INIP Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Jurkat T lymphoblast cell line, offering a loss-of-function model for INIP, a core subunit of the SOSS complex involved in DNA double-strand break repair and ATM signaling. The polyclonal format provides a heterogeneous gene-disrupted pool without clonal selection, enabling unbiased functional studies in a leukemia-relevant background.
Jurkat cells, originally isolated from an acute T cell leukemia patient, are an extensively characterized suspension line used for investigating T cell receptor signaling, immune responses, and apoptosis. They exhibit leukemic genomic features that render them particularly suitable for examining the consequences of DNA repair gene disruption in a malignant context. This host system therefore supports research into how genome maintenance failures influence leukemogenesis and therapeutic responsiveness.
INIP functions within the SOSS heterotrimeric complex through direct interactions with INTS3 and NABP1 (hSSB1). In response to DNA double-strand breaks induced by ionizing radiation or chemotherapeutics, INIP promotes recruitment of the MRN complex (MRE11?CRAD50?CNBS1), leading to ATM kinase activation. ATM then phosphorylates downstream effectors such as CHK2, p53, and H2AX (??H2AX), which coordinate cell cycle arrest and facilitate RAD51-dependent homologous recombination. Thus, INIP acts as an upstream organizer of damage sensing and repair, linking genotoxic stress to checkpoint signaling and recombinational repair.
Ablation of INIP in Jurkat cells compromises homologous recombination repair capacity, accentuating genomic instability in a T lymphoblast background already primed by leukemic alterations. This model enables dissection of DNA damage response pathways in the context of aberrant T cell signaling and apoptosis regulation. It further allows exploration of synthetic lethal interactions with other DNA repair defects, providing a system to test strategies that exploit genomic fragility for therapeutic benefit.
These polyclonal knockout cells are suited for a wide array of experimental approaches, including Western blotting for phospho-ATM and ??H2AX, immunofluorescence detection of RAD51 and 53BP1 foci, flow cytometry for cell cycle and apoptosis analysis, and clonogenic survival assays after treatment with DNA-damaging agents. Co-immunoprecipitation can assess SOSS complex assembly, and RT-qPCR can measure transcript level changes in repair genes. Applications span DNA damage response studies, genome stability research, leukemia biology, and drug target validation for DNA repair inhibitors. For further inquiries, please contact Ascent Research.
