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- W2945294727 startingPage "2157" @default.
- W2945294727 abstract "Wnt signaling pathways direct key physiological decisions in development. Here, we establish a role for a pleckstrin homology domain-containing protein, PLEKHA4, as a modulator of signaling strength in Wnt-receiving cells. PLEKHA4 oligomerizes into clusters at PI(4,5)P2-rich regions of the plasma membrane and recruits the Cullin-3 (CUL3) E3 ubiquitin ligase substrate adaptor Kelch-like protein 12 (KLHL12) to these assemblies. This recruitment decreases CUL3-KLHL12-mediated polyubiquitination of Dishevelled, a central intermediate in canonical and non-canonical Wnt signaling. Knockdown of PLEKHA4 in mammalian cells demonstrates that PLEKHA4 positively regulates canonical and non-canonical Wnt signaling via these effects on the Dishevelled polyubiquitination machinery. In vivo knockout of the Drosophila melanogaster PLEKHA4 homolog, kramer, selectively affects the non-canonical, planar cell polarity (PCP) signaling pathway. We propose that PLEKHA4 tunes the sensitivities of cells toward the stimulation of Wnt or PCP signaling by sequestering a key E3 ligase adaptor controlling Dishevelled polyubiquitination within PI(4,5)P2-rich plasma membrane clusters." @default.
- W2945294727 created "2019-05-29" @default.
- W2945294727 creator A5012613988 @default.
- W2945294727 creator A5014115738 @default.
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- W2945294727 creator A5088817211 @default.
- W2945294727 date "2019-05-01" @default.
- W2945294727 modified "2023-10-13" @default.
- W2945294727 title "PLEKHA4/kramer Attenuates Dishevelled Ubiquitination to Modulate Wnt and Planar Cell Polarity Signaling" @default.
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- W2945294727 doi "https://doi.org/10.1016/j.celrep.2019.04.060" @default.
- W2945294727 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6594551" @default.
- W2945294727 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31091453" @default.
- W2945294727 hasPublicationYear "2019" @default.