The KMT2C Knockout Jurkat Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of Jurkat cells with targeted disruption of the KMT2C gene. This loss-of-function model is generated without single-cell cloning, yielding a heterogeneous mixture of edited alleles that collectively ablate KMT2C expression, suitable for pooled knockout studies in T-cell leukemia research.
The Jurkat host cell line is an immortalized acute T-cell leukemia line derived from the peripheral blood of a patient. It serves as a well-characterized model for T-cell receptor (TCR) signaling, cytokine responses, and leukemogenesis, making it an appropriate background to interrogate oncogenic enhancer regulation.
KMT2C encodes a catalytic subunit of the MLL3/4 histone methyltransferase complex, which includes core components ASH2L, RBBP5, WDR5, DPY30, and UTX. This complex catalyzes monomethylation of histone H3 at lysine 4 (H3K4me1) at enhancer regions, priming chromatin for gene activation. KMT2C activity is modulated by upstream factors such as Notch1 intracellular domain, P53, STAT3, and ??-catenin, and it regulates downstream targets including CDKN1A, BAX, MYC, and CCND1, thereby influencing cell cycle progression, apoptosis, and differentiation. Through interactions with PTIP and NCOA6, KMT2C integrates signaling from Notch, Wnt, and p53 pathways to coordinate transcriptional programs.
In Jurkat cells, disruption of KMT2C impairs enhancer function, leading to altered expression of genes critical for T-cell homeostasis and leukemic transformation. As KMT2C mutations are observed in T-cell acute lymphoblastic leukemia and other malignancies, this model enables dissection of KMT2C’s tumor-suppressive roles, where it antagonizes Notch1-driven transcription and supports p53-dependent checkpoints. The polyclonal nature preserves genetic heterogeneity, mirroring the clonal diversity of tumors.
This product is ideal for investigating enhancer-mediated gene regulation in T-cell acute lymphoblastic leukemia, screening epigenetic agents such as BET inhibitors, and mapping signal-dependent enhancer landscapes. Representative assays include western blotting for H3K4me1, ChIP-qPCR at developmentally regulated enhancers, RNA-seq transcriptomics, flow cytometry for Annexin V apoptosis, cell cycle profiling, and TCR signaling activation readouts. For additional details or technical support, please contact Ascent Research.
