ArticleGenes to cells : devoted to molecular & cellular mechanisms2013
WNK4 is an essential effector of anterior formation in FGF signaling.
Article in Genes to cells : devoted to molecular & cellular mechanisms, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Exome sequencing identifies genetic variants in anophthalmia and microphthalmia.American journal of medical genetics. Part A · 2022Article
- Energy Shortage in Human and Mouse Models of SLC4A11-Associated Corneal Endothelial Dystrophies.Investigative ophthalmology & visual science · 2020Article
- WNK4 is an Adipogenic Factor and Its Deletion Reduces Diet-Induced Obesity in Mice.EBioMedicine · 2017Article
- WDR26 is a new partner of Axin1 in the canonical Wnt signaling pathway.FEBS letters · 2016Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
With no lysine (K) (WNK) kinase family is conserved among many species and regulates SPAK/OSR1 and ion cotransporters. WNK is also involved in developmental and cellular processes, but the molecular mechanisms underlying its regulation in these processes remain unknown. In this study, we found that WNK4 is involved in fibroblast growth factor (FGF) signaling during Xenopus development. In Xenopus embryos, depletion of WNK4 by antisense morpholino oligonucleotides (MOs) results in a severe defect in anterior development and impaired expression of endogenous anterior markers. Defects in head formation or expression of anterior marker genes caused by suppression of endogenous WNK4 expression could be rescued by expression of wild-type WNK4, but not mutant WNK4 lacking its kinase activity. It is notable that morphants of Xenopus WNK4 inhibited the expression of anterior marker genes and the target genes induced by FGF signaling. Moreover, knockdown of Wnk4 significantly reduced the phosphorylation level of Osr1 induced by FGF. These results provide the first evidence that FGF signaling regulates WNK4 function required for anterior formation in Xenopus development.
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