The KDM3B Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T-lymphocyte cell line. This product features targeted disruption of the KDM3B gene, which encodes a histone H3 lysine 9 demethylase. The polyclonal nature of the knockout pool ensures a heterogeneous loss-of-function model without single-cell cloning, offering a representative genetic background for population-level studies. The CRISPR/Cas9-mediated gene disruption abolishes KDM3B enzymatic activity, enabling functional investigations of this epigenetic regulator in a T-cell context. These cells are supplied as a viable, ready-to-use culture, ideal for downstream applications in immunology and cancer research.
The parental Jurkat cell line is an immortalized human T-lymphocyte model derived from an acute T-cell leukemia patient. Jurkat cells are widely employed to study T-cell receptor (TCR) signaling, cytokine production, and immune response mechanisms. They exhibit robust activation responses upon TCR stimulation, including calcium flux, activation of transcription factors such as NFAT, NF-??B, and AP-1, and subsequent expression of interleukin-2 and activation markers. This well-characterized background makes Jurkat an optimal host for examining the epigenetic control of T-cell function and leukemogenesis. The knockout cells thus provide a physiologically relevant system for dissecting KDM3B-dependent regulatory networks in T lymphocytes.
KDM3B functions as a histone H3K9me1/2 demethylase and transcriptional coactivator, promoting chromatin remodeling and gene activation. It removes repressive methyl marks to facilitate open chromatin. In Jurkat T cells, KDM3B operates downstream of TCR signaling via calcineurin and NFAT. It interacts with ARID5B, SMAD2/3, PRMT5, HSP90, and 14-3-3 proteins. Its activity is modulated by upstream signals like androgen receptor and HIF1A, and it regulates targets including MYC, CCND1, IL2, CD69, and immune checkpoint genes.
Loss of KDM3B in Jurkat polyclonal cells provides a model to study epigenetic control of T-cell activation and proliferation. Its disruption leads to sustained repressive H3K9me2 marks, dampening activation-induced transcription. This model enables examination of cytokine output, cell cycle progression, and immune checkpoint regulation in a leukemic T-cell context. It also aids research into KDM3B’s roles in metabolic syndrome and spermatogenic failure. Researchers can explore histone modification and oncogenic signaling in a system that mimics aspects of acute T-cell leukemia.
Typical applications include high-throughput screening for epigenetic or immunomodulatory drugs, target validation in leukemia, and mechanistic studies of TCR signaling. Assays include ChIP-qPCR for H3K9me2, RNA-seq, RT-qPCR, Western blotting, flow cytometry for CD69, proliferation assays, co-immunoprecipitation, and reporter assays. For details, contact Ascent Research.
