The HMBOX1 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HEK293T human embryonic kidney epithelial cell line. This product supplies a genetically diverse pool of cells with targeted disruptions of the HMBOX1 gene, generated through CRISPR/Cas9-mediated gene editing. The polyclonal format avoids clonal biases and allows assessment of knockout effects across a population. It serves as a loss-of-function model for studying HMBOX1 biology in cellular homeostasis and disease.
HEK293T cells are derived from the parental HEK293 line and stably express the SV40 large T antigen, facilitating episomal plasmid replication. This property underpins their widespread use in transient protein expression and lentiviral packaging. Hypothesized to be of neuronal origin, these epithelial cells combine robust growth with high transfectability, establishing them as a platform for gene function studies, protein interaction analyses, and reporter assays. Introducing an HMBOX1 knockout into this system yields a dedicated model for dissecting pathway-specific mechanisms.
HMBOX1 is a homeobox transcription factor that binds telomeric DNA and negatively regulates NF-??B signaling by stabilizing I??B??, thereby restricting pro-inflammatory gene expression (e.g., IL-6). It is modulated by upstream stimuli including TNF-??, IL-1??, and p53, partly through miR-21. HMBOX1 interacts with shelterin components TRF2 and POT1 and influences targets such as hTERT, CDKN1A (p21), BAX, and BCL2, linking telomere maintenance to apoptosis. The protein also engages the Wnt/??-catenin pathway via ??-catenin and TCF/LEF factors. Loss of HMBOX1 is thus expected to enhance NF-??B activity and disturb telomere dynamics.
In HEK293T cells, HMBOX1 disruption should relieve NF-??B inhibition, leading to elevated transcriptional activity of RelA/p65, which may alter proliferation and inflammatory responses. Concurrently, impaired HMBOX1 function can compromise telomere protection by disrupting shelterin interactions, potentially impacting hTERT regulation and genomic stability. The polyclonal knockout population enables study of these combined effects without clonal artifacts, serving as a physiologically relevant model for probing the intersection of telomere biology and innate immune signaling. This is especially useful for investigating HMBOX1??s putative tumor suppressor functions and its role in cell cycle and apoptosis regulation.
This knockout cell product supports diverse experimental workflows. Western blotting, RT-qPCR, and immunofluorescence can quantify changes in HMBOX1, I??B??, BAX, and BCL2. Telomere Q-FISH and NF-??B luciferase reporter assays provide functional readouts of telomere alteration and pathway activation. Annexin V staining and flow cytometry detect apoptosis and cell cycle shifts, while co-immunoprecipitation and ChIP-seq dissect protein interactions and DNA binding. RNA-seq captures global transcriptomic changes. These applications facilitate drug screening for NF-??B or telomere modulators and disease modeling for gastric, colorectal, and hepatocellular cancers. For detailed technical specifications and ordering information, please contact Ascent Research.
