Involved in pre-mRNA splicing. Functions in association with cyclin-dependent kinases (CDKs) (PubMed:18216018). Inhibited by the CDK-specific inhibitor CDKN1A/p21 (PubMed:11980906). May play a role in the regulation of RNA polymerase II (pol II). May be a candidate proto-oncogene in head and neck squamous cell carcinomas (HNSCC) (PubMed:12414649, PubMed:15700036). Interacts with POLR2A via its hyperphosphorylated C-terminal domain (CTD) (By similarity). Interacts with CDK11A, CDK12 and CDK13 (PubMed:11980906, PubMed:18216018). Isoforms 1 and 2, but not isoform 3, interact with CDK11B. May form a ternary complex with CDK11B and casein kinase II (CKII) (PubMed:18216018). Interacts with pre-mRNA-splicing factors, including at least SRSF1, SRSF2 AND SRSF7/SLU7 (PubMed:11980906, PubMed:18216018). Found in nuclear intrachromatin granules clusters (IGC), also called nuclear speckles, which are storage compartments for nuclear proteins involved in mRNA processing. Ccnl1 is an immediate-early gene with independently regulated isoforms. Widely expressed. Overexpression in primary tumors of head and neck squamous cell carcinomas (HNSCC). Contains a RS region (arginine-serine dipeptide repeat) within the C-terminal domain which is the hallmark of the SR family of splicing factors. This region probably plays a role in protein-protein interactions. CCNL1 is amplified in several HNSCC. May play a critical role in the formation of loco-regional metastases and an unfavorable clinical outcome of HNSCC. May be produced at very low levels due to a premature stop codon in the mRNA, leading to nonsense-mediated mRNA decay. May be produced at very low levels due to a premature stop codon in the mRNA, leading to nonsense-mediated mRNA decay. Belongs to the cyclin family. Cyclin L subfamily. Probable cloning artifact. Probable cloning artifact.