The HTATIP2 Knockout Jurkat Polyclonal Cells are a population of Jurkat T lymphoblasts engineered to harbor CRISPR/Cas9-mediated disruption of the HTATIP2 gene. This polyclonal knockout model enables loss-of-function investigations of HTATIP2, also known as TIP30, a multifunctional tumor suppressor and transcriptional corepressor. The cell population is supplied as a ready-to-use suspension culture, providing a heterogeneous pool of edited cells suitable for functional genomics, cancer biology, and virology studies. By targeting the endogenous HTATIP2 locus, these cells circumvent the need for transient siRNA or shRNA approaches, offering a stable genetic background for long-term assays.
The parental Jurkat cell line is a widely characterized human T lymphoblast model originally derived from the peripheral blood of a 14-year-old male with acute T-cell leukemia (clone E6-1). As an immortalized suspension cell line, Jurkat cells have been extensively employed to dissect T-cell receptor signaling, apoptosis regulation, and human immunodeficiency virus (HIV) infection mechanisms. Their rapid proliferation and highly tractable genetic landscape make them a robust platform for studying oncogenic processes and immune cell biology. The Jurkat background is particularly relevant for research into hematological malignancies and lymphocyte-dependent signaling networks.
HTATIP2 encodes a 30-kDa protein that functions as a pro-apoptotic tumor suppressor and transcriptional corepressor. It interacts with DNA-PKcs (PRKDC) to enhance DNA damage-induced apoptosis and is regulated by TP53 and ESR1, while being targeted by HIV-1 Tat. HTATIP2 promotes BAX expression and Caspase-3 activation and represses MMP2 to inhibit metastasis. It forms complexes with POLR2E and ERCC3 (XPB), linking DNA repair to transcriptional regulation.
In the Jurkat T-cell leukemia context, disruption of HTATIP2 generates a powerful tool to examine its role in lymphomagenesis and therapy resistance. Since HTATIP2 acts as a pro-apoptotic barrier, its loss may confer a survival advantage under genotoxic stress, providing a model to investigate mechanisms of chemoresistance. The Jurkat polyclonal knockout population is therefore ideal for studying how HTATIP2 deficiency alters cell death signaling in a leukemia background. Moreover, given the interaction between HIV-1 Tat and HTATIP2, these cells enable dissection of host factor roles in viral replication and Tat-mediated transcriptional dysregulation, making them valuable for HIV/AIDS research.
This knockout cell model supports a broad spectrum of applications. Researchers can perform tumor suppressor gene functional analysis via Western blotting and RT-qPCR. Apoptosis studies are enabled by Annexin V/propidium iodide flow cytometry and Caspase-3 activity assays. Drug target validation uses MTS proliferation and soft agar colony formation assays. Co-immunoprecipitation maps protein interactions. HIV host factor studies benefit from the Jurkat background. For further technical information, please contact Ascent Research.
