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J. Biol. Chem., Vol. 279, Issue 13, 12190-12205, March 26, 2004

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ZNF143 Mediates Basal and Tissue-specific Expression of Human Transaldolase^*

Craig E. Grossman, Yueming Qian, Katalin Banki¶, and Andras Perl||

From the Departments of Medicine, Microbiology and Immunology, and ^¶Pathology, State University of New York, Upstate Medical University, College of Medicine, Syracuse, New York 13210

Transaldolase regulates redox-dependent apoptosis through controlling NADPH and ribose 5-phosphate production via the pentose phosphate pathway. The minimal promoter sufficient to drive chloramphenicol acetyltransferase reporter gene activity was mapped to nucleotides –49 to –1 relative to the transcription start site of the human transaldolase gene. DNase I footprinting with nuclear extracts of transaldolase-expressing cell lines unveiled protection of nucleotides –29 to –16. Electrophoretic mobility shift assays identified a single dominant DNA-protein complex that was abolished by consensus sequence for transcription factor ZNF143/76 or mutation of the ZNF76/143 motif within the transaldolase promoter. Mutation of an AP-2 recognition sequence, partially overlapping the ZNF143 motif, increased TAL-H promoter activity in HeLa cells, without significant impact on HepG2 cells, which do not express AP-2. Cooperativity of ZNF143 with AP-2 was supported by supershift analysis of HeLa cells where AP-2 may act as cell type-specific repressor of TAL promoter activity. However, overexpression of full-length ZNF143, ZNF76, or dominant-negative DNA-binding domain of ZNF143 enhanced, maintained, or abolished transaldolase promoter activity, respectively, in HepG2 and HeLa cells, suggesting that ZNF143 initiates transcription from the transaldolase core promoter. ZNF143 overexpression also increased transaldolase enzyme activity. ZNF143 and transaldolase expression correlated in 21 different human tissues and were coordinately upregulated 14- and 34-fold, respectively, in lactating mammary glands compared with nonlactating ones. Chromatin immunoprecipitation studies confirm that ZNF143/73 associates with the transaldolase promoter in vivo. Thus, ZNF143 plays a key role in basal and tissue-specific expression of transaldolase and regulation of the metabolic network controlling cell survival and differentiation.

Received for publication, July 2, 2003 , and in revised form, December 31, 2003.

^* This work was supported in part by Grant RO1 DK49221 from the National Institutes of Health. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

^|| To whom correspondence should be addressed: State University of New York, College of Medicine, 750 East Adams St., Syracuse, NY 13210. Tel.: 315-464-4192; Fax: 315-464-4176; E-mail: perla{at}upstate.edu.

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