The HMBOX1 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphoblastoid cell line. This product provides a loss-of-function model for studying the human HMBOX1 gene, a homeobox-containing transcription factor. The polyclonal knockout pool is generated by CRISPR/Cas9-mediated gene disruption, yielding a heterogeneous population of edited cells suitable for functional analyses. Researchers can employ this model to dissect HMBOX1’s roles in NF-??B signaling inhibition, telomere maintenance, and apoptosis regulation without the need for single-cell cloning.
Jurkat cells are a widely used immortalized T lymphocyte cell line originally derived from the peripheral blood of a 14-year-old male patient with acute T-cell leukemia. They serve as a well-established model system for studying T-cell signaling, activation, and apoptosis, and are extensively employed in immunological and leukemia research. The Jurkat background is particularly relevant for exploring NF-??B signaling dynamics, as these cells exhibit robust activation of this pathway in response to stimuli such as TNF?? and other inflammatory cytokines. This host cell line thus offers a physiologically relevant context for investigating the interplay between HMBOX1 and inflammatory signaling networks.
HMBOX1 (Homeobox containing 1) is a transcription factor that functions as a negative regulator of NF-??B signaling. Mechanistically, HMBOX1 binds directly to the NF-??B p65 subunit, preventing its nuclear translocation and thereby suppressing the transcriptional activation of pro-inflammatory cytokines such as IL-6 and IL-8. This regulatory interaction is positioned downstream of the I??B???CIKK complex, which normally releases p65/p50 dimers upon stimulation by TNF?? through its receptor. In addition to its role in inflammatory signaling, HMBOX1 participates in telomere biology through interactions with the shelterin complex components TPP1 and POT1, as well as the DNA repair protein Ku70, contributing to telomere length regulation and genomic stability. The protein thus integrates immunological and genomic maintenance functions, making it a gene of interest in cancer biology and inflammatory disorders.
In Jurkat T lymphoblastoid cells, knockout of HMBOX1 is expected to derepress NF-??B activity, leading to enhanced transcription of pro-inflammatory and pro-survival genes. This polyclonal knockout model enables dissection of HMBOX1-dependent modulation of T-cell receptor signaling and cytokine networks, which are central to immune responses and leukemogenesis. Given that Jurkat cells are derived from a T-cell leukemia, the HMBOX1 knockout background provides a physiologically pertinent platform to investigate how loss of this homeobox protein alters telomere dynamics and apoptosis sensitivity, processes frequently dysregulated in hematological malignancies. Researchers can employ this model to compare wild-type and HMBOX1-deficient Jurkat cells in assays assessing NF-??B nuclear translocation, cytokine secretion, and apoptotic responses.
Typical applications include luciferase-based NF-??B reporter assays to quantify pathway activation, western blotting for p65 subcellular localization, ELISA measurement of IL-6 and IL-8 secretion, Annexin V/PI flow cytometry to evaluate apoptosis, and telomere length qPCR analysis. This product is suitable for investigating hepatocellular carcinoma, other cancers, and inflammatory disorders where HMBOX1 has been implicated. For further information or technical support, please contact Ascent Research.
