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논문 기본 정보

자료유형
학술저널
저자정보
김정환 (경상대학교) Min Seok Woo (Gyeongsang National University) Atif Ali Khan Khalil (Gyeongsang National University) Frank J. Gonzalez (National Institutes of Health)
저널정보
한국분자세포생물학회 Molecules and Cells Molecules and Cells Vol.47 No.1
발행연도
2024.1
수록면
1 - 9 (9page)
DOI
10.1016/j.mocell.2024.100148

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Growth arrest and DNA damage-inducible beta (GADD45b) plays a critical role in intracellular events such as cell growth and apoptosis. Although the functional study of GADD45b has been conducted, the mechanism for the transcriptional regulation of GADD45b is largely unknown. Due to the drastic induction of hepatic GADD45b mRNA by peroxisome proliferator-activated receptor alpha activation in wild-type mice, we investigated a key factor that affects the upregulation of GADD45b mRNA. Interestingly, we found that GADD45b-promoter luciferase activity was dramatically increased as the 5′-flanking regions were closer to the transcription start site in Hepa1c1c7 cells. Additionally, we found 2 E2F (E2F-myc activator/cell cycle regulator) binding motifs in the region (−150/−1) of the GADD45b promoter. Notably, E2F3 mRNA was significantly increased only in wild-type mice treated with WY-14643, a peroxisome proliferator-activated receptor alpha agonist, followed by the induction of GADD45b mRNA. Furthermore, gene functional studies and Chromatin Immunoprecipitation assays revealed that E2F3 could regulate the GADD45b gene via the E2F binding motif. Thus, we suggest that E2F3 may play a key role in regulating the GADD45b gene as a positive transcription factor.

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