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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
biochemistry, genetics and molecular biology
The C-type lectin receptor CLECSF8 (CLEC4D) is expressed by myeloid cells and triggers cellular activation through syk kinase
Journal of Biological Chemistry, Volume 287, No. 31, Year 2012
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Description
CLECSF8 is a poorly characterized member of the "Dectin-2 cluster" of C-type lectin receptors and was originally thought to be expressed exclusively by macrophages. We show here that CLECSF8 is primarily expressed by peripheral blood neutrophils and monocytes and weakly by several subsets of peripheral blood dendritic cells. However, expression of this receptor is lost upon in vitro differentiation of monocytes into dendritic cells or macrophages. Like the other members of the Dectin-2 family, which require association of their transmembrane domains with signaling adaptors for surface expression, CLECSF8 is retained intracellularly when expressed in non-myeloid cells. However, we demonstrate that CLECSF8 does not associate with any known signaling adaptor molecule, including DAP10, DAP12, or the FcRγ chain, and we found that the C-type lectin domain of CLECSF8 was responsible for its intracellular retention. Although CLECSF8 does not contain a signaling motif in its cytoplasmic domain, we show that this receptor is capable of inducing signaling via Syk kinase in myeloid cells and that it can induce phagocytosis, proinflammatory cytokine production, and the respiratory burst. These data therefore indicate that CLECSF8 functions as an activation receptor on myeloid cells and associates with a novel adaptor molecule. Characterization of the CLECSF8-deficient mice and screening for ligands using oligosaccharide microarrays did not provide further insights into the physiological function of this receptor. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.
Available Materials
https://efashare.b-cdn.net/share/pmc/articles/PMC3406680/bin/supp_287_31_25964__index.html
https://efashare.b-cdn.net/share/pmc/articles/PMC3406680/bin/supp_M112.384164_jbc.M112.384164-1.pdf
https://efashare.b-cdn.net/share/pmc/articles/PMC3406680/bin/supp_M112.384164_jbc.M112.384164-2.pdf
Authors & Co-Authors
Graham, Lisa M.
South Africa, Cape Town
University of Cape Town
Gupta, Vandana
South Africa, Cape Town
University of Cape Town
Schäfer, Georgia
South Africa, Cape Town
University of Cape Town
Reid, Delyth M.
United Kingdom, Aberdeen
University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Kimberg, Matti
South Africa, Cape Town
University of Cape Town
Dennehy, Kevin M.
South Africa, Cape Town
University of Cape Town
Germany, Tubingen
Universitätsklinikum Und Medizinische Fakultät Tübingen
Hornsell, William G.
South Africa, Cape Town
University of Cape Town
Guler, Reto
South Africa, Cape Town
University of Cape Town
Campanero-Rhodes, Maria A.
United Kingdom, London
Imperial College London
Spain, Madrid
Csic - Instituto de Quimica Fisica Rocasolano Iqfr
Palma, Angelina S.
United Kingdom, London
Imperial College London
Portugal, Caparica
Faculdade de Ciências e Tecnologia da Universidade Nova de Lisboa
Feizi, Ten
United Kingdom, London
Imperial College London
Kim, Stella K.
United States, San Francisco
University of California, San Francisco
Sobieszczuk, Peter
New Zealand, Auckland
Auckland Cancer Society Research Centre
Willment, Janet Anne
South Africa, Cape Town
University of Cape Town
United Kingdom, Aberdeen
University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Brown, Gordon D.A.
South Africa, Cape Town
University of Cape Town
United Kingdom, Aberdeen
University of Aberdeen School of Medicine, Medical Sciences and Nutrition
Statistics
Citations: 101
Authors: 15
Affiliations: 8
Identifiers
Doi:
10.1074/jbc.M112.384164
ISSN:
00219258
e-ISSN:
1083351X