The HMG20B Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population with targeted disruption of the HMG20B gene in the HAP1 host background. This loss-of-function model is designed for studies requiring depletion of HMG20B protein and enables systematic investigation of the gene??s cellular functions without the use of complete clonal isolation.
The HAP1 cell line is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line. Its haploid karyotype makes it an exceptional tool for genetic perturbation studies, as it simplifies the creation of complete gene knockouts without the complication of heterozygous alleles. HAP1 cells retain key signaling pathways relevant to CML and broader cancer biology, making them a versatile model for hematological malignancies and functional genomics.
HMG20B (also known as BRAF35) encodes a non-histone chromosomal protein that functions as a key component of the REST corepressor complex. In this complex, HMG20B interacts with REST, CoREST, HDAC1/2, LSD1, and BRG1 to facilitate histone deacetylase and demethylase activities, leading to transcriptional repression of neuronal genes such as BDNF and SYN1. Beyond its role in neuronal gene silencing, HMG20B participates in DNA repair by interacting with BRCA2 and regulating RAD51-mediated homologous recombination, thereby contributing to genomic stability. Upstream regulators of HMG20B include REST and E2F transcription factors, which integrate cell cycle signals with chromatin remodeling. Thus, HMG20B sits at the intersection of epigenetic silencing, cell cycle control, and DNA damage response pathways.
In the HAP1 near-haploid background, disruption of HMG20B generates a homogeneous loss-of-function model that is particularly suited for deciphering its dual role in transcriptional repression and DNA repair. The CML origin of HAP1 cells provides a disease-relevant context for studying HMG20B function in hematological cancers, where aberrant REST complex activity has been implicated. Moreover, the haploid nature minimizes genetic redundancy, allowing clear interpretation of phenotypic outcomes in assays such as cell cycle analysis, drug sensitivity profiling, and haploid genetic screens. This model enables systematic interrogation of HMG20B-dependent mechanisms without the confounding effects of wild-type alleles.
Researchers can employ this polyclonal knockout pool in a wide range of applications. Chromatin biology studies benefit from ChIP-seq and western blotting to assess histone modification changes and REST complex integrity. Neuroscience-oriented projects may use RT-qPCR or RNA-seq to examine derepression of neuronal genes. Cancer biologists can investigate cell cycle defects via flow cytometry and DNA repair dysfunction by quantifying DNA damage foci with immunofluorescence. Additionally, the cells are compatible with drug sensitivity assays and haploid genetic screens to identify synthetic lethal interactions or validate drug targets. For further information or to discuss customization, please contact Ascent Research.
