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Publication : Molecular cloning and posttranscriptional regulation of macrophage inflammatory protein-1 alpha in alveolar macrophages.

First Author  Shi MM Year  1995
Journal  Biochem Biophys Res Commun Volume  211
Issue  1 Pages  289-95
PubMed ID  7779098 Mgi Jnum  J:25962
Mgi Id  MGI:73666 Doi  10.1006/bbrc.1995.1809
Citation  Shi MM, et al. (1995) Molecular cloning and posttranscriptional regulation of macrophage inflammatory protein-1 alpha in alveolar macrophages. Biochem Biophys Res Commun 211(1):289-95
abstractText  Macrophage inflammatory protein-1 alpha (MIP-1 alpha) belongs to the chemokine superfamily of chemoattractant pro-inflammatory cytokines. MIP-1 alpha is chemotactic for monocytes and neutrophils and thus, plays an important role in initiation and control of inflammation. We have isolated and sequenced a cDNA clone encoding rat MIP-1 alpha. This 0.75 kb cDNA includes a single open reading frame of 92 amino acids. Expression of MIP-1 alpha mRNA was characterized in NR8383, a rat alveolar macrophage cell line (RAM). In resting RAM cells, MIP-1 alpha mRNA decayed rapidly, with a half life of less than 2 hours. Lipopolysaccharide (LPS) treatment of RAM cells resulted in a dose-dependent increase in MIP-1 alpha steady state mRNA expression. The induction of MIP-1 alpha mRNA by LPS was partially the result of mRNA stabilization, as half life increased to over 6 hours.
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