ArticlePloS one2014
The variable hinge region of novel PKCs determines localization to distinct regions of the immunological synapse.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Interfacial actin protrusions mechanically enhance killing by cytotoxic T cells.Science immunology · 2019Article
- Spatial and Temporal Control of T Cell Activation Using a Photoactivatable Agonist.Journal of visualized experiments : JoVE · 2018Article
- Cell Type-Specific Regulation of Immunological Synapse Dynamics by B7 Ligand Recognition.Frontiers in immunology · 2016Review
- Spatio-Temporal Regulation of PKC Isoforms Imparts Signaling Specificity.Frontiers in immunology · 2016Review
- Lipid-based patterning of the immunological synapse.Biochemical Society transactions · 2014Review
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Authors and funding
4 authors.
Funding
Abstract
The immunological synapse (IS) formed between a T cell and its cognate antigen-presenting cell (APC) enables the directional secretion of cytolytic and inflammatory molecules. Synaptic architecture is established in part by a two-step cascade of novel protein kinase C (nPKC) isozymes. PKCε and PKCη arrive at the IS first, and occupy the entire synaptic membrane. Then, PKCθ accumulates in a smaller zone at the center of the contact. We investigated the molecular basis for this differential recruitment behavior using chimeric nPKC constructs and total internal reflection fluorescence microscopy. Our studies revealed that the V3 linker just N-terminal to the kinase domain plays a crucial role in specifying nPKC localization. Substitution of this linker switched the scope and the kinetics of PKCθ accumulation to that of PKCε and PKCη, and vice versa. Although the V3 was necessary for synaptic compartmentalization, it was not sufficient, as the tandem C1 domains were also required to mediate membrane association. Together, these results suggest a model whereby the V3 linker controls nPKC sub-compartmentalization after initial C1 domain-mediated accumulation at the IS.
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