The KDM1B Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Jurkat T-lymphocytes with disrupted KDM1B, the histone demethylase also known as LSD2. This loss-of-function model enables investigation of KDM1B-dependent epigenetic regulation without clonal selection bias, suitable for studies in gene regulation, signal transduction, and drug discovery.
The Jurkat cell line, derived from a patient with acute T-cell leukemia, serves as an immortalized model for T-cell receptor (TCR) signaling, apoptosis, and activation. Its well-characterized pathways make it ideal for exploring epigenetic mechanisms in T-cell malignancies and immune responses, providing a relevant background for KDM1B functional studies.
KDM1B specifically demethylates H3K4me1/me2, leading to transcriptional repression. It functions within the CoREST complex, interacting with RCOR1 and HDAC1, and is regulated by REST. KDM1B is activated downstream of TCR and Notch signaling, targeting regulatory regions of genes such as OCT4, NANOG, and Grb10. This demethylase thus integrates external signals with chromatin modification, influencing stem cell maintenance and imprinting.
In Jurkat T-cells, KDM1B knockout may alter H3K4 methylation at enhancers and promoters, potentially affecting T-cell activation, differentiation, or apoptosis. This model allows interrogation of demethylase activity in acute lymphoblastic leukemia, glioblastoma, and germ cell tumors, and can be used to study interactions among CoREST, HDAC1, and REST in modulating oncogenic gene expression.
Researchers can use these polyclonal cells for transcriptome analysis by RNA-seq, ChIP-qPCR for H3K4 methylation, and RT-qPCR for target genes. Protein loss is verified by Western blotting, while functional assays include flow cytometry for activation markers and apoptosis, along with drug sensitivity testing using LSD1/KDM1 inhibitors. This model supports drug target validation and mechanistic studies in T-cell leukemia. For additional information regarding this product, please contact Ascent Research.
