Cell cycle regulator of non-homologous end joining is a protein that in humans is encoded by the CYRENgene.
It prevents classical non-homologous end joining, a method of repair of double-stranded DNA breaks.[1] This protein is therefore important in regulating DNA repair.
When alternatively spliced, is predicted to produce three different micropeptides.[2]
MRI-1 was previously found to be a modulator of retrovirus infection.[2]
MRI-2 may be important in non-homologous end joining (NHEJ) of DNA double strand breaks. In Co-Immunoprecipitation experiments, MRI-2 bound to Ku70 and Ku80, two subunits of Ku, which play a major role in the NHEJ pathway.[2]
MRI-3
References
↑Arnoult N, Correia A, Ma J, Merlo A, Garcia-Gomez S, Maric M, Tognetti M, Benner CW, Boulton SJ, Saghatelian A, Karlseder J (September 2017). "Regulation of DNA repair pathway choice in S and G2 phases by the NHEJ inhibitor CYREN". Nature. 549 (7673): 548–552. doi:10.1038/nature24023. PMID28959974.
↑ 2.02.12.2Slavoff SA, Heo J, Budnik BA, Hanakahi LA, Saghatelian A (April 2014). "A human short open reading frame (sORF)-encoded polypeptide that stimulates DNA end joining". The Journal of Biological Chemistry. 289 (16): 10950–7. doi:10.1074/jbc.c113.533968. PMID24610814.
