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J. Biol. Chem., Vol. 277, Issue 47, 45172-45180, November 22, 2002

This Article Full Text Full Text (PDF) All Versions of this Article: 277/47/45172    most recent M204117200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Das, S. Articles by Tsichlis, P. N. Search for Related Content PubMed PubMed Citation Articles by Das, S. Articles by Tsichlis, P. N. Social Bookmarking                      What's this?

Differential Splicing Generates Tvl-1/RFXANK Isoforms with Different Functions^*

Santasabuj Das^§, Jun-Hsiang Lin^¶, Joseph Papamatheakis, Yuri Sykulev, and Philip N. Tsichlis^**

From the  Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, Pennsylvania 19107 and the  Foundation for Research and Technology, Institute of Molecular Biology and Biotechnology, Heraklion, 711 10 Crete, Greece

Earlier studies have shown that Tvl-1 gives rise to at least two differentially spliced mRNAs, one of which (Tvl-S) encodes a protein that lacks amino acids 91-112. DNA binding of RFX complexes assembled in the presence of Tvl-S is impaired. As a result, Tvl-S does not support the expression of Class II major histocompatibility complex (MHC) genes. Here, we show that the reason Tvl-S is inactive as a transcriptional regulator of Class II MHC genes is that the RFX complexes assembled in the presence of Tvl-S are unstable. Additionally, we show that interferon-, which induces Class II MHC gene expression in 293 cells, promotes a shift in the splicing pattern of RFXANK/Tvl-1 toward the transcriptionally active Tvl-L isoform, suggesting that differential splicing of Tvl-1 is a signal-regulated process. Finally, we show that Tvl-1 regulates the expression of non-MHC genes. One such gene encodes the ephrin receptor EphA3. Since both Tvl-L and Tvl-S are identical in their ability to induce the expression of EphA3, we conclude that Tvl-1 regulates the expression of non-MHC genes by RFX-independent mechanisms.

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