ArticleThe Journal of cell biology2020
A polybasic domain in aPKC mediates Par6-dependent control of membrane targeting and kinase activity.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 40 citations in OpenAlex.
- aPKC-ζ III promotes trophoblast fusion by altering Par-3 interactions with Hippo signaling kinase LATS1.Stem cell reports · 2026Article
- LGL-1 and the RhoGAP protein PAC-1 redundantly polarize thebioRxiv : the preprint server for biology · 2026Article
- Polarity protein Par6 facilitates the processive phosphorylation of Lgl via a dynamic interaction with aPKC.Communications biology · 2025Article
- Capture, mutual inhibition and release mechanism for aPKC-Par6 and its multisite polarity substrate Lgl.Nature structural & molecular biology · 2025Article
- A PAR6-aPKC-LGL structure reveals how LGL antagonizes aPKC.Nature structural & molecular biology · 2025Article
- Review
- Membrane extraction in native lipid nanodiscs reveals dynamic regulation of Cdc42 complexes during cell polarization.Biophysical journal · 2025Article
- A PDZ-kinase allosteric relay mediates Par complex regulator exchange.bioRxiv : the preprint server for biology · 2024Article
- Atypical Protein Kinase C Promotes its own Asymmetric Localisation by Phosphorylating Cdc42 in thebioRxiv : the preprint server for biology · 2024Article
- The Drosophila neuroblast polarity cycle at a glance.Journal of cell science · 2024Article
- Into the fold: advances in understanding aPKC membrane dynamics.The Biochemical journal · 2023Article
- Article
- Apical polarity and actomyosin dynamics control Kibra subcellular localization and function in Drosophila Hippo signaling.Developmental cell · 2023Article
- Cooperative regulation of C1-domain membrane recruitment polarizes atypical protein kinase C.The Journal of cell biology · 2023Article
- An acytokinetic cell division creates PIP2-enriched membrane asymmetries leading to slit diaphragm assembly in Drosophila nephrocytes.Development (Cambridge, England) · 2023Article
- Control of atypical PKCι membrane dissociation by tyrosine phosphorylation within a PB1-C1 interdomain interface.The Journal of biological chemistry · 2023Article
- PI(4,5)P2: signaling the plasma membrane.The Biochemical journal · 2022Article
- Apical-basal polarity and the control of epithelial form and function.Nature reviews. Molecular cell biology · 2022Review
- Hypoxia controls plasma membrane targeting of polarity proteins by dynamic turnover of PI4P and PI(4,5)P2.eLife · 2022Article
- A novel non‑selective atypical PKC agonist could protect neuronal cell line from Aβ‑oligomer induced toxicity by suppressing Aβ generation.Molecular medicine reports · 2022Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Mechanisms coupling the atypical PKC (aPKC) kinase activity to its subcellular localization are essential for cell polarization. Unlike other members of the PKC family, aPKC has no well-defined plasma membrane (PM) or calcium binding domains, leading to the assumption that its subcellular localization relies exclusively on protein-protein interactions. Here we show that in both Drosophila and mammalian cells, the pseudosubstrate region (PSr) of aPKC acts as a polybasic domain capable of targeting aPKC to the PM via electrostatic binding to PM PI4P and PI(4,5)P2. However, physical interaction between aPKC and Par-6 is required for the PM-targeting of aPKC, likely by allosterically exposing the PSr to bind PM. Binding of Par-6 also inhibits aPKC kinase activity, and such inhibition can be relieved through Par-6 interaction with apical polarity protein Crumbs. Our data suggest a potential mechanism in which allosteric regulation of polybasic PSr by Par-6 couples the control of both aPKC subcellular localization and spatial activation of its kinase activity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.