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]
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.
CCL3 | |||||||||||||||||||||||||||||||||||||||||||||||||||
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Aliases | CCL3, G0S19-1, LD78ALPHA, MIP-1-alpha, MIP1A, SCYA3, C-C motif chemokine ligand 3 | ||||||||||||||||||||||||||||||||||||||||||||||||||
External IDs | OMIM: 182283 HomoloGene: 88430 GeneCards: CCL3 | ||||||||||||||||||||||||||||||||||||||||||||||||||
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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]
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.