UniProt functional annotation for P17927



	UniProt functional annotation for P17927

UniProt code: P17927.

Organism: Homo sapiens (Human).

Taxonomy: Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo.

Function: Membrane immune adherence receptor that plays a critical role in the capture and clearance of complement-opsonized pathogens by erythrocytes and monocytes/macrophages (PubMed:2963069). Mediates the binding by these cells of particles and immune complexes that have activated complement to eliminate them from the circulation (PubMed:2963069). Acts also in the inhibition of spontaneous complement activation by impairing the formation and function of the alternative and classical pathway C3/C5 convertases, and by serving as a cofactor for the cleavage by factor I of C3b to iC3b, C3c and C3d,g, and of C4b to C4c and C4d (PubMed:2972794, PubMed:8175757). Plays also a role in immune regulation by contributing, upon ligand binding, to the generation of regulatory T cells from activated helper T cells (PubMed:25742728). {ECO:0000269|PubMed:25742728, ECO:0000269|PubMed:2963069, ECO:0000269|PubMed:2972794, ECO:0000269|PubMed:8175757}.

Function: (Microbial infection) Acts as a receptor for Epstein-Barr virus. {ECO:0000269|PubMed:23416052}.

Subunit: Interacts (via Sushi 1 and Sushi 2 domains) with complement factor C4b (PubMed:2972794, PubMed:8175757). Interacts (via Sushi 8 and Sushi 9 domains) with complement factor C3b (PubMed:2972794, PubMed:8175757). Interacts (via Sushi 24 and Sushi 25 domains) with MBL2 (PubMed:23460739, PubMed:29563915). Interacts with FCN2 (PubMed:2972794). Interacts (via Sushi 24 and Sushi 25 domains) with C1QA (PubMed:9324355, PubMed:29563915). {ECO:0000269|PubMed:23460739, ECO:0000269|PubMed:29563915, ECO:0000269|PubMed:2972794, ECO:0000269|PubMed:8175757, ECO:0000269|PubMed:9324355}.

Subunit: (Microbial infection) Interacts with Epstein-Barr virus gp350. {ECO:0000269|PubMed:23460739}.

Subcellular location: Membrane {ECO:0000269|PubMed:1385479}; Single- pass type I membrane protein.

Tissue specificity: Present on erythrocytes, a subset of T cells, mature B cells, follicular dendritic cells, monocytes and granulocytes. {ECO:0000269|PubMed:1534036, ECO:0000269|PubMed:25742728, ECO:0000269|PubMed:6233222}.

Polymorphism: CR1 contains a system of antigens called the Knops blood group system. Polymorphisms within this system are involved in malarial rosetting, a process associated with cerebral malaria, the major cause of mortality in Plasmodium falciparum malaria. Common Knops system antigens include McCoy (McC) and Sl(a)/Vil (Kn4, or Swain-Langley; Vil or Villien). Sl(a-) phenotype is more common in persons of African descent and may protect against fatal malaria.

Polymorphism: Other polymorphic forms of CR1 contain 23, 37 or 44 Sushi (CCP/SCR) domains instead of the 30 Sushi (CCP/SCR) domains. The most frequent alleles are the F allotype (shown here) and the S allotype (37 repeat Sushi domains). The gene frequencies of the F allotype and S allotype are 0.87 and 0.11 in Caucasians, 0.82 and 0.11 in African Americans, 0.89 and 0.11 in Mexicans.

Polymorphism: Genetic variations in CR1 resulting in CR1 deficiency are involved in protection against severe malaria [MIM:611162]. Parasitized red blood cells (RBCs) from children suffering from severe malaria often adhere to complement receptor 1 (CR1) on uninfected RBCs to form clumps of cells known as rosettes. CR1-deficient red blood cells show greatly reduced rosetting and CR1 deficiency occurs in healthy individuals from malaria-endemic regions.

Similarity: Belongs to the receptors of complement activation (RCA) family. {ECO:0000305}.

Annotations taken from UniProtKB at the EBI.


Organism:		Homo sapiens (Human).
Taxonomy:		Eukaryota; Metazoa; Chordata; Craniata; Vertebrata; Euteleostomi; Mammalia; Eutheria; Euarchontoglires; Primates; Haplorrhini; Catarrhini; Hominidae; Homo.



Function:		Membrane immune adherence receptor that plays a critical role in the capture and clearance of complement-opsonized pathogens by erythrocytes and monocytes/macrophages (PubMed:2963069). Mediates the binding by these cells of particles and immune complexes that have activated complement to eliminate them from the circulation (PubMed:2963069). Acts also in the inhibition of spontaneous complement activation by impairing the formation and function of the alternative and classical pathway C3/C5 convertases, and by serving as a cofactor for the cleavage by factor I of C3b to iC3b, C3c and C3d,g, and of C4b to C4c and C4d (PubMed:2972794, PubMed:8175757). Plays also a role in immune regulation by contributing, upon ligand binding, to the generation of regulatory T cells from activated helper T cells (PubMed:25742728). {ECO:0000269\|PubMed:25742728, ECO:0000269\|PubMed:2963069, ECO:0000269\|PubMed:2972794, ECO:0000269\|PubMed:8175757}.



Function:		(Microbial infection) Acts as a receptor for Epstein-Barr virus. {ECO:0000269\|PubMed:23416052}.


Subunit:		Interacts (via Sushi 1 and Sushi 2 domains) with complement factor C4b (PubMed:2972794, PubMed:8175757). Interacts (via Sushi 8 and Sushi 9 domains) with complement factor C3b (PubMed:2972794, PubMed:8175757). Interacts (via Sushi 24 and Sushi 25 domains) with MBL2 (PubMed:23460739, PubMed:29563915). Interacts with FCN2 (PubMed:2972794). Interacts (via Sushi 24 and Sushi 25 domains) with C1QA (PubMed:9324355, PubMed:29563915). {ECO:0000269\|PubMed:23460739, ECO:0000269\|PubMed:29563915, ECO:0000269\|PubMed:2972794, ECO:0000269\|PubMed:8175757, ECO:0000269\|PubMed:9324355}.
Subunit:		(Microbial infection) Interacts with Epstein-Barr virus gp350. {ECO:0000269\|PubMed:23460739}.
Subcellular location:		Membrane {ECO:0000269\|PubMed:1385479}; Single- pass type I membrane protein.
Tissue specificity:		Present on erythrocytes, a subset of T cells, mature B cells, follicular dendritic cells, monocytes and granulocytes. {ECO:0000269\|PubMed:1534036, ECO:0000269\|PubMed:25742728, ECO:0000269\|PubMed:6233222}.
Polymorphism:		CR1 contains a system of antigens called the Knops blood group system. Polymorphisms within this system are involved in malarial rosetting, a process associated with cerebral malaria, the major cause of mortality in Plasmodium falciparum malaria. Common Knops system antigens include McCoy (McC) and Sl(a)/Vil (Kn4, or Swain-Langley; Vil or Villien). Sl(a-) phenotype is more common in persons of African descent and may protect against fatal malaria.
Polymorphism:		Other polymorphic forms of CR1 contain 23, 37 or 44 Sushi (CCP/SCR) domains instead of the 30 Sushi (CCP/SCR) domains. The most frequent alleles are the F allotype (shown here) and the S allotype (37 repeat Sushi domains). The gene frequencies of the F allotype and S allotype are 0.87 and 0.11 in Caucasians, 0.82 and 0.11 in African Americans, 0.89 and 0.11 in Mexicans.
Polymorphism:		Genetic variations in CR1 resulting in CR1 deficiency are involved in protection against severe malaria [MIM:611162]. Parasitized red blood cells (RBCs) from children suffering from severe malaria often adhere to complement receptor 1 (CR1) on uninfected RBCs to form clumps of cells known as rosettes. CR1-deficient red blood cells show greatly reduced rosetting and CR1 deficiency occurs in healthy individuals from malaria-endemic regions.
Similarity:		Belongs to the receptors of complement activation (RCA) family. {ECO:0000305}.