Chemokine (C-C motif) ligand 3 (CCL3) also known as macrophage inflammatory protein 1-alpha (MIP-1-alpha) is a protein that in humans is encoded by the CCL3 gene.^[3]

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CCL3
Available structures PDB Human UniProt search: PDBe RCSB List of PDB id codes 1B50, 1B53, 2X69, 2X6G, 3FPU, 3H44, 3KBX, 4RA8, 4ZKB, 5D65, 5COR
Identifiers
Aliases	CCL3, G0S19-1, LD78ALPHA, MIP-1-alpha, MIP1A, SCYA3, C-C motif chemokine ligand 3
External IDs	OMIM: 182283 HomoloGene: 88430 GeneCards: CCL3
Gene location (Human) Chr. Chromosome 17 (human)[1] Band 17q12 Start 36,088,256 bp[1] End 36,090,169 bp[1]
RNA expression pattern Bgee Human Mouse (ortholog) Top expressed in bone marrow spleen monocyte bone marrow cells gallbladder placenta lymph node appendix blood upper lobe of left lung n/a More reference expression data BioGPS More reference expression data
Gene ontology Molecular function protein kinase activity cytokine activity CCR5 chemokine receptor binding chemokine activity CCR1 chemokine receptor binding kinase activity phospholipase activator activity calcium-dependent protein kinase C activity protein binding identical protein binding chemoattractant activity CCR chemokine receptor binding Cellular component cytoplasm cytosol intracellular anatomical structure extracellular region extracellular space Biological process G protein-coupled receptor signaling pathway signaling negative regulation of bone mineralization positive regulation of protein kinase B signaling release of sequestered calcium ion into cytosol by sarcoplasmic reticulum response to cholesterol positive regulation of calcium-mediated signaling regulation of sensory perception of pain protein kinase B signaling monocyte chemotaxis negative regulation of osteoclast differentiation astrocyte cell migration positive regulation of cell migration positive regulation of natural killer cell chemotaxis chemokine-mediated signaling pathway T cell chemotaxis cell-cell signaling cellular response to tumor necrosis factor eosinophil chemotaxis cellular response to organic cyclic compound cellular calcium ion homeostasis negative regulation of gene expression neutrophil chemotaxis cell activation MAPK cascade chemotaxis positive regulation of GTPase activity positive regulation of neuron apoptotic process positive regulation of calcium ion import macrophage chemotaxis positive regulation of gene expression cytoskeleton organization osteoblast differentiation cellular response to interleukin-1 immune response positive regulation of ERK1 and ERK2 cascade regulation of cell shape positive regulation of tumor necrosis factor production cellular response to interferon-gamma lymphocyte chemotaxis inflammatory response granulocyte chemotaxis response to toxic substance eosinophil degranulation lipopolysaccharide-mediated signaling pathway calcium ion transport calcium-mediated signaling exocytosis positive regulation of calcium ion transport positive chemotaxis positive regulation of inflammatory response regulation of signaling receptor activity cytokine-mediated signaling pathway regulation of behavior positive regulation of microglial cell activation positive regulation of microglial cell migration Sources:Amigo / QuickGO
Orthologs Species Human Mouse Entrez 6348 n/a Ensembl ENSG00000278567 ENSG00000277632 ENSG00000274221 n/a UniProt P10147 n/a RefSeq (mRNA) NM_002983 n/a RefSeq (protein) NP_002974 n/a Location (UCSC) Chr 17: 36.09 – 36.09 Mb n/a PubMed search [2] n/a
Wikidata
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CCL3 is a cytokine belonging to the CC chemokine family that is involved in the acute inflammatory state in the recruitment and activation of polymorphonuclear leukocytes^[4] through binding to the receptors CCR1, CCR4 and CCR5.^[3]

Sherry et al. (1988) demonstrated 2 protein components of MIP1, called by them alpha (CCL3, this protein) and beta (CCL4).^[5][3]

CCL3 produces a monophasic fever of rapid onset whose magnitude is equal to or greater than that of fevers produced with either recombinant human tumor necrosis factor or recombinant human interleukin-1. However, in contrast to these two endogenous pyrogens, the fever induced by MIP-1 is not inhibited by the cyclooxygenase inhibitor ibuprofen and CCL3 may participate in the febrile response that is not mediated through prostaglandin synthesis and clinically cannot be ablated by cyclooxygenase.^[6]

CCL3 has been shown to interact with CCL4.^[7] Attracts macrophages, monocytes and neutrophils.

• Macrophage inflammatory proteins