| ID | Sequence | Length | GC content |
|---|---|---|---|
| GAGUCCGUUCUGGGUGUCUUGGCUCUAUGGCUCGCCUCUGCCAGCUCCU… | 1818 nt | 0.4153 | |
| AGAGCGGCAGCCUUUUCCCGCGCGUGCUGCCUUCGCCGCUCGGGCCGCC… | 1901 nt | 0.4156 | |
| AGAGCGGCAGCCUUUUCCCGCGCGUGCUGCCUUCGCCGCUCGGGCCGCC… | 1640 nt | 0.4146 | |
| AGAGCGGCAGCCUUUUCCCGCGCGUGCUGCCUUCGCCGCUCGGGCCGCC… | 1684 nt | 0.4103 | |
| AGAGCGGCAGCCUUUUCCCGCGCGUGCUGCCUUCGCCGCUCGGGCCGCC… | 1764 nt | 0.4161 | |
| AGAGCGGCAGCCUUUUCCCGCGCGUGCUGCCUUCGCCGCUCGGGCCGCC… | 1634 nt | 0.4094 | |
| AGAGCGGCAGCCUUUUCCCGCGCGUGCUGCCUUCGCCGCUCGGGCCGCC… | 1814 nt | 0.4168 |
The protein encoded by this gene possesses kinase activity that phosphorylates regulators involved in signal transduction. It phosphorylates I kappa-Balpha, p105, and c-Jun. It acts as a docking site for complex-mediated phosphorylation. The gene is located within the Smith-Magenis syndrome region on chromosome 17. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2015]
A longitudinal mRNA expression analysis in post-mortem human blood samples demonstrated that the COPS3 is involved in nucleotide-excision repair and DNA damage recognition and shows an up-regulated expression pattern after death, with pathway analysis suggesting active processes promoting DNA damage repair are a source of early postmortem gene expression changes [Antiga et al. DOI:10.1038/s41598-021-96095-z].