The HMG20B Knockout Jurkat Polyclonal Cells are a genetically engineered cell pool generated by CRISPR/Cas9-mediated disruption of the HMG20B gene in the Jurkat immortalized T lymphocyte line. As a polyclonal population, this product contains a heterogeneous mix of edited alleles, providing a robust loss-of-function model without clonal selection artifacts. This knockout model is designed for studying the functional consequences of HMG20B ablation in human T cells, particularly its role in transcriptional repression and chromatin remodeling.
The Jurkat cell line is a well-established human T lymphocyte line derived from the peripheral blood of a 14-year-old male with acute T cell leukemia. These suspension-adapted cells are widely utilized to investigate T cell receptor (TCR) signaling, apoptosis, and cytokine production. Their rapid proliferation and ease of manipulation make them a versatile host for genetic perturbation and functional genomics studies, including the interrogation of epigenetic regulators like HMG20B in a lymphoid context.
HMG20B (also known as BRAF35) functions as a critical non-catalytic subunit of the BRAF-HDAC (BHC) repressor complex. It forms a stable core with the histone demethylase LSD1 (KDM1A), the scaffold protein CoREST (RCOR1), and histone deacetylases HDAC1/HDAC2. This complex is recruited by the transcriptional repressor REST to neuronal gene promoters, where it orchestrates chromatin compaction through coordinated histone deacetylation and demethylation. Known downstream targets of this repressive machinery include BDNF, SYN1, and SCN2A, whose expression is silenced in non-neuronal cells. HMG20B also interacts with BHC80 (PHF21A) and has been implicated in Wnt pathway modulation, linking it to broader signaling networks.
In Jurkat T cells, knockout of HMG20B disrupts the REST/CoREST repressor complex, potentially derepressing neuronal-specific genes in a lymphoid environment. This model enables dissection of HMG20B’s contribution to epigenetic silencing independent of neuronal differentiation, offering insights into how chromatin-modifying complexes operate in immune cells. Given the increasing recognition of REST and its cofactors in T cell function and disease, this knockout tool is valuable for probing the cross-talk between epigenetic repression and T cell biology, as well as for studying the pathological roles of HMG20B in hepatocellular carcinoma and pancreatic cancer, where aberrant expression is observed.
This polyclonal knockout product supports a broad range of experimental workflows. Researchers can employ chromatin immunoprecipitation (ChIP-qPCR) to assess changes in histone marks at target promoters, RNA sequencing (RNA-seq) to map global transcriptome alterations, and quantitative PCR (RT-qPCR) to validate derepression of BDNF and SYN1. Co-immunoprecipitation (co-IP) and western blotting are suitable for examining complex stability, while luciferase reporter assays can measure REST-dependent transcriptional activity. Additionally, flow cytometry permits immunophenotyping and apoptosis assays, and the cells can serve in high-throughput screens for HDAC inhibitors or epigenetic modulators. For further details and custom inquiries, please contact Ascent Research.
