Src family protein tyrosine kinase (PTK) modulates the effect of SGK1 and WNK4 on ROMK channels
作者： P. Yue , D.-H. Lin , C.-Y. Pan , Q. Leng , G. Giebisch
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摘要: WNK4 (with no lysine kinase 4) inhibits ROMK channel activity in the distal nephron by stimulating clathrin-dependent endocytosis, an effect attenuated SGK1 (serum-glucocorticoids-induced kinase)-mediated phosphorylation. It has been suggested that increased because of SGK1-mediated inhibition plays a role promoting renal K secretion response to elevated serum or high (HK) intake. In contrast, intravascular volume depletion also increases but fails stimulate channels and secretion. Because HK intake decreases Src family protein tyrosine (PTK) inhibitor channels, it is possible PTK may modulate effects on WNK4. Here, we show c-Src prevents from attenuating WNK4's activity. This was WNK4-dependent had harboring mutation at site phosphorylation (R1Y337A) absence Moreover, expression diminished increase serine WNK4, suggesting enhances WNK4-mediated suppressing SGK1-induced notion supported observation not able interaction between mutants (WNK4(S1169A) WNK4(S1169D)) which SGK1-phosphorylation (serine 1169) mutated alanine aspartate. We conclude hereby restoring thus
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