ArticleMolecular and cellular biology2004
Immune functions in mice lacking Clnk, an SLP-76-related adaptor expressed in a subset of immune cells.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 30 citations in OpenAlex.
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- The neuroimmune axis of Alzheimer's disease.Genome medicine · 2023Review
- Identification of Immune-Related Gene Signatures in Lung Adenocarcinoma and Lung Squamous Cell Carcinoma.Frontiers in immunology · 2021Article
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- Single-cell transcriptomic analysis of tissue-resident memory T cells in human lung cancer.The Journal of experimental medicine · 2019Article
- The Role of Adaptor Proteins in the Biology of Natural Killer T (NKT) Cells.Frontiers in immunology · 2019Review
- Significant concordance of genetic variation that increases both the risk for obsessive-compulsive disorder and the volumes of the nucleus accumbens and putamen.The British journal of psychiatry : the journal of mental science · 2018Article
- IFN-γ induction by neutrophil-derived IL-17A homodimer augments pulmonary antibacterial defense.Mucosal immunology · 2016Article
- Proteomic analysis of the SH2 domain-containing leukocyte protein of 76 kDa (SLP76) interactome in resting and activated primary mast cells [corrected].Molecular & cellular proteomics : MCP · 2013Article
- Independent and cooperative roles of adaptor molecules in proximal signaling during FcepsilonRI-mediated mast cell activation.Molecular and cellular biology · 2010Article
- Adapters in the organization of mast cell signaling.Immunological reviews · 2009Review
- Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The SLP-76 family of immune cell-specific adaptors is composed of three distinct members named SLP-76, Blnk, and Clnk. They have been implicated in the signaling pathways coupled to immunoreceptors such as the antigen receptors and Fc receptors. Previous studies using gene-targeted mice and deficient cell lines showed that SLP-76 plays a central role in T-cell development and activation. Moreover, it is essential for normal mast cell and platelet activation. In contrast, Blnk is necessary for B-cell development and activation. While the precise function of Clnk is not known, it was reported that Clnk is selectively expressed in mast cells, natural killer (NK) cells, and previously activated T-cells. Moreover, ectopic expression of Clnk was shown to rescue T-cell receptor-mediated signal transduction in an SLP-76-deficient T-cell line, suggesting that, like its relatives, Clnk is involved in the positive regulation of immunoreceptor signaling. Stimulatory effects of Clnk on immunoreceptor signaling were also reported to occur in transfected B-cell and basophil leukemia cell lines. Herein, we attempted to address the physiological role of Clnk in immune cells by the generation of Clnk-deficient mice. The results of our studies demonstrated that Clnk is dispensable for normal differentiation and function of T cells, mast cells, and NK cells. Hence, unlike its relatives, Clnk is not essential for normal immune functions.
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