SCUBA

CX3CR1 — C-X3-C motif chemokine receptor 1

CX3CR1 belongs to a gene co-expression module in 3 of 28 SCUBA cell types. Each module groups genes that rise and fall together in that cell type; the genes it shares a module with are its closest co-expression partners there.

CX3CR1's module in each cell type

Cell typeModuleShares the module with
Gamma-delta T cellsCytotoxic Effector Program
cytotoxicity
ADGRG1, ANXA4, CADM1, FCGR3A, FGFBP2, FGL2, GNLY, GZMB +14 more
MonocytesNon-classical Monocyte Migration
Migration & adhesion
ADGRE1, ITGA4, ITGAL, LILRA1, LTB, SCLT1, SH2D3C, UTRNView in SCUBA
Mucosal-associated invariant T cellNK-like Cytotoxic
cytotoxicity
AKR1C3, BNC2, CLIC3, FCGR3A, FGFBP2, GNLY, IGFBP7, KIR3DL1 +3 more

About the gene

SynonymsCCRL1, CMKBRL1, CMKDR1, GPR13, V28
Chromosome3: 39263495-39281735
Predicted locationMembrane
Essential geneNo
Protein classDisease related genes, G-protein coupled receptors, Human disease related genes, Plasma proteins, Potential drug targets, Predicted membrane proteins
Molecular functionG-protein coupled receptor, Receptor, Transducer
Biological processAdaptive immunity, Host-virus interaction, Immunity, Inflammatory response, Innate immunity

Function

Receptor for the C-X3-C chemokine fractalkine (CX3CL1) present on many early leukocyte cells; CX3CR1-CX3CL1 signaling exerts distinct functions in different tissue compartments, such as immune response, inflammation, cell adhesion and chemotaxis. CX3CR1-CX3CL1 signaling mediates cell migratory functions (By similarity). Responsible for the recruitment of natural killer (NK) cells to inflamed tissues (By similarity). Acts as a regulator of inflammation process leading to atherogenesis by mediating macrophage and monocyte recruitment to inflamed atherosclerotic plaques, promoting cell survival (By similarity). Involved in airway inflammation by promoting interleukin 2-producing T helper (Th2) cell survival in inflamed lung (By similarity). Involved in the migration of circulating monocytes to non-inflamed tissues, where they differentiate into macrophages and dendritic cells (By similarity). Acts as a negative regulator of angiogenesis, probably by promoting macrophage chemotaxis. Plays a key role in brain microglia by regulating inflammatory response in the central nervous system (CNS) and regulating synapse maturation (By similarity). Required to restrain the microglial inflammatory response in the CNS and the resulting parenchymal damage in response to pathological stimuli (By similarity). Involved in brain development by participating in synaptic pruning, a natural process during which brain microglia eliminates extra synapses during postnatal development (By similarity). Synaptic pruning by microglia is required to promote the maturation of circuit connectivity during brain development (By similarity). Acts as an important regulator of the gut microbiota by controlling immunity to intestinal bacteria and fungi (By similarity). Expressed in lamina propria dendritic cells in the small intestine, which form transepithelial dendrites capable of taking up bacteria in order to provide defense against pathogenic bacteria (By similarity). Required to initiate innate and adaptive immune responses against dissemination of commensal fungi (mycobiota) component of the gut: expressed in mononuclear phagocytes (MNPs) and acts by promoting induction of antifungal IgG antibodies response to confer protection against disseminated C.albicans or C.auris infection. Also acts as a receptor for C-C motif chemokine CCL26, inducing cell chemotaxis. (Microbial infection) Acts as a coreceptor with CD4 for HIV-1 virus envelope protein. (Microbial infection) Acts as a coreceptor with CD4 for HIV-1 virus envelope protein. May have more potent HIV-1 coreceptothr activity than isoform 1. (Microbial infection) Acts as a coreceptor with CD4 for HIV-1 virus envelope protein. May have more potent HIV-1 coreceptor activity than isoform 1

Human Protein Atlas · Open Targets · UniProt

Gene annotation from the Human Protein Atlas and UniProt; see sources & licences.