The KLF12 Knockout Jurkat Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the KLF12 gene in the Jurkat human T lymphoblastoid cell line. The CRISPR/Cas9-mediated gene disruption produces loss-of-function mutations across the KLF12 locus, generating a versatile knockout resource without clonal selection biases. This polyclonal model provides a heterogeneous pool of knockout cells, enabling robust functional screening and eliminating the need for in-house genome editing. The cells are supplied live and ready for immediate use in downstream assays.
Jurkat cells are derived from acute T-cell leukemia and serve as a classic model for T-cell receptor signaling, immune activation, and leukemogenesis. They harbor deficiencies in p53 and PTEN, rendering them susceptible to proliferation and survival pathway perturbations. Their lymphoid origin and well-defined signaling circuits make them an appropriate background for analyzing transcription factor function in T-cell biology. The cell line’s rapid proliferation facilitates large-scale experimental designs.
KLF12 is a transcriptional repressor that inhibits proliferation and promotes apoptosis by antagonizing Sp1-mediated activation. It interacts with Sp1 at gene promoters and recruits corepressor complexes containing CtBP and HDACs. KLF12 is regulated by upstream factors including TGF-??1 and miR-10b, and acts in the TGF-?? pathway downstream of Smad2/3 phosphorylation. Its targets include Cyclin D1, c-Myc, MMP-9, and Bcl-2 family members, linking KLF12 to cell cycle progression and survival control.
In Jurkat cells, KLF12 knockout relieves transcriptional repression, leading to enhanced cell cycle progression and increased viability. This effect is magnified by the p53/PTEN-deficient background, highlighting the gene’s role in restraining T-cell leukemogenesis. The polyclonal composition captures a range of mutational events, providing a more physiologically relevant model for studying the consequences of KLF12 loss in a heterogeneous cancer context. This model thus serves as a powerful tool for dissecting the molecular underpinnings of KLF12-mediated tumor suppression in T-ALL.
Typical applications include functional analysis of KLF12 in T-cell signaling, TGF-?? pathway studies, and drug screening for modulators of KLF12 activity. Proliferation (CFSE), apoptosis (Annexin V), and activation marker (CD69, CD25) assays by flow cytometry are directly applicable. Molecular characterization can be performed via Western blotting, RT-qPCR, RNA-seq, and ChIP-qPCR for target gene validation and phospho-Smad2/3 analysis. Additionally, co-culture and signaling assays can probe interactions with upstream regulators such as TGF-??1. For further details and ordering information, contact Ascent Research.
