The HMGB2 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HAP1 cell line, designed for disruption of the HMGB2 gene. This product provides a genetically mixed knockout population suitable for loss-of-function studies in a near-haploid genetic background, enabling investigation of HMGB2-dependent processes in chromatin biology, transcriptional regulation, and inflammatory signaling.
HAP1 is a fibroblast-like cell line with a near-haploid karyotype, originally derived from the KBM-7 chronic myeloid leukemia line. Its haploid genetic makeup simplifies functional genomics and cancer research by eliminating allelic redundancy, making it an ideal host for studying genes involved in chromatin dynamics, DNA damage repair, and oncogenic signaling pathways.
HMGB2 is a non-histone chromosomal protein that bends DNA and facilitates transcription factor assembly and chromatin remodeling. It functions both as a nuclear architectural factor and as an extracellular damage-associated molecular pattern. HMGB2 interacts with HMGB1, RAGE, TLR2, TLR4, and the NF-??B subunit p65/RelA, integrating signals from upstream regulators such as TNF-??, IL-1??, and lipopolysaccharide. Downstream, it promotes expression of pro-inflammatory cytokines IL-6 and TNF-??, matrix metalloproteinases, and proliferation genes. Its knockout impairs NF-??B-mediated signaling, disrupts DNA repair, and alters gene expression profiles, positioning HMGB2 at the intersection of pathways involving RAGE, TLR4/MyD88, p38 MAPK, and p53.
In HAP1 cells, the near-haploid background accentuates phenotypes from HMGB2 loss, particularly in DNA damage response and transcriptional regulation. This system enables direct assessment of reduced NF-??B activity, altered cytokine production, and defective chromatin remodeling, with minimal compensation from a second allele. The model thus serves as a powerful platform for studying HMGB2??s role in hepatocellular carcinoma, glioblastoma, rheumatoid arthritis, sepsis, and systemic lupus erythematosus.
This polyclonal knockout population supports diverse experimental applications, including western blotting, RT-qPCR, immunofluorescence, and ChIP-qPCR to analyze protein expression and chromatin localization. NF-??B reporter assays, cytokine ELISA, and wound healing assays facilitate functional studies of inflammatory signaling and cell migration. It is ideally suited for researchers in chromatin biology, inflammation, cancer signaling, and functional genomics. For further information, please contact Ascent Research.
