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.[5] This protein is therefore important in regulating
DNA repair.
When alternatively spliced, is predicted to produce three different
micropeptides.[6]
MRI-1 was previously found to be a modulator of retrovirus infection.[6]
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.[6]
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.[5] This protein is therefore important in regulating
DNA repair.
When alternatively spliced, is predicted to produce three different
micropeptides.[6]
MRI-1 was previously found to be a modulator of retrovirus infection.[6]
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.[6]