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GPR183 was identified by the up-regulation of its expression upon Epstein-Barr virus infection of primary B lymphocytes. Additionally we are shipping GPR183 Proteins (4) and many more products for this protein.
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Inhibition of Gpr183 significantly upregulates Notch (show NOTCH1 Antibodies) signaling and abolishes embryonic hematopoietic stem and progenitor cells emergence.
this study concludes that EBI2 expression is directly influenced by EBV infection and that BRRF1 is necessary and sufficient for EBI2 upregulation during infection.
These results demonstrate a role for EBI2 in astrocyte function and suggest that modulation of this receptor may be beneficial in neuroinflammatory disorders.
EBI2 is expressed in primary human monocytes and macrophages.
This model of ligand docking yields important structural insight into the molecular mechanisms mediating EBI2 function.
Data indicate that EBI2 expression modulates CXCL13 (show CXCL13 Antibodies) binding affinity to CXCR5 (show CXCR5 Antibodies).
Molecular characterization of oxysterol binding to the Epstein-Barr virus-induced gene 2 (GPR183).
Based on the constitutive signaling and cellular expression pattern of EBI2, it is suggested that it may function in conjunction with BILF1 in the reprogramming of the cell during EBV infection
Structural motifs of importance for the constitutive activity of EBI2: analysis of receptor activation in the absence of an agonist.
mice lacking EBI2 in T cells or CD25 (show IL2RA Antibodies) in dendritic cells have reduced T follicular helper cells and mount defective T-cell-dependent plasma cell and germinal centre responses
findings establish an essential role for EBI2 in CD4 (show CD4 Antibodies)(+) DC positioning and homeostasis and in facilitating capture and presentation of blood-borne particulate antigens
EBI2 is a negative regulator of type I interferons in plasmacytoid and myeloid dendritic cells.
Regulated expression of EBI2 on DC populations is therefore critical for the generation and correct positioning of splenic DCs and the initiation of immune responses.
Regulation of B cell migration by EBI2 has an important role in controlling the positioning of activated B cells within lymphoid follicles in the early phases of B cell responses during cell differentiation and affinity maturation.
These findings establish a role for EBI2 in helping control B cell position at multiple stages during the Ab response
ligand targeting EBI2. In turn, this molecule provides a useful tool for further characterization of EBI2 as well as serving as a potent lead compound.
important role for EBI2 in promoting B cell localization in the outer follicle, and show that differential expression of this receptor helps position B cells appropriately for mounting T-dependent antibody responses
EBI2 provides a previously uncharacterized dimension to B (show TDO2 Antibodies) cell migration that is crucial for coordinating rapid versus long-term antibody responses.
This gene was identified by the up-regulation of its expression upon Epstein-Barr virus infection of primary B lymphocytes. This gene is predicted to encode a G protein-coupled receptor that is most closely related to the thrombin receptor. Expression of this gene was detected in B-lymphocyte cell lines and lymphoid tissues but not in T-lymphocyte cell lines or peripheral blood T lymphocytes. The function of this gene is unknown.
G protein-coupled receptor 183
, EBV-induced G protein-coupled receptor 2
, Epstein-Barr virus induced gene 2 (lymphocyte-specific G protein-coupled receptor)
, G-protein coupled receptor 183
, Epstein-Barr virus induced gene 2
, G-protein coupled receptor 183-A
, G-protein coupled receptor 183-like
, EBV-induced G-protein coupled receptor 2
, epstein-Barr virus-induced G-protein coupled receptor 2
, EBV-induced G-protein coupled receptor 2 homolog