CCL2

CCL2 (C-C Motif Chemokine Ligand 2) is a Protein Coding gene, and is affiliated with the lncRNA class. Diseases associated with CCL2 include Neural Tube Defects and Human Immunodeficiency Virus Type 1. Among its related pathways are Ectoderm Differentiation and PEDF Induced Signaling. Gene Ontology (GO) annotations related to this gene include protein kinase activity and heparin binding. An important paralog of this gene is CCL7.

C-C Motif Chemokine Ligand 2

Acts as a ligand for C-C chemokine receptor CCR2 (PubMed:9837883, PubMed:10587439, PubMed:10529171).
Signals through binding and activation of CCR2 and induces a strong chemotactic response and mobilization of intracellular calcium ions (PubMed:9837883, PubMed:10587439).
Exhibits a chemotactic activity for monocytes and basophils but not neutrophils or eosinophils (PubMed:8627182, PubMed:9792674, PubMed:8195247).
May be involved in the recruitment of monocytes into the arterial wall during the disease process of atherosclerosis (PubMed:8107690).

Angiogenesis Source: BHF-UCL
Animal organ morphogenesis Source: ProtInc
Astrocyte cell migration Source: BHF-UCL
Cell adhesion Source: ProtInc
Cell surface receptor signaling pathway Source: ProtInc
Cellular homeostasis Source: BHF-UCL
Cellular response to fibroblast growth factor stimulus Source: UniProtKB
Cellular response to interferon-gamma Source: UniProtKB
Cellular response to interleukin-1 Source: UniProtKB
Cellular response to lipopolysaccharide Source: BHF-UCL
Cellular response to organic cyclic compound Source: UniProtKB
Cellular response to tumor necrosis factor Source: UniProtKB
Chemokine-mediated signaling pathway Source: GO_Central
Chemotaxis Source: ProtInc
Cytokine-mediated signaling pathway Source: BHF-UCL
Cytoskeleton organization Source: UniProtKB
Eosinophil chemotaxis Source: GO_Central
G protein-coupled receptor signaling pathway Source: GO_Central
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger Source: ProtInc
Helper T cell extravasation Source: BHF-UCL
Humoral immune response Source: ProtInc
Inflammatory response Source: UniProtKB
Lipopolysaccharide-mediated signaling pathway Source: UniProtKB
Lymphocyte chemotaxis Source: GO_Central
Macrophage chemotaxis Source: BHF-UCL
MAPK cascade Source: UniProtKB
Monocyte chemotaxis Source: BHF-UCL
Negative regulation of G1/S transition of mitotic cell cycle Source: BHF-UCL
Negative regulation of glial cell apoptotic process Source: UniProtKB
Negative regulation of natural killer cell chemotaxis Source: UniProtKB
Negative regulation of neuron apoptotic process Source: UniProtKB
Negative regulation of vascular endothelial cell proliferation Source: BHF-UCL
Neutrophil chemotaxis Source: GO_Central
PERK-mediated unfolded protein response Source: Reactome
Positive regulation of apoptotic cell clearance Source: BHF-UCL
Positive regulation of calcium ion import Source: BHF-UCL
Positive regulation of endothelial cell apoptotic process Source: BHF-UCL
Positive regulation of ERK1 and ERK2 cascade Source: GO_Central
Positive regulation of GTPase activity Source: GO_Central
Positive regulation of nitric-oxide synthase biosynthetic process Source: BHF-UCL
Positive regulation of NMDA glutamate receptor activity Source: ARUK-UCL
Positive regulation of synaptic transmission, glutamatergic Source: UniProtKB
Positive regulation of T cell activation Source: BHF-UCL
Protein kinase B signaling Source: UniProtKB
Protein phosphorylation Source: ProtInc
Receptor signaling pathway via JAK-STAT Source: ProtInc
Regulation of cell shape Source: UniProtKB
Response to bacterium Source: BHF-UCL
Sensory perception of pain Source: UniProtKB
Signal transduction Source: ProtInc
Viral genome replication Source: ProtInc

Secreted

Processing at the N-terminus can regulate receptor and target cell selectivity (PubMed:8627182). Deletion of the N-terminal residue converts it from an activator of basophil to an eosinophil chemoattractant (PubMed:8627182).
N-Glycosylated.