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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Long-term depletion of Cereblon induces mitochondrial dysfunction in cancer cells
Sung Goo Park 1,2,* (Principal Investigator), Seulki Park1,2 (Researcher), Kidae Kim4 (Researcher), Gi-Ok Haam5 (Researcher), Hyun Seung Ban5 (Senior Researcher), Jung-Ae Kim2,6 (Senior Researcher), Byoung Chul Park1,3 (Senior Researcher), Sunhong Kim7,# (Senior Researcher), Jeong-Hoon Kim1,2,# (Senior Researcher)
1Disease Target Structure Research Center, KRIBB,
2Functional Genomics and 3Proteome Structural Biology, Korea University of Science and Technology,
4Center for Genome Science, KCDC,
55Biotherapeutics Translational Research Center and 6Personalized Genomic Medicine Research Center, KRIBB,
7Drug Discovery Center, LG Chem
Cereblon (CRBN) is a multi-functional protein that acts as a substrate receptor of the E3 ligase complex and a molecular chaperone. While CRBN is proposed to function in mitochondria, its specific roles are yet to be established. Here, we showed that knockdown of CRBN triggers oxidative stress and calcium overload in mitochondria, leading to disruption of mitochondrial membrane potential. Notably, long-term CRBN depletion using PROteolysis TArgeting Chimera (PROTAC) induced irreversible mitochondrial dysfunction, resulting in cell death. Our collective findings indicate that CRBN is required for mitochondrial homeostasis in cells.
Abstract, Accepted Manuscript(in press) [Submitted on October 5, 2020, Accepted on December 30, 2020]
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