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Novel Protein kinase C θ: Coronin 1A complex in T lymphocytes

Overview of attention for article published in Cell Communication and Signaling, March 2015
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Title
Novel Protein kinase C θ: Coronin 1A complex in T lymphocytes
Published in
Cell Communication and Signaling, March 2015
DOI 10.1186/s12964-015-0100-3
Pubmed ID
Authors

Kerstin Siegmund, Nikolaus Thuille, Nina Posch, Friedrich Fresser, Gottfried Baier

Abstract

Protein kinase C-θ (PKCθ) plays an important role in signal transduction down-stream of the T cell receptor and T cells deficient of PKCθ show impaired NF-κB as well as NFAT/AP-1 activation resulting in strongly decreased IL-2 expression and proliferation. However, it is not yet entirely clear, how the function of PKCθ - upon T cell activation - is regulated on a molecular level. Employing a yeast two-hybrid screen and co-immunoprecipitation analyses, we here identify coronin 1A (Coro1A) as a novel PKCθ-interacting protein. We show that the NH2-terminal WD40 domains of Coro1A and the C2-like domain of PKCθ are sufficient for the interaction. Furthermore, we confirm a physical interaction by GST-Coro1A mediated pull-down of endogenous PKCθ protein. Functionally, wild-type but not Coro1A lacking its actin-binding domain negatively interferes with PKCθ-dependent NF-κB, Cyclin D1 and IL-2 transactivation when analysed with luciferase promoter activation assays in Jurkat T cells. This could be phenocopied by pharmacological inhibitors of actin polymerization and PKC, respectively. Mechanistically, Coro1A overexpression attenuates both lipid raft and plasma membrane recruitment of PKCθ in CD3/CD28-activated T cells. Using primary CD3(+) T cells, we observed that (opposite to PKCθ) Coro1A does not localize preferentially to the immunological synapse. In addition, we show that CD3(+) T cells isolated from Coro1A-deficient mice show impaired IKK/NF-κB transactivation. Together, these findings both in Jurkat T cells as well as in primary T cells indicate a regulatory role of Coro1A on PKCθ recruitment and function downstream of the TCR leading to NF-κB transactivation.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 14 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 14 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 3 21%
Researcher 3 21%
Student > Master 3 21%
Unspecified 2 14%
Lecturer > Senior Lecturer 1 7%
Other 2 14%
Readers by discipline Count As %
Agricultural and Biological Sciences 5 36%
Immunology and Microbiology 3 21%
Unspecified 2 14%
Biochemistry, Genetics and Molecular Biology 2 14%
Chemistry 1 7%
Other 1 7%

Attention Score in Context

This research output has an Altmetric Attention Score of 1. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 19 April 2015.
All research outputs
#4,190,371
of 5,011,922 outputs
Outputs from Cell Communication and Signaling
#103
of 128 outputs
Outputs of similar age
#140,284
of 169,390 outputs
Outputs of similar age from Cell Communication and Signaling
#7
of 7 outputs
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So far Altmetric has tracked 128 research outputs from this source. They receive a mean Attention Score of 3.1. This one is in the 1st percentile – i.e., 1% of its peers scored the same or lower than it.
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