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New role of human ribosomal protein S3: Regulation of cell cycle via phosphorylation by cyclin-dependent kinase 2.
Han, Se Hee; Chung, Ji Hyung; Kim, Joon; Kim, Key-Sun; Han, Ye Sun.
Afiliación
  • Han SH; Center for Diagnosis, Treatment and Care System of Dementia, Korea Institute of Science and Technology, Seoul 02792, Republic of Korea.
  • Chung JH; Department of Applied Bioscience, College of Life Science, CHA University, Pocheon 11160, Republic of Korea.
  • Kim J; Laboratory of Biochemistry, Division of Life Sciences and Biotechnology, Korea University, Seoul 02841, Republic of Korea.
  • Kim KS; Center for Diagnosis, Treatment and Care System of Dementia, Korea Institute of Science and Technology, Seoul 02792, Republic of Korea.
  • Han YS; Department of Advanced Technology Fusion, Konkuk University, Seoul 05029, Republic of Korea.
Oncol Lett ; 13(5): 3681-3687, 2017 May.
Article en En | MEDLINE | ID: mdl-28521470
Human ribosomal protein S3 (hRpS3) is a component of the 40S ribosomal subunit that associated in protein synthesis. hRpS3 has additional ribosomal functions such as DNA repair, transcription, metastasis, and apoptosis via interaction with numerous signaling molecules and has different modifications. Cyclin-dependent kinases (CDKs) are heterodimeric serine/threonine protein kinases that regulate cell cycle progression. Among its members, the Cdk1-cyclin B complex is known to control cell progression in the G2/M phase, while Cdk2-cyclin E/A complexes function in G1/S and S/G2 transition. In our previous study, we observed interaction between hRpS3 and Cdk1. The present study investigated the interaction between hRpS3 and Cdk2. Cdk2 phosphorylated hRps3 at amino acid residues S6 and T221 during the S-phase. Furthermore, hRpS3 knockdown delayed cell cycle progression by modulating the expression of cell cycle-related proteins, including cyclin B1 and cyclin E1. These findings suggest that hRpS3 is involved in Cdk2-mediated cell cycle regulation.
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Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Oncol Lett Año: 2017 Tipo del documento: Article

Texto completo: 1 Colección: 01-internacional Banco de datos: MEDLINE Idioma: En Revista: Oncol Lett Año: 2017 Tipo del documento: Article