The CCNT2 Knockout SK-HEP-1 Polyclonal Cells product consists of a pool of SK-HEP-1 cells that have undergone CRISPR/Cas9-mediated disruption of the CCNT2 gene, generating a heterogeneous population of knockout cells. This polyclonal format provides a versatile loss-of-function model for investigating cyclin T2 function without the need for single-cell clone isolation, making it particularly suitable for population-level studies such as drug screening and functional genomics.
The SK-HEP-1 host cell line was originally established from the ascitic fluid of a patient with liver adenocarcinoma. It exhibits a unique hybrid phenotype, co-expressing epithelial and endothelial markers, including Factor VIII and Weibel-Palade bodies. This dual identity has led to its widespread use as a model for liver sinusoidal endothelial cells, angiogenesis, and hepatic cancer biology, enabling the study of cross-talk between endothelial differentiation and malignant transformation.
CCNT2 encodes cyclin T2, a regulatory subunit of the positive transcription elongation factor b (P-TEFb) complex. Following association with its catalytic partner CDK9, cyclin T2 drives transcriptional elongation by phosphorylating Ser2 of the RNA polymerase II C-terminal domain (CTD) and negative elongation factors, thereby releasing promoter-proximal pausing. This process controls the expression of rapid-response genes such as c-MYC, FOS, JUN, and the anti-apoptotic factor MCL1. P-TEFb activity is tightly regulated by reversible sequestration into the inhibitory 7SK snRNP (containing HEXIM1 and LARP7) and by recruitment factors including BRD4 and AFF4. Notably, the HIV Tat protein usurps this machinery to enhance viral transcription.
Disruption of CCNT2 in SK-HEP-1 cells is expected to impair P-TEFb-dependent elongation, leading to reduced expression of proliferation and survival genes. Given the endothelial?Cepithelial character of the host line, this knockout model enables dissection of cyclin T2’s role in both angiogenic signaling and hepatocellular carcinoma progression. Researchers can employ it to assess the dependency of liver cancer cells on transcriptional elongation and to explore how loss of CCNT2 influences endothelial marker expression and cell cycle regulation.
These polyclonal knockout cells are suitable for a broad range of applications, including transcript elongation analysis by RNA-seq, ChIP-qPCR assessment of RNA Pol II CTD phosphorylation, and RT-qPCR quantification of elongation-responsive genes. They serve as a robust platform for P-TEFb inhibitor screening via cell viability or gene expression readouts, and for functional interrogation of the HIV Tat?CP-TEFb axis in a hepatic context. The model also supports cancer dependency studies and functional genomics approaches to investigate cyclin T2 biology. For further information or custom requests, please contact Ascent Research.
