CCL3

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 CCL gene.[3]

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 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 • GO:0001948 protein binding • identical protein binding • chemoattractant activity • CCR chemokine receptor binding Cellular component • cytoplasm • cytosol • intracellular • extracellular region • extracellular 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 • GO:0032320, GO:0032321, GO:0032855, GO:0043089, GO:0032854 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 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
View/Edit Human

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.

See also

• Macrophage inflammatory proteins

References

1. ENSG00000277632, ENSG00000274221 GRCh38: Ensembl release 89: ENSG00000278567, ENSG00000277632, ENSG00000274221 - Ensembl, May 2017
2. "Human PubMed Reference:". National Center for Biotechnology Information, U.S. National Library of Medicine.
3. "Entrez Gene: CCL3 chemokine (C-C motif) ligand 3".
4. 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.
5. 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.
6. 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. doi:10.1126/science.2646711. PMID 2646711.
7. 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.

Further reading

• Menten P, Wuyts A, Van Damme J (Dec 2002). "Macrophage inflammatory protein-1". Cytokine & Growth Factor Reviews. 13 (6): 455–81. doi:10.1016/S1359-6101(02)00045-X. PMID 12401480.
• Muthumani K, Desai BM, Hwang DS, Choo AY, Laddy DJ, Thieu KP, Rao RG, Weiner DB (Apr 2004). "HIV-1 Vpr and anti-inflammatory activity". DNA and Cell Biology. 23 (4): 239–47. doi:10.1089/104454904773819824. PMID 15142381.
• Joseph AM, Kumar M, Mitra D (Jan 2005). "Nef: "necessary and enforcing factor" in HIV infection". Current HIV Research. 3 (1): 87–94. doi:10.2174/1570162052773013. PMID 15638726.
• Zhao RY, Elder RT (Mar 2005). "Viral infections and cell cycle G2/M regulation". Cell Research. 15 (3): 143–9. doi:10.1038/sj.cr.7290279. PMID 15780175.
• Zhao RY, Bukrinsky M, Elder RT (Apr 2005). "HIV-1 viral protein R (Vpr) & host cellular responses". The Indian Journal of Medical Research. 121 (4): 270–86. PMID 15817944.
• Li L, Li HS, Pauza CD, Bukrinsky M, Zhao RY (2006). "Roles of HIV-1 auxiliary proteins in viral pathogenesis and host-pathogen interactions". Cell Research. 15 (11–12): 923–34. doi:10.1038/sj.cr.7290370. PMID 16354571.