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Nucleic Acids Research, 2002, Vol. 30, No. 11 2398-2406
© 2002 Oxford University Press

An alternatively spliced isoform of transcriptional repressor ATF3 and its induction by stress stimuli

Yoshinori Hashimoto1,4, Chun Zhang1, Junya Kawauchi1, Issei Imoto2,3, Mimi T. Adachi1,3, Johji Inazawa2,3, Teruo Amagasa4, Tsonwin Hai5 and Shigetaka Kitajima1,3,*

1Department of Biochemical Genetics, 2Department of Molecular Cytogenetics, 3Integrated Genomics and Advanced Medical Frontier Research Unit, Medical Research Institute and 4Maxillofacial Surgery, Graduate School, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan and 5Department of Molecular and Cellular Biochemistry, Neurobiotechnology Center, Ohio State University, Columbus, OH, USA

Activating transcription factor 3 (ATF3) is a member of the ATF/CREB family of transcription factors and its expression is increased by various pathophysiological conditions and in several cancer cells. In this study, we describe two alternatively spliced ATF3{Delta}Zip mRNAs: ATF3{Delta}Zip2a and ATF3{Delta}Zip2b. Both variants encoded the same truncated protein of 135 amino acids, which lacked the leucine zipper domain and was incapable of binding to the ATF/CRE motif. The ATF3{Delta}Zip2 protein was shown to be localized in the nuclei and counteracted the transcriptional repression by the full-length ATF3. Western blot analysis showed that ATF3{Delta}Zip2 was expressed in cells exposed to A23187. Further study showed that, similar to the full-length ATF3, the expression of ATF3{Delta}Zip2 was induced by a wide range of stress stimuli. However, its expression was not detectable in cancer cells that constitutively over-expressed ATF3. Taken together, our results suggest that ATF3{Delta}Zip2, a protein derived from alternatively spliced mRNAs, is induced by various stress signals and may modulate the activity of the full-length ATF3 protein during stress response.

* To whom correspondence should be addressed at: Department of Biochemical Genetics, Medical Research Institute, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8510, Japan. Tel: +81 3 5803 5822; Fax: +81 3 5803 0248; Email: kita.bgen{at}mri.tmd.ac.jp


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