Anti-Ccl3 Antibody Fluoro488 Conjugated

Macrophage inflammatory protein-1 alpha (MIP-1 alpha), also called CCL3, LD78. The cDNA for CCL3 predicts a mature peptide of 69 amino acids with a molecular mass of 7,889 daltons. CCL3 is a member of a newly identified superfamily of small inducible proteins involved in inflammatory responses, wound healing and tumorigenesis. CCL3 is a chemokine that has pro-inflammatory and stem cell inhibitory activities in vitro. It constitutes an important second signal for mast cell degranulation in the conjunctiva in vivo and consequently for acute-phase disease.

Expressed in the brain, with expression in the hippocampus, the neuropil in the dentate gyrus, where expression is higher in the outer half of the molecular layer than in the inner half, and in the neuropil of CA4 and CA3.

Atherosclerosis, Cardiovascular, Cell Biology, Drug Metabolism, Heart Disease, Metabolic Signaling Pathways, Metabolism, Oxidative Stress, Pathways and Processes, Redox Metabolism, Signal Transduction, Vascular Inflammation

Lineage-defining transcription factor which initiates Th1 lineage development from naive Th precursor cells both by activating Th1 genetic programs and by repressing the opposing Th2 and Th17 genetic programs. Activates transcription of a set of genes important for Th1 cell function, including those encoding IFN-gamma and the chemokine receptor CXCR3. Activates IFNG and CXCR3 genes in part by recruiting chromatin remodeling complexes including KDM6B, a SMARCA4-containing SWI/SNF-complex, and an H3K4me2-methyltransferase complex to their promoters and all of these complexes serve to establish a more permissive chromatin state conducive with transcriptional activation. Can activate Th1 genes also via recruitment of Mediator complex and P-TEFb (composed of CDK9 and CCNT1/cyclin-T1) in the form of the super elongation complex (SEC) to super-enhancers and associated genes in activated Th1 cells. Inhibits the Th17 cell lineage commitment by blocking RUNX1-mediated transactivation of Th17 cell-specific transcriptinal regulator RORC. Inhibits the Th2 cell lineage commitment by suppressing the production of Th2 cytokines, such as IL-4, IL-5, and IL- 13, via repression of transcriptional regulators GATA3 and NFATC2. Protects Th1 cells from amplifying aberrant type-I IFN response in an IFN-gamma abundant microenvironment by acting as a repressor of type-I IFN transcription factors and type-I IFN-stimulated genes. Acts as a regulator of antiviral B-cell responses; controls chronic viral infection by promoting the antiviral antibody IgG2a isotype switching and via regulation of a broad antiviral gene expression program.

1. Cook, D. N.; Beck, M. A.; Coffman, T. M.; Kirby, S. L.; Sheridan, J. F.; Pragnell, I. B.; Smithies, O. Requirement of MIP-1-alpha for an inflammatory response to viral infection. Science 269: 1583-1585, 1995. 2. Miyazaki, D.; Nakamura, T.; Toda, M.; Cheung-Chau, K.-W.; Richardson, R. M.; Ono, S. J. Macrophage inflammatory protein-1-alpha as a costimulatory signal for mast cell-mediated immediate hypersensitivity reactions. J. Clin. Invest. 115: 434-442, 2005. 3. Nakao, M.; Nomiyama, H.; Shimada, K. Structures of human genes coding for cytokine LD78 and their expression. Molec. Cell. Biol. 10: 3646-3658, 1990. 4. Wolpe, S. D.; Cerami, A. Macrophage inflammatory proteins 1 and 2: members of a novel superfamily of cytokines. FASEB J. 3: 2565-2573, 1989.