The NEK1 interactor, C21ORF2, is required for efficient DNA damage repair

• Published in: Acta biochimica et biophysica Sinica Vol. 47; no. 10; pp. 834 - 841
• Main Authors: Fang, Xiao, Lin, Han, Wang, Xiaohui, Zuo, Qiuhong, Qin, Jun, Zhang, Pumin
• Format: Journal Article
• Language: English
• Published: China Oxford University Press 01.10.2015
• Subjects: 21号染色体; Cell Cycle Proteins - metabolism; Cell Proliferation - physiology; Cell Proliferation - radiation effects; DNA Damage - physiology; DNA Repair - physiology; DNA Repair - radiation effects; DNA损伤修复; HEK293 Cells; HeLa Cells; Humans; NIMA-Related Kinase 1; orf2蛋白; Original; Protein-Serine-Threonine Kinases - metabolism; Proteins - metabolism; Radiation Dosage; 开放阅读框; 细胞功能; 脱氧核糖核酸; 遗传性疾病; 非同源末端连接; DNA damage repair; NEK1 interactor; C21ORF2; G2-phase checkpoint; ionizing radiation
• ISSN: 1672-9145; 1745-7270
• DOI: 10.1093/abbs/gmv076

Defective DNA damage response is a threat to genome stability and a proven cause of tumorigenesis. C210RF2 （chromosome 21 open reading frame 2） is a novel gene on chromosome 21, and the C21ORF2 protein is found to interact with NEKI. Earlier studies showed that C21ORF2 might be as- sociated with some human genetic diseases including Down syndrome. However, the cellular functions of C21ORF2 remain unknown. In the present study, we reported that C21ORF2 affected cell proliferation after DNA damage induced by ionizing radiation, and DNA repair was less efficient in C21ORF2-depleted cells compared with control cells. However, C21ORF2-knockdown cells did not show defects in the activation of the G2-phase DNA damage checkpoint. Furthermore, homologous recombination, but not non-homologous end joining repair, was found to be impaired after C21ORF2 attenuation, which could be rescued by the overexpression of NEK1, indicating that C21ORF2 functions in the same pathway as NEK1 in DNA damage repair.