CCNT2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji Burkitt lymphoma B lymphocyte line, providing a loss-of-function model for Cyclin T2 (CCNT2). This heterogeneous pool carries targeted disruption of the CCNT2 gene, which encodes the regulatory subunit of the positive transcription elongation factor b (P-TEFb) complex, enabling detailed dissection of P-TEFb-dependent transcription.
The parental Raji cell line is an Epstein-Barr virus (EBV)-positive human B lymphocyte model widely used in immunology, oncology, and virology. Raji cells maintain B-cell traits like surface immunoglobulin expression and antigen presentation, and they proliferate robustly due to constitutive NF-??B signaling and MYC overexpression, making them ideal for studying lymphomagenesis and virus-host interactions.
CCNT2 partners with CDK9 in the P-TEFb complex to phosphorylate the RNA polymerase II C-terminal domain and the negative elongation factors DSIF and NELF, thereby releasing paused polymerases into productive elongation. This process is activated by upstream signals including NF-??B and BRD4, and is regulated by reversible sequestration into the 7SK snRNP containing HEXIM1 and 7SK RNA. HIV-1 Tat hijacks P-TEFb by directly recruiting the complex to the viral promoter, making CCNT2 essential for viral transcription. Key downstream targets include the proto-oncogene MYC and HIV-1 transcripts, linking CCNT2 to cell proliferation, survival, and viral pathogenesis.
In Raji B lymphocytes, CCNT2 disruption impairs P-TEFb-driven transcriptional programs sustaining rapid proliferation and immunoglobulin expression. Given the cell??s reliance on MYC and NF-??B, the knockout model enables interrogation of how elongation checkpoints influence Burkitt lymphoma biology. The EBV-positive background further permits studies of viral-host transcriptional crosstalk, particularly involving BRD4 and NF-??B pathways converging on P-TEFb.
These cells support functional genomics studies using RNA-seq, ChIP-qPCR for polymerase occupancy, and HIV-1 Tat-dependent reporter assays to investigate viral reactivation. Drug target validation for CDK9 inhibitors and other transcriptional therapeutics can be performed via proliferation, apoptosis, and co-immunoprecipitation of P-TEFb components. Flow cytometry enables monitoring of B-cell markers and cell cycle profiles. Researchers may also explore synthetic lethal interactions in B-cell lymphoma contexts. For further details, contact Ascent Research.
