|CD191|| CCR1 (chemokine [CC motif] receptor 1) (*See available information under CD CKR), CC-CKR-1|
|Molecule Type||Antigen Expression||Molecular Weight|
Min / Max
|Non-lineage Restricted Molecule|
Type 3 glycoprotein, 7 span
|41 / 41|
|CD191 is expressed on T cells, monocytes, macrophages, NK cells, T lymphocytes, dendritic cells, hematopoietic cells and stem cell subsets. High levels of expression are found among T cell memory cells. Expression is show at low levels in most tissues and not in B cells and granulocytes. mRNA expression data show low levels in most tissues with a high level in caudate nucleus.|
MOLECULAR FAMILY NAME: Belongs to the chemokine receptor family.
|LIGANDS AND MOLECULE ASSOCIATED WITH CD191|
The ligands of the chemokine receptor include MIP-1α, RANTES, MCP-3 and MPIF-1.
|CD191 is a member of the β chemokine receptor family and mediates the effects of its several chemokine ligands. Ligand binding causes a calcium flux but the downstream consequences are not known. Chemokines and their receptors mediate signal transduction which are critical for the recruitment of effector immune cells to the site of inflammation. Knockout studies of the mouse homolog suggested the role of CD191 in host protection from inflammatory damage and protection from the susceptibility to viral and parasitic infection. CD191 is involved in leukocyte chemotaxis and appears to be responsible for affecting stem cell proliferation. It is believed that CD191 as well as CD193 (CCR3) regulate T cell and dendritic cells in the process of antigen presentation.|
CD191 binds C-C type chemokines and transducer signals by increasing intracellular calcium ion levels.
DISEASE RELEVANCE AND FUNCTION OF CD191 IN INTACT ANIMAL
A knockout mouse model suggests that CD191 provides a degree of protection from inflammatory damage and protection from parasitic and viral infection.
PROTEINS AND DNA ELEMENTS WHICH REGULATE TRANSCRIPTION OF CD191: No information.
SUBSTRATES: No information.
ENZYMES WHICH MODIFY CD191: No information.
For further information see Sato, K. et al (1999) Blood 93: 34-42.
Database accession numbers
Revised June 25, 2008