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J. Biol. Chem., Vol. 277, Issue 48, 46822-46830, November 29, 2002

This Article Full Text Full Text (PDF) All Versions of this Article: 277/48/46822    most recent M206299200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted 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 Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Ray, B. K. Articles by Ray, A. Search for Related Content PubMed PubMed Citation Articles by Ray, B. K. Articles by Ray, A. Social Bookmarking                      What's this?

SAF-2, a Splice Variant of SAF-1, Acts as a Negative Regulator of Transcription^*

Bimal K. Ray, Ryan Murphy, Papiya Ray, and Alpana Ray

From the Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri 65211

Serum amyloid A-activating factor-1 (SAF-1), a Cys₂His₂-type zinc finger transcription factor, regulates inflammation-induced expression of serum amyloid A protein that is linked to the pathogenesis of reactive amyloidosis, rheumatoid arthritis, and atherosclerosis. Here we report the identification of a novel splice variant, SAF-2, of the SAF family bearing strong sequence similarity to SAF-1. The N-terminal 426 amino acids of both SAF-1 and SAF-2 are identical containing two polyalanine tracts, one proline-rich domain, and six zinc fingers. However, the C terminus of SAF-2 containing two additional zinc fingers is different from SAF-1, which indicates the capability of different biochemical function. We show that SAF-2 interacts more avidly with the SAF-binding element, but its transactivation potential is much lower than SAF-1. Furthermore, co-expression of SAF-2 markedly suppresses SAF-1-regulated promoter function. Finally, we show that the level of SAF-2 protein is reduced during many inflammatory conditions, whereas the SAF-1 protein level remains unchanged. Together, these data suggest that the relative abundance of SAF-2 plays a critical role in the fine tuned regulation of inflammation-responsive genes that are controlled by SAF-1.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBank^TM/EBI Data Bank with accession number(s) AF489858.

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				A. Ray, A. Shakya, D. Kumar, M. D. Benson, and B. K. Ray Inflammation-Responsive Transcription Factor SAF-1 Activity Is Linked to the Development of Amyloid A Amyloidosis J. Immunol., August 15, 2006; 177(4): 2601 - 2609. [Abstract] [Full Text] [PDF]

				A. Ray, A. Shakya, D. Kumar, and B. K. Ray Overexpression of Serum Amyloid A-Activating Factor 1 Inhibits Cell Proliferation by the Induction of Cyclin-Dependent Protein Kinase Inhibitor p21WAF-1/Cip-1/Sdi-1 Expression J. Immunol., April 15, 2004; 172(8): 5006 - 5015. [Abstract] [Full Text] [PDF]