Sap185p appear to control the function of Nha1p in K+ homeostasis via Sit4p.
机译:我们在这里证明 SAP155 编码酵母 Saccharomyces cerevisiae 中的K + 外排负调节剂。 SAP155 的过表达减少外排,而缺失则增加外排。相反,称为 SAP185 SAP155 的同系物编码K + 外排的正调节剂: SAP185 增加流出,而缺失则减少流出。 SAP4 SAP190 这两个同系物对K + 体内稳态没有影响。 SAP155 SAP185 均需要功能 SIT4 ,该功能编码对G 1重要的PP2A样磷酸酶 -S在整个细胞周期中的过渡。向外整流的K + 通道Tok1p或假定的质膜K + / H + 反向转运蛋白Kha1p的过表达会增加野生型和sit4Δ菌株。但是,Na + -K + / H + 反转运蛋白Nha1p的过表达在 sit4 Δ应变,表明Sit4p向Nha1p发出信号。总之,Sap155p和Sap185p的联合活动似乎通过Sit4p控制Nha1p在K + 体内稳态中的功能。

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