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The Human C‐Type Lectin‐Like Receptor CLEC‐1 is Upregulated by TGF‐β and Primarily Localized in the Endoplasmic Membrane Compartment
Author(s) -
Sattler S.,
Reiche D.,
Sturtzel C.,
Karas I.,
Richter S.,
Kalb M. L.,
Gregor W.,
Hofer E.
Publication year - 2012
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/j.1365-3083.2011.02665.x
Subject(s) - endoplasmic reticulum , microbiology and biotechnology , receptor , c type lectin , transforming growth factor , biology , downregulation and upregulation , proinflammatory cytokine , subfamily , intracellular , innate immune system , immunology , inflammation , gene , biochemistry
The orphan receptor CLEC‐1 is part of a subfamily of C‐type lectin‐like receptors, which is encoded in the human natural killer gene complex and comprises several pattern recognition receptors important for innate immune functions. As information on human CLEC‐1 is still very limited, we aimed to further characterize this receptor. Similar to another subfamily member, LOX‐1, expression of CLEC‐1 mRNA was detected in myeloid cells as well as in endothelial cells. CLEC‐1 protein displayed N‐linked glycosylation and formed dimers. However, in contrast to other members of the subfamily, expression levels were upregulated by transforming growth factor (TGF)‐β, but not significantly affected by proinflammatory stimuli. It is intriguing that human CLEC‐1 could only be detected intracellularly with a staining pattern resembling endoplasmic reticulum proteins. Neither TGF‐β nor inflammatory stimuli could promote significant translocation to the cell surface. These findings are in accordance with a primarily intracellular localization and function of human CLEC‐1.