The BAZ2B Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population carrying targeted disruption of the BAZ2B gene in the human Jurkat T?lymphocyte background. This loss?of?function model enables investigation of BAZ2B?dependent chromatin remodeling and epigenetic silencing in a well?characterized immune cell system. The polyclonal format preserves the functional heterogeneity of the knockout pool, making it suitable for assays where clonal isolation is not required, and facilitates robust statistical comparisons between edited and parental populations.
Jurkat cells are an immortalized human T?cell line originally isolated from a patient with acute T?cell leukemia. They serve as a widely used model for T?cell receptor signaling, activation?induced apoptosis, and adaptive immunity. Their genetic tractability and well?documented signaling networks make them an ideal host for CRISPR?based functional genomics studies. The Jurkat background is particularly relevant for dissecting the role of chromatin?modifying enzymes in leukemogenesis and T?cell biology.
BAZ2B encodes a chromatin remodeling factor that acts as a key component of the nucleolar remodeling complex (NoRC). Within NoRC, BAZ2B heterodimerizes with TIP5 (BAZ2A) and recruits the ATP?dependent remodeler SNF2H (SMARCA5), along with HDAC1 and DNMT1, to rDNA loci. The complex is tethered to rDNA promoters by the transcription termination factor TTF1, where it establishes a repressive chromatin environment through histone deacetylation and DNA methylation. This cascade silences ribosomal RNA (rRNA) gene transcription, thereby suppressing ribosome biogenesis and constraining cellular growth. BAZ2B function is further influenced by upstream regulators including MYC and growth factor signaling, and its silencing feeds into downstream effects on rDNA loci, rRNA output, and genes governing proliferation and differentiation.
In Jurkat cells, disruption of BAZ2B provides a platform to examine how epigenetic silencing pathways intersect with T?cell signaling and leukemic transformation. Given the role of NoRC in modulating nucleolar activity in response to growth cues, this knockout model is particularly valuable for exploring the link between chromatin?level gene regulation and cell cycle control in a malignant lymphocyte context. It can uncover dependencies on BAZ2B?mediated silencing that may be exploitable in acute T?cell leukemia or other cancers driven by deregulated ribosome biogenesis.
Typical applications include chromatin immunoprecipitation (ChIP?qPCR) to assess histone modifications (e.g., H3K9me3, H4K16ac) at rDNA, RT?qPCR for pre?rRNA transcripts to measure transcriptional output, and western blotting to quantify BAZ2B and its NoRC partners. The cells can be employed in bromodomain?targeted drug screening campaigns to identify compounds that disrupt BAZ2B?chromatin interactions. Functional assays such as flow cytometry?based cell cycle analysis, apoptosis and proliferation measurements, and transcriptome?wide RNA?seq further enable comprehensive phenotypic characterization. For additional information or custom requirements, please contact Ascent Research.
