| ID | Sequence | Length | GC content |
|---|---|---|---|
| AAACACUUCGCCACUGCAGGGGUGGAGACUGGCUCUGUUCGGAUGCCGG… | 1504 nt | 0.5745 | |
| GUCAGGGAAGCGGCGCGCGCGCGCGGGCGGCGGGCGGGCUGGGGAUCCG… | 1889 nt | 0.5998 | |
| GUCAGGGAAGCGGCGCGCGCGCGCGGGCGGCGGGCGGGCUGGGGAUCCG… | 1673 nt | 0.5971 | |
| AAACACUUCGCCACUGCAGGGGUGGAGACUGGCUCUGUUCGGAUGCCGG… | 1720 nt | 0.5802 | |
| GUCAGGGAAGCGGCGCGCGCGCGCGGGCGGCGGGCGGGCUGGGGAUCCG… | 2026 nt | 0.5997 |
The protein encoded by this gene belongs to the highly conserved cyclin family, whose members are characterized by a dramatic periodicity in protein abundance through the cell cycle. Cyclins function as regulators of CDK kinases. Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event. This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activtiy is required for cell cycle G1/S transition. This protein has been shown to interact with and be involved in the phosphorylation of tumor suppressor protein Rb. The CDK4 activity associated with this cyclin was reported to be necessary for cell cycle progression through G2 phase into mitosis after UV radiation. Several transcript variants encoding different isoforms have been found for this gene. [provided by RefSeq, Oct 2008] CIViC Summary for CCND3 Gene Cyclin D has been shown in many cancer types to be misregulated. Well established for their oncogenic properties, the cyclins and the cyclin-dependent kinases (CDK's) they activate have been the focus of major research and development efforts over the past decade. The methods by which the cyclins are misregulated are widely variable, ranging from genomic amplification to changes in promoter methylation. Cyclin D3 loss has been reported in T-ALL, a seemingly unique trend when compared to the amplifcations and overexpressions of the other cyclin D's. In a mouse study, the targeted therapeutic palbociclib significantly increased the median survival of the cyclin D3 knockouts.
No relevant information is available at the moment.