ArticleDevelopmental cell2016
aPKC Inhibition by Par3 CR3 Flanking Regions Controls Substrate Access and Underpins Apical-Junctional Polarization.
Article in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 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
41 citing papers in PubMed, 75 citations in OpenAlex.
- aPKC-ζ III promotes trophoblast fusion by altering Par-3 interactions with Hippo signaling kinase LATS1.Stem cell reports · 2026Article
- Generating models for isoform-specific PKM-KIBRA interactions with BIFC, stabilization and AlphaFold 3.Molecular brain · 2026Article
- Design, Optimization and Mechanistic Insights Into Terpenoid-Derived Inhibitors of Protein Kinase C Iota.Chemical biology & drug design · 2026Article
- Photochemical nanomotors reverse anxiety- and depressive-related behaviors in rodents via spatiotemporal polarity dynamics tuning.Nature communications · 2026Article
- Penetrant PKCβ mutation in ATLL displays a mixed gain-of-function.The Biochemical journal · 2025Article
- Oligomerization and positive feedback on membrane recruitment encode dynamically stable PAR-3 asymmetries in thebioRxiv : the preprint server for biology · 2025Article
- 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
- Cell polarity proteins promote macropinocytosis in response to metabolic stress.Nature communications · 2024Article
- Quantitative perturbation-phenotype maps reveal nonlinear responses underlying robustness of PAR-dependent asymmetric cell division.PLoS biology · 2024Article
- 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
- Into the fold: advances in understanding aPKC membrane dynamics.The Biochemical journal · 2023Article
- Morphogenesis and development of human telencephalic organoids in the absence and presence of exogenous extracellular matrix.The EMBO journal · 2023Article
- Article
- Control of atypical PKCι membrane dissociation by tyrosine phosphorylation within a PB1-C1 interdomain interface.The Journal of biological chemistry · 2023Article
- aPKC regulates apical constriction to prevent tissue rupture in the Drosophila follicular epithelium.Current biology : CB · 2022Article
- Apical-basal polarity and the control of epithelial form and function.Nature reviews. Molecular cell biology · 2022Review
- The Roles of Par3, Par6, and aPKC Polarity Proteins in Normal Neurodevelopment and in Neurodegenerative and Neuropsychiatric Disorders.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Review
- Par-3 family proteins in cell polarity & adhesion.The FEBS journal · 2022Review
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
Atypical protein kinase C (aPKC) is a key apical-basal polarity determinant and Par complex component. It is recruited by Par3/Baz (Bazooka in Drosophila) into epithelial apical domains through high-affinity interaction. Paradoxically, aPKC also phosphorylates Par3/Baz, provoking its relocalization to adherens junctions (AJs). We show that Par3 conserved region 3 (CR3) forms a tight inhibitory complex with a primed aPKC kinase domain, blocking substrate access. A CR3 motif flanking its PKC consensus site disrupts the aPKC kinase N lobe, separating P-loop/αB/αC contacts. A second CR3 motif provides a high-affinity anchor. Mutation of either motif switches CR3 to an efficient in vitro substrate by exposing its phospho-acceptor site. In vivo, mutation of either CR3 motif alters Par3/Baz localization from apical to AJs. Our results reveal how Par3/Baz CR3 can antagonize aPKC in stable apical Par complexes and suggests that modulation of CR3 inhibitory arms or opposing aPKC pockets would perturb the interaction, promoting Par3/Baz phosphorylation.
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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.