SGD Paper 
Manlandro CM, et al. (2005) Ability of Sit4p to promote K+ efflux via Nha1p is modulated by Sap155p and Sap185p. Eukaryot Cell 4(6):1041-9
Abstract: 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 G(1)-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 sit4Delta strains. However, overexpression of the Na(+)-K(+)/H(+) antiporter, Nha1p, is without effect in a sit4Delta 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.
| Status: Published | Type: Journal Article | PubMed ID: 15947196 |
Topics addressed in this paper
Number of different genes curated to this paper: 9
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