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Originally published In Press as doi:10.1074/jbc.M300508200 on March 6, 2003

J. Biol. Chem., Vol. 278, Issue 20, 17792-17799, May 16, 2003
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Distinct Functional Interactions of Human Skn-1 Isoforms with Ese-1 during Keratinocyte Terminal Differentiation*

Adriana CabralDagger , David F. FischerDagger §, Wilbert P. Vermeij, and Claude Backendorf

From the Laboratory of Molecular Genetics, Leiden Institute of Chemistry, Leiden University, P. O. Box 9502, 2300 RA Leiden, The Netherlands

Among the three major POU proteins expressed in human skin, Oct-1, Tst-1/Oct-6, and Skn-1/Oct-11, only the latter induced SPRR2A, a marker of keratinocyte terminal differentiation. In this study, we have identified three Skn-1 isoforms, which encode proteins with various N termini, generated by alternative promoter usage. These isotypes showed distinct expression patterns in various skin samples, internal squamous epithelia, and cultured human keratinocytes. Skn-1a and Skn-1d1 bound the SPRR2A octamer site with comparable affinity and functioned as transcriptional activators. Skn-1d2 did not affect SPRR2A expression. Skn-1a, the largest protein, functionally cooperated with Ese-1/Elf-3, an epithelial-specific transcription factor, previously implicated in SPRR2A induction. This cooperativity, which depended on an N-terminal pointed-like domain in Skn-1a, was not found for Skn-1d1. Actually, Skn-1d1 counteracted the cooperativity between Skn-1a and Ese-1. Apparently, the human Skn-1 locus encodes multifunctional protein isotypes, subjected to biochemical cross-talk, which are likely to play a major role in the fine-tuning of keratinocyte terminal differentiation.

* This work was supported by the J. A. Cohen Institute (Leiden) and by European Community Grant BMH4-CT96-0319.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger These authors contributed equally to this work.

§ Present address: Netherlands Institute for Brain Research, Meibergdreef 33, 1105 AZ Amsterdam, The Netherlands.

To whom correspondence should be addressed: Laboratory of Molecular Genetics, Gorlaeus Laboratories, P. O. Box 9502, 2300 RA Leiden, The Netherlands. Tel.: 31-71-527-4409; Fax: 31-71-527-4537; E-mail: backendo@chem.leidenuniv.nl.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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