RAE1 promotes BMAL1 shuttling and regulates degradation and activity of CLOCK: BMAL1 heterodimer
| Autor: | Yingying Zhang, Xulei Zheng, Hao Tan, Yilu Lu, Dachang Tao, Bojun Qiu, Xu Zhao, Yongxin Ma, Jiarong Zeng, Tengjiao Ma, Yunqiang Liu |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Transcriptional Activation Cancer Research endocrine system Nucleocytoplasmic Transport Proteins Immunology Circadian clock CLOCK Proteins Transfection Article 03 medical and health sciences Cellular and Molecular Neuroscience Mice 0302 clinical medicine Nuclear Matrix-Associated Proteins Circadian Clocks Gene Knockdown Techniques Animals Humans Circadian rhythm lcsh:QH573-671 Gene knockdown Chemistry lcsh:Cytology HEK 293 cells Ubiquitination ARNTL Transcription Factors Promoter Cell Biology Cell biology Circadian Rhythm PER2 Nuclear Pore Complex Proteins 030104 developmental biology HEK293 Cells Cytoplasm Proteolysis NIH 3T3 Cells Protein Multimerization 030217 neurology & neurosurgery Plasmids |
| Zdroj: | Cell Death & Disease Cell Death and Disease, Vol 10, Iss 2, Pp 1-12 (2019) |
| ISSN: | 2041-4889 |
| Popis: | Circadian rhythm is an autoregulatory rhythm, which is sustained by various mechanisms. The nucleocytoplasmic shuttling of BMAL1 is essential for CLOCK translocation between cytoplasm and nucleus and maintenance of the correct pace of the circadian clock. Here we showed that RAE1 and NUP98 can promote the degradation of BMAL1 and CLOCK. Knockdown of RAE1 and NUP98 suppressed BMAL1 shuttling, leading to cytoplasm accumulation of CLOCK. Furthermore, Chip assay showed that knockdown of RAE1 and NUP98 can enhance the interaction between CLOCK: BMAL1 and E-box region in the promoters of Per2 and Cry1 while reducing its transcription activation activity. Our present study firstly revealed that RAE1 and NUP98 are critical regulators for BMAL1 shuttling. |
| Databáze: | OpenAIRE |
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