The CCNL2 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population disrupting the CCNL2 gene. This loss-of-function model enables investigation of cyclin L2, the regulatory subunit of CDK11, in pre-mRNA splicing and transcription. The polyclonal pool retains heterogeneity from gene editing, ensuring robust functional studies without clonal selection bias.
The host HEK293T cell line is derived from human embryonic kidney epithelial cells and constitutively expresses the SV40 large T antigen. This feature supports high-level protein expression, efficient viral production, and high transfectability, making HEK293T a standard system for molecular and cellular biology applications.
The CCNL2 gene product cyclin L2 forms complexes with CDK11A and CDK11B to phosphorylate key spliceosome components, including SF3B1, PRPF19, SRSF proteins, and U2 snRNP subunits, as well as the TFIIH transcription factor complex. Through these activities, the cyclin L2?CCDK11 holoenzyme regulates alternative splicing of crucial transcripts such as BCL2L1, generating isoforms that modulate apoptosis. The complex is activated by upstream signals that control cyclin expression and CDK11 kinase activity.
In HEK293T cells, disruption of CCNL2 impairs splicing fidelity and shifts isoform expression, particularly of BCL2L1, affecting cell survival and cycle progression. The polyclonal knockout population captures the diversity of editing outcomes, providing a physiologically relevant model to dissect cyclin L2 function in a manipulable human cell background. Because HEK293T cells are highly transfectable and support robust biochemical analyses, this knockout tool is particularly valuable for studying the direct impact of cyclin L2 loss on spliceosome dynamics and downstream gene expression programs.
These polyclonal knockout cells are suitable for functional splicing assays using RT-PCR and RNA-seq, western blotting for splice variants, co-immunoprecipitation to assess CDK11 interactions, immunofluorescence for nuclear speckles, and cell viability or clonogenic survival assays. They facilitate CRISPR-based screens and drug target validation in cancer and neurological disease research. For more information, please contact Ascent Research.
