CCL3

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]
End	36,090,169 bp[1]
RNA expression pattern
	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
	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
	6348
	n/a
	ENSG00000278567; ENSG00000277632; ENSG00000274221
	n/a
	P10147
	n/a
	NM_002983
	n/a
	NP_002974
	n/a
	Wikidata
View/Edit Human

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]

Function

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]

Interactions

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

References

ENSG00000277632, ENSG00000274221 GRCh38: Ensembl release 89: ENSG00000278567, ENSG00000277632, ENSG00000274221 - Ensembl, May 2017
"Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
"Entrez Gene: CCL3 chemokine (C-C motif) ligand 3".
Wolpe SD, Davatelis G, Sherry B, Beutler B, Hesse DG, Nguyen HT, Moldawer LL, Nathan CF, Lowry SF, Cerami A (1988). "Macrophages secrete a novel heparin-binding protein with inflammatory and neutrophil chemokinetic properties". The Journal of Experimental Medicine. 167 (2): 570–81. doi:10.1084/jem.167.2.570. PMC 2188834. PMID 3279154.
Sherry B, Tekamp-Olson P, Gallegos C, Bauer D, Davatelis G, Wolpe SD, Masiarz F, Coit D, Cerami A (1988). "Resolution of the two components of macrophage inflammatory protein 1, and cloning and characterization of one of those components, macrophage inflammatory protein 1 beta". The Journal of Experimental Medicine. 168 (6): 2251–9. doi:10.1084/jem.168.6.2251. PMC 2189160. PMID 3058856.
Davatelis G, Wolpe SD, Sherry B, Dayer JM, Chicheportiche R, Cerami A (1989). "Macrophage inflammatory protein-1: a prostaglandin-independent endogenous pyrogen". Science. 243 (4894 Pt 1): 1066–8. Bibcode:1989Sci...243.1066D. doi:10.1126/science.2646711. PMID 2646711.
Guan E, Wang J, Norcross MA (Apr 2001). "Identification of human macrophage inflammatory proteins 1alpha and 1beta as a native secreted heterodimer". The Journal of Biological Chemistry. 276 (15): 12404–9. doi:10.1074/jbc.M006327200. PMID 11278300.

External links

Human CCL3 genome location and CCL3 gene details page in the UCSC Genome Browser.

CCL3

Function

Interactions

See also

References

External links

Further reading