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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 CCL3gene.[1]
Sherry et al. (1988) demonstrated 2 protein components of MIP1, called by them alpha (CCL3, this protein) and beta (CCL4).[3][1]
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.[4]
Interactions
CCL3 has been shown to interact with CCL4.[5]
Attracts macrophages, monocytes and neutrophils.
↑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. PMID11278300.
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. PMID15142381.
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. PMID15638726.
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. PMID15817944.
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. PMID16354571.
