Genomic organization of the CC chemokine MIP-3 α/CCL20/LARC/EXODUS/SCYA20, showing gene structure, splice variants, and chromosome localization
Date
2001
Authors
Nelson, R.
Boyd, J.
Gladue, R.
Paradis, T.
Thomas, R.
Cunningham, A.
Lira, P.
Brissette, W.
Hayes, L.
Hames, L.
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Journal article
Citation
Genomics, 2001; 73(1):28-37
Statement of Responsibility
Robin T. Nelson, James Boyd, Ronald P. Gladue, Timothy Paradis, Ranjeny Thomas, Ann C. Cunningham, Paul Lira, William H. Brissette, Lisa Hayes, Lynn M. Hames, Kuldeep S. Neote and Shaun R. McColl
Conference Name
Abstract
We describe the genomic organization of a recently identified CC chemokine, MIP3α/CCL20 (HGMW-approved symbol SCYA20). The MIP-3α/CCL20 gene was cloned and sequenced, revealing a four exon, three intron structure, and was localized by FISH analysis to 2q35–q36. Two distinct cDNAs were identified, encoding two forms of MIP-3α/CCL20, Ala MIP-3α/CCL20 and Ser MIP-3α/CCL20, that differ by one amino acid at the predicted signal peptide cleavage site. Examination of the sequence around the boundary of intron 1 and exon 2 showed that use of alternative splice acceptor sites could give rise to Ala MIP-3α/CCL20 or Ser MIP-3α/CCL20. Both forms of MIP-3α/CCL20 were chemically synthesized and tested for biological activity. Both flu antigen plus IL-2-activated CD4+ and CD8+ T lymphoblasts and cord blood-derived dendritic cells responded to Ser and Ala MIP-3α/CCL20. T lymphocytes exposed only to IL-2 responded inconsistently, while no response was detected in naive T lymphocytes, monocytes, or neutrophils. The biological activity of Ser MIP-3α/CCL20 and Ala MIP-3α/CCL20 and the tissue-specific preference of different splice acceptor sites are not yet known.
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Copyright © 2001 Academic Press. All rights reserved.