The HMGB2 Knockout HeLa Polyclonal Cells product is a heterogeneous cell population derived from HeLa cells following CRISPR/Cas9-mediated disruption of the HMGB2 gene, creating a polyclonal loss-of-function model. This format avoids clonal selection artifacts and preserves genetic variability, making it ideal for experiments requiring pooled knockout cultures. The cells are supplied as a convenient research tool for investigating HMGB2-dependent processes in cancer biology and gene regulation.
HeLa cells, the host line, are human cervical adenocarcinoma cells positive for HPV18, exhibiting robust growth, high transfectability, and well-defined signaling pathways. Their epithelial origin and transformed nature make them a standard model for studying tumor suppressor mechanisms, DNA damage responses, and oncogenic signaling, with particular relevance to p53 and NF-??B pathway analysis.
HMGB2 functions as a chromatin architectural protein that bends DNA and facilitates nucleosome remodeling, promoting transcription factor access and DNA repair. It is regulated by p53 and inflammatory cytokines, and it interacts with proteins such as RAG1, TBP, and p53 itself. Downstream, HMGB2 influences the expression of key apoptosis and cell cycle regulators including BAX, Bcl-2, and CDKN1A (p21), mediating signals through NF-??B and p53 transcriptional networks. Disruption of HMGB2 in these cells impairs DNA damage-induced responses and perturbs the balance between pro-survival and pro-apoptotic gene programs.
In the HeLa context, where HPV18 oncoproteins E6 and E7 subvert p53 and Rb tumor suppressor functions, HMGB2 knockout further uncouples chromatin-mediated regulation of transcription and repair. This enables dissection of cooperative interactions between viral oncogenesis and host chromatin dynamics, particularly how HMGB2 deficiency impacts cell cycle checkpoints, apoptosis susceptibility, and senescence entry. The polyclonal configuration reflects the heterogeneity of tumor cell populations, providing a more physiologically relevant model for studying adaptive responses and drug effects.
Representative applications include Western blotting, RT-qPCR, immunofluorescence, and flow cytometry for expression analysis, as well as apoptosis assays, cell cycle profiling, and ??-H2AX foci quantification to assess DNA damage. These cells are suited for cancer biology research, drug sensitivity screens, DNA repair mechanism studies, gene regulation investigations, and senescence assays. The polyclonal knockout format is compatible with pooled CRISPR screens and high-throughput phenotypic analyses. For further details, please contact Ascent Research.
