ANKRD12 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the ANKRD12 gene in the Jurkat human T lymphoblast line. This gene-disrupted model enables loss-of-function studies of the transcriptional corepressor ANKRD12 in the context of T cell acute lymphoblastic leukemia (T-ALL) research. The polyclonal pool contains a spectrum of edits and is suited for pooled functional screens or isolation of clonal derivatives.
Jurkat cells are an immortalized human T lymphocyte line derived from acute T cell leukemia, widely used to investigate T cell signaling, activation, and apoptosis. Their genome commonly harbors activating Notch1 mutations that drive constitutive Notch signaling, making them a highly relevant host for studying pathway modulators like ANKRD12. This background provides a sensitized system for assessing repressor function and downstream transcriptional consequences.
ANKRD12 functions as a corepressor of the Notch signaling pathway by binding the transcription factor CSL/RBP-J?? and recruiting HDAC3, N-CoR, and SMRT complexes to repress transcription of Notch target genes, including HES1, HES5, MYC, and CCND1. This repressive activity counteracts the activation mediated by the Notch intracellular domain (NICD) and MAML1 coactivators, positioning ANKRD12 as a critical negative regulator of Notch-dependent proliferation and differentiation programs. Its function is influenced by upstream factors such as CSL/RBP-J?? availability and HDAC3 catalytic activity.
In Jurkat cells with hyperactive Notch signaling, ANKRD12 knockout releases transcriptional repression, leading to upregulation of target genes and mimicking aspects of T-ALL pathogenesis or neurodevelopmental disorders. This model allows investigation of how corepressor loss cooperates with oncogenic signaling to promote leukemic phenotypes and may reveal new therapeutic targets by identifying synthetic lethal interactions or drug sensitivities arising from ANKRD12 deficiency.
Applications encompass Western blotting for protein depletion, RT-qPCR for HES1 and MYC expression, RNA-seq transcriptomics, Notch reporter assays, flow cytometry for activation markers, and functional assays for proliferation, apoptosis, and drug response. These tools enable detailed dissection of Notch signaling, transcriptional repression, and T-ALL biology. For further information, please contact Ascent Research.
