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CD69 encodes a member of the calcium dependent lectin superfamily of type II transmembrane receptors. Additionally we are shipping CD69 Antibodies (459) and CD69 Proteins (17) and many more products for this protein.
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Data show that a subset of inflammation-induced CD69(+) Kupffer cells which can feedback inhibit CD4 (show CD4 ELISA Kits) T cell response via cell surface TGF-beta1 (show TGFB1 ELISA Kits) at the late stage of immune response against infection.
Specific niches for lung-resident memory CD8 (show CD8A ELISA Kits)+ T cells at the site of tissue regeneration enable CD69-independent maintenance.
this study shows that CD69 serves as a key mediator of the pathogenesis of psoriasis by controlling LAT1-CD98 (show SLC7A5 ELISA Kits)-mediated metabolic cues
Loss of CD69 is associated with enhanced protection against vaccinia virus infection.
The data highlight the contribution of CD69 as a nonredundant key regulator of BIC/miR (show MLXIP ELISA Kits)-155-dependent regulatory T cell development and homeostasis.
Data show that after tumor necrosis factor alpha-induced protein 8 like-2 (TIPE2 (show TNFAIP8L2 ELISA Kits)) gene was down-regulated, the expression of the CD69 antigen was increased, and the proliferation of T lymphocytes and the secretion of cytokines IL-2 (show IL2 ELISA Kits) and IFN-gamma (show IFNG ELISA Kits) were enhanced.
The generation of cancer-specific CD8 (show CD8A ELISA Kits)(+) CD69(+)-expressing lymphocytes that inhibit colon cancer growth has been described.
Maintenance of immune tolerance by Foxp3 (show FOXP3 ELISA Kits)+ regulatory T cells requires CD69 expression.
AIM(-/-) mice were highly susceptible to steatosis-associated HCC (show FAM126A ELISA Kits) development, whereas no AIM(+/+) mouse developed the disease despite comparable liver inflammation and fibrosis in response to a long-term high-fat diet.
CD69 interference with S1P1 (show S1PR1 ELISA Kits) function regulates peripheral T cell retention.
Higher CD69 expression were less sensitive to bendamustine and is associated with chronic lymphocytic leukemia.
In vitro functional assays showed that CD69(+) Treg cells exerted an important suppressive effect on the activation of T effector cells
results demonstrate the functional and mechanistic interplays between CD69 and S100A8 (show S100A8 ELISA Kits)/S100A9 (show S100A9 ELISA Kits) in supporting Treg-cell differentiation
Elevated expression of CD69 and CD161 (show KLRB1 ELISA Kits) on NK cells can be considered as immunological risk markers in RSA and IVF (show SCN5A ELISA Kits) failure.
Human tumor-infiltrating CD4 (show CD4 ELISA Kits)+CD69+ T cells suppress T cell proliferation via membarene -bound TGF-beta1 (show TGFB1 ELISA Kits).
these findings identify CD69 and galectin-1 (show LGALS1 ELISA Kits) to be a novel regulatory receptor-ligand pair that modulates Th17 effector cell differentiation and function.
REVIEW: CD69 exerts a complex immunoregulatory role in humans, and that it could be considered as a target molecule for the therapy of immune-mediated diseases
Following coculture with GTKO/CD46 (show CD46 ELISA Kits) pig mesenchymal stromal cells, it is possible that upregulation of CD69 on human T cells initiates signaling events that would regulate CD4 (show CD4 ELISA Kits)+ and CD8 (show CD8A ELISA Kits)+ T cell activation and differentiation.
In patients with allergic rhinitis CD69 antigen is overexpressed on human peripheral blood natural killer cells reflecting their activation status.
This is the first report of the regulation of CD69 expression by LMP-1 (show PDLIM7 ELISA Kits), and this novel finding may, thus, represent an important link between the EBV oncoprotein LMP-1 (show PDLIM7 ELISA Kits) and its critical role in the development of EBV-associated diseases.
This gene encodes a member of the calcium dependent lectin superfamily of type II transmembrane receptors. Expression of the encoded protein is induced upon activation of T lymphocytes, and may play a role in proliferation. Furthermore, the protein may act to transmit signals in natural killer cells and platelets.
, early activation antigen CD69
, Very Early Activation Antigen
, C-type lectin domain family 2, member C
, CD69 antigen (p60, early T-cell activation antigen)
, activation inducer molecule (AIM/CD69)
, early T-cell activation antigen p60
, early lymphocyte activation antigen
, leukocyte surface antigen Leu-23