CR2
CR2 (Complement C3d Receptor 2) is a Protein Coding gene. Diseases associated with CR2 include Immunodeficiency, Common Variable, 7 and Systemic Lupus Erythematosus 9. Among its related pathways are Complement and coagulation cascades and 4-1BB Pathway. Gene Ontology (GO) annotations related to this gene include protein homodimerization activity and transmembrane signaling receptor activity. An important paralog of this gene is CR1.
Full Name
Complement C3d Receptor 2
Alternative Names
Complement C3d Receptor 2; Complement Component (3d/Epstein Barr Virus) Receptor 2; Complement Component 3d Receptor 2; Epstein-Barr Virus Receptor; EBV Receptor; C3DR; Complement Receptor Type 2; Complement C3d Receptor;
Function
Receptor for complement C3, for the Epstein-Barr virus on human B-cells and T-cells and for HNRNPU (PubMed:7753047).
Participates in B lymphocytes activation (PubMed:7753047).
(Microbial infection) Acts as a receptor for Epstein-Barr virus.
Biological Process
B cell differentiation Source: UniProtKB
B cell proliferation Source: UniProtKB
Complement activation, alternative pathway Source: ARUK-UCL
Complement activation, classical pathway Source: UniProtKB-KW
Immune response Source: UniProtKB
Regulation of complement activation Source: Reactome
Cellular Location
Cell membrane
Involvement in disease
Systemic lupus erythematosus 9 (SLEB9):
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.
Immunodeficiency, common variable, 7 (CVID7):
A primary immunodeficiency characterized by antibody deficiency, hypogammaglobulinemia, recurrent bacterial infections and an inability to mount an antibody response to antigen. The defect results from a failure of B-cell differentiation and impaired secretion of immunoglobulins; the numbers of circulating B-cells is usually in the normal range, but can be low.
Topology
Extracellular: 21-971
Helical: 972-999
Cytoplasmic: 1000-1033
Loading...
Datasheet