The BRMS1L Knockout Jurkat Polyclonal Cells provide a defined loss-of-function model generated through CRISPR/Cas9-mediated disruption of the BRMS1L gene in Jurkat T lymphocytes. This product is supplied as a polyclonal knockout cell population, offering a pooled gene-edited model suitable for functional studies of the metastasis suppressor BRMS1L. The polyclonal format retains population-level heterogeneity, enabling robust and reproducible phenotypic analysis in cellular assays. As with all CRISPR-engineered products, the knockout is achieved via targeted genomic disruption, leading to functional ablation of BRMS1L protein expression without introducing exogenous sequences.
The host Jurkat cell line is an immortalized suspension cell line derived from an acute T-cell leukemia patient. Jurkat cells serve as a well-established model for T-cell receptor signaling, proliferation, and apoptosis, and are extensively utilized in immunology and cancer biology research. Their lymphoid origin and ease of culture make them particularly suitable for high-throughput functional genomics screens and mechanistic investigations into hematological malignancies. The parental Jurkat line has been extensively characterized, providing a reproducible background for knockout studies and ensuring comparability across independent experiments.
BRMS1L (Breast Cancer Metastasis Suppressor 1-Like) is a core component of the SIN3A-histone deacetylase (HDAC) transcriptional corepressor complex, where it interacts directly with SIN3A, HDAC1, HDAC2, BRMS1, and MTA1. This complex deacetylates histones at promoters of target genes, leading to transcriptional repression. BRMS1L selectively suppresses genes that drive epithelial-mesenchymal transition (EMT) and cell migration, including MMP9, VEGF, and CXCR4. Its activity is regulated by upstream EMT-inducing transcription factors such as SNAI1 and ZEB1, as well as by TGF-?? and PI3K/AKT signaling pathways. By repressing pro-metastatic gene expression, BRMS1L functions as a critical barrier to cancer cell dissemination and invasion.
Knockout of BRMS1L in Jurkat T leukemia cells is expected to relieve transcriptional repression of EMT-associated genes, potentially conferring enhanced migratory and invasive properties to this lymphoid cell line. This model enables dissection of the SIN3A-HDAC repressive machinery in a T-cell context and provides a platform to investigate the role of metastasis suppressors in hematopoietic malignancies. The Jurkat background facilitates studies on how transcriptional corepressors influence T-cell activation, proliferation, and survival, linking epigenetic regulation to leukemia biology.
The BRMS1L Knockout Jurkat Polyclonal Cells are ideally suited for a range of applications, including chromatin immunoprecipitation (ChIP) assays to assess histone acetylation changes at target promoters, RT-qPCR and RNA-seq for transcriptomic profiling of EMT and apoptosis genes, and functional assays such as Transwell migration/invasion, proliferation, and apoptosis assessments. These cells also serve as a valuable tool for screening small molecules aimed at reactivating metastasis suppressor function or targeting the SIN3A-HDAC complex. For further information or to discuss custom projects, please contact Ascent Research.
