The HMGB2 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population generated from HEK293T human embryonic kidney epithelial cells. This product provides a heterogeneous knockout model with targeted disruption of the HMGB2 gene, suitable for loss-of-function studies in chromatin biology, inflammation, and cancer research. The polyclonal format avoids clonal selection biases while maintaining effective HMGB2 depletion at the population level.
HEK293T is a derivative of the HEK293 cell line that stably expresses the SV40 large T antigen, enabling high-copy-number episomal plasmid replication and superior transient transfection efficiency. These cells are widely employed for recombinant protein expression and lentiviral production due to their rapid growth and epithelial morphology. The HEK293T background provides a robust and well-characterized platform for dissecting HMGB2-dependent pathways, including responses to extracellular stimuli.
HMGB2 functions as a DNA architectural protein that modulates chromatin structure, gene expression, and DNA repair, playing critical roles in cell proliferation and differentiation. When released extracellularly, it acts as a damage-associated molecular pattern (DAMP) and engages RAGE and TLR4 receptors, triggering MyD88-dependent NF-??B and MAP kinase signaling cascades. Upstream regulators include TNF-??, IL-1??, LPS, Sp1, and HIF-1??, while downstream effectors encompass MMP9, Cyclin D1, and Snail. HMGB2 forms complexes with RAGE, TLR4, p53, histones, and nucleosome remodeling factors, thereby coordinating transcriptional responses that influence senescence, inflammation, and tumor progression. In cancer, HMGB2 overexpression promotes proliferation, invasion, and metastasis through the regulation of cell cycle genes and matrix metalloproteinases.
Knockout of HMGB2 in HEK293T cells enables dissection of its dual roles in chromatin regulation and extracellular signaling. The high transfection efficiency of HEK293T facilitates rescue experiments with wild-type or mutant HMGB2 constructs, allowing functional domain validation. Researchers can stimulate these knockout cells with ligands such as TNF-?? or LPS and measure NF-??B reporter activity or MMP9 secretion to assess pathway dependency. The polyclonal population mitigates clonal artifacts, offering a representative view of HMGB2 depletion effects in a widely used expression system.
This model supports a range of experimental techniques, including ChIP-qPCR for chromatin binding analysis, RNA-seq for transcriptomic profiling, and co-immunoprecipitation for protein interaction studies. Functional assays for proliferation, apoptosis, and migration/invasion enable phenotypic characterization in cancer biology contexts. The cells are also applicable to drug sensitivity testing to validate HMGB2 as a target in inflammatory or neoplastic diseases. Furthermore, they are suitable for senescence research, given the link between HMGB2 and p53 signaling. For technical inquiries or to place an order, please contact Ascent Research.
