The KDM5C Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population providing loss-of-function studies of KDM5C. This heterogeneous pool of Jurkat T lymphoblastoid cells carries Cas9-mediated gene disruptions, enabling investigation of chromatin remodeling and transcriptional regulation in a leukemia-relevant model. The polyclonal format allows robust assessment of KDM5C-dependent phenotypes across a biologically variable background without clonal selection.
Jurkat cells, derived from the peripheral blood of a 14-year-old male with acute T cell leukemia, are a widely used suspension lymphoblastoid line. They serve as a canonical model for T cell signaling, activation, and apoptosis, and are extensively applied in leukemia biology, immune receptor signal transduction, and drug screening. Their high proliferative capacity and defined signaling networks make them suitable for studying epigenetic influences on lymphoid malignancies.
KDM5C is a histone H3K4 demethylase that removes methyl groups from H3K4me2/me3, acting as a transcriptional repressor within complexes containing the REST corepressor and HDAC1/2. Its activity is regulated by MYC, miR-138, and REST, and it targets genes like CDKN1A and BCL2 to suppress expression. KDM5C knockout thus increases H3K4 methylation, derepressing these and other targets to alter cell cycle and survival control.
In Jurkat cells, loss of KDM5C likely shifts the epigenetic landscape at regulatory regions, affecting T cell receptor signaling, proliferation, and apoptosis. As a repressor of tumor-suppressor and survival genes, its disruption may modulate leukemogenic gene programs. The polyclonal population avoids clonal bias, offering a representative view of KDM5C’s role in T lymphoblastoid cell biology.
Applications include epigenetic drug screening with demethylase inhibitors, histone modification mapping by ChIP-qPCR, and transcriptomic analysis via RNA-seq. Typical assays involve western blotting for H3K4me2/me3 and KDM5C, RT-qPCR of CDKN1A and BCL2, and flow cytometry for proliferation and apoptosis. This model also aids studies of X-linked intellectual disability (Claes-Jensen syndrome) by providing a T cell platform. For further information, contact Ascent Research.
