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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Aug 2016.

CD226 molecule

CD226, DNAM-1, PTA1, DNAX accessory molecule-1
This gene encodes a glycoprotein expressed on the surface of NK cells, platelets, monocytes and a subset of T cells. It is a member of the Ig-superfamily containing 2 Ig-like domains of the V-set. The protein mediates cellular adhesion of platelets and megakaryocytic cells to vascular endothelial cells. The protein also plays a role in megakaryocytic cell maturation. [provided by RefSeq, Jul 2008] (from NCBI)
Top mentioned proteins: NKG2D, poliovirus receptor, CAN, NKp46, NKp30
Papers on CD226
Suppression of metastases using a new lymphocyte checkpoint target for cancer immunotherapy.
Smyth et al., Hannover, Germany. In Cancer Discov, Feb 2016
The anti-metastatic activity of anti-CD96 was dependent on NK cells, CD226 (DNAM-1) and IFN-γ, but independent of activating Fc receptors.
Identification of CD112R as a novel checkpoint for human T cells.
Edil et al., Hangzhou, China. In J Exp Med, Feb 2016
UNASSIGNED: T cell immunoglobulin and ITIM domain (TIGIT) and CD226 emerge as a novel T cell cosignaling pathway in which CD226 and TIGIT serve as costimulatory and coinhibitory receptors, respectively, for the ligands CD155 and CD112.
Expression of DNAM-1 (CD226) on inflammatory monocytes.
Shibuya et al., Japan. In Mol Immunol, Jan 2016
DNAM-1 is an activating receptor expressed on NK cells and T cells and plays an important role in cytotoxicity of these cells against target cells.
Melanoma Cells Control Antimelanoma CTL Responses via Interaction between TIGIT and CD155 in the Effector Phase.
Shimada et al., Japan. In J Invest Dermatol, Jan 2016
This suggested that antimelanoma cytotoxic T lymphocyte responses are controlled not only by an imbalance in CD226 (an activating molecule that binds to CD155) and TIGIT expression on T cells but also by the expression levels of CD155 on melanoma cells.
Recurrent activating mutations of CD28 in peripheral T-cell lymphomas.
Chan et al., Xi'an, China. In Leukemia, Jan 2016
We found increased transcription of the CD28-responsive genes CD226 and TNFA in cells expressing the T195P mutant in response to CD3 and CD86 co-stimulation and increased downstream activation of NF-κB by both D124V and T195P mutants, suggesting a potential therapeutic target in CD28-mutated PTCLs.Leukemia accepted article preview online, 31 December 2015.
CD155/CD226-interaction impacts on the generation of innate CD8(+) thymocytes by regulating iNKT-cell differentiation.
Bernhardt et al., Hannover, Germany. In Eur J Immunol, Jan 2016
UNASSIGNED: The cell surface receptor CD155 influences a variety of immune processes by binding to its ligands CD226, CD96 or TIGIT.
Critical roles of co-activation receptor DNAX accessory molecule-1 in natural killer cell immunity.
Zhu et al., Wuhan, China. In Immunology, Nov 2015
DNAX accessory molecule-1 (DNAM-1) is an activating receptor molecule expressed on the surface of NK cells.
Balancing natural killer cell activation through paired receptors.
Smyth et al., Australia. In Nat Rev Immunol, Apr 2015
These molecules include CD226, T cell immunoreceptor with immunoglobulin and ITIM domains (TIGIT), CD96, and cytotoxic and regulatory T cell molecule (CRTAM).
TIGIT and CD226: tipping the balance between costimulatory and coinhibitory molecules to augment the cancer immunotherapy toolkit.
Wherry et al., Philadelphia, United States. In Cancer Cell, 2015
In this issue of Cancer Cell, Johnston and colleagues identify the TIGIT/CD226 pathway, which provides significant interest for combination with PD-1 pathway blockade to improve anticancer CD8(+) T cell responses, because it acts by a novel mechanism to regulate CD8(+) T cell functions within the tumor microenvironment.
The immunoreceptor TIGIT regulates antitumor and antiviral CD8(+) T cell effector function.
Grogan et al., San Francisco, United States. In Cancer Cell, 2015
This effect was abrogated by blockade of TIGIT's complementary costimulatory receptor, CD226, whose dimerization is disrupted upon direct interaction with TIGIT in cis.
NKG2D and DNAM-1 Ligands: Molecular Targets for NK Cell-Mediated Immunotherapeutic Intervention in Multiple Myeloma.
Cippitelli et al., Roma, Italy. In Biomed Res Int, 2014
Enhancement of NK cell-mediated recognition of multiple myeloma cells was reported by us and others showing increased surface expression of NKG2D and DNAM-1 ligands on tumor cells following treatment with a number of chemotherapeutic agents, such as genotoxic drugs or inhibitors of proteasome, histone deacetylases, GSK3, and HSP-90.
The receptors CD96 and CD226 oppose each other in the regulation of natural killer cell functions.
Smyth et al., Melbourne, Australia. In Nat Immunol, 2014
CD96, CD226 (DNAM-1) and TIGIT belong to an emerging family of receptors that interact with nectin and nectin-like proteins.
[Nectins and nectin-like receptors DNAM-1 and CRTAM: new ways for tumor escape].
Toutirais et al., Rennes, France. In Med Sci (paris), 2014
DNAM-1 and CRTAM are emerging NK receptors of immune cells that were described to interact with nectin and Necl.
Costimulatory molecule DNAM-1 is essential for optimal differentiation of memory natural killer cells during mouse cytomegalovirus infection.
Lanier et al., San Francisco, United States. In Immunity, 2014
Similarly, DNAM-1-deficient (Cd226(-/-)) Ly49H(+) NK cells exhibited intrinsic defects in expansion and differentiation into memory cells.
Cancer-Induced Alterations of NK-Mediated Target Recognition: Current and Investigational Pharmacological Strategies Aiming at Restoring NK-Mediated Anti-Tumor Activity.
Olive et al., Marseille, France. In Front Immunol, 2013
Thus, evasion to Natural killer (NK) cell-mediated anti-tumor activity is commonly described and is mediated by various mechanisms, mainly cancer cell-induced down-regulation of NK-activating receptors (NCRs, NKG2D, DNAM-1, and CD16) as well as up-regulation of inhibitory receptors (killer-cell immunoglobulin-like receptors, KIRs, NKG2A).
CD8 T cell defect of TNF-α and IL-2 in DNAM-1 deficient mice delays clearance in vivo of a persistent virus infection.
Oldstone et al., Los Angeles, United States. In Virology, 2012
DNAM-1 -/- CD8 T cells had significant reductions in TNF-alpha and IL-2 that were associated on adoptive transfer with the inability to terminate the persistent Arenaviridae infection.
Crystal structure of cell adhesion molecule nectin-2/CD112 and its binding to immune receptor DNAM-1/CD226.
Yan et al., Beijing, China. In J Immunol, 2012
A soluble nectin-2 immunoglobulin-like V-set domain (nectin-2v) has been successfully prepared and demonstrates binding to both soluble ectodomain and cell surface-expressed full-length DNAX accessory molecule (DNAM)-1.
Influence of MIF, CD40, and CD226 polymorphisms on risk of rheumatoid arthritis.
Fan et al., Changzhou, China. In Mol Biol Rep, 2012
CD226 gene polymorphisms may not be associated with rheumatoid arthritis susceptibility.
The TIGIT/CD226 axis regulates human T cell function.
Hafler et al., New Haven, United States. In J Immunol, 2012
TIGIT can inhibit T cell functions by competing with CD226 and can also directly inhibit T cells in a T cell-intrinsic manner.
Autoimmune disease-associated CD226 gene variants are not involved in giant cell arteritis susceptibility in the Spanish population.
González-Gay et al., Granada, Spain. In Clin Exp Rheumatol, 2012
CD226 polymorphisms, rs727088, rs34794968 and rs763361 were not involved in giant cell arteritis susceptibility in the Spanish population.
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