한빛사 논문
Seoung Min Bong1,†, Seung-Hyun Bae1,2,†, Bomin Song1, HyeRan Gwak1, Seung-Won Yang1, Sunshin Kim1, Seungyoon Nam3, Krishnaraj Rajalingam4, Se Jin Oh5, Tae Woo Kim5, SangYoun Park6, Hyonchol Jang1,2,* and Byung Il Lee1,2,*
1Research Institute, National Cancer Center, Goyang-si, Gyeonggi 10408, Republic of Korea,
2Department of Cancer Biomedical Science, National Cancer Center Graduate School of Cancer Science and Policy, Goyang-si, Gyeonggi 10408, Republic of Korea,
3Department of Life Sciences, College of BioNano Technology and Department of Genome Medicine and Science, Graduate School of Medicine, Gachon University, Incheon 21565, Republic of Korea,
4Cell Biology Unit, University Medical Center Mainz, JGU, Mainz, Germany,
5Department of Biomedical Sciences, Graduate School of Medicine, Korea University, Seoul 02841, Republic of Korea,
6School of Systems Biomedical Science, Soongsil University, Seoul 06978, Republic of Korea
†The authors wish it to be known that, in their opinion, the first two authors should be regarded as Joint First Authors.
*Corresponding author
Abstract
API5 (APoptosis Inhibitor 5) and nuclear FGF2 (Fibroblast Growth Factor 2) are upregulated in various human cancers and are correlated with poor prognosis. Although their physical interaction has been identified, the function related to the resulting complex is unknown. Here, we determined the crystal structure of the API5–FGF2 complex and identified critical residues driving the protein interaction. These findings provided a structural basis for the nuclear localization of the FGF2 isoform lacking a canonical nuclear localization signal and identified a cryptic nuclear localization sequence in FGF2. The interaction between API5 and FGF2 was important for mRNA nuclear export through both the TREX and eIF4E/LRPPRC mRNA export complexes, thus regulating the export of bulk mRNA and specific mRNAs containing eIF4E sensitivity elements, such as c-MYC and cyclin D1. These data show the newly identified molecular function of API5 and nuclear FGF2, and provide a clue to understanding the dynamic regulation of mRNA export.
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