HERC4 Knockout Jurkat Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population in which the HERC4 gene has been disrupted. This loss-of-function model enables investigation of HERC4 in T lymphocyte biology. The polyclonal pool comprises a heterogeneous mix of edited cells, minimizing clonal selection bias and providing a robust platform for diverse assays.
The Jurkat host cell line is a human T lymphocyte model originally derived from the peripheral blood of a 14-year-old male with acute T cell leukemia. Established in the late 1970s, Jurkat cells are widely used for studying T cell receptor signaling, apoptosis, and immunology. Their continuous proliferation and well-characterized signaling networks make them an ideal system for dissecting ubiquitin-mediated regulatory mechanisms.
HERC4 encodes a putative E3 ubiquitin ligase that operates within the ubiquitin-proteasome system, catalyzing ubiquitin transfer to substrate proteins for 26S proteasomal degradation. Its direct regulators and targets are unknown, but it likely interacts with E2 ubiquitin-conjugating enzymes and proteasome subunits. Representative pathway components include ubiquitin, E1 activating enzyme, E2 conjugating enzymes, HERC4 E3 ligase, and the 26S proteasome. Through protein quality control, HERC4 may influence cell cycle progression and apoptosis. Knockout likely disrupts degradation of key substrates, enabling dissection of its physiological roles.
In Jurkat T cells, HERC4 loss allows exploration of ubiquitin-mediated proteolysis in T cell receptor signaling and leukemic cell survival. Given potential involvement in tumorigenesis, this knockout model can help elucidate contributions to malignant phenotypes such as proliferation and apoptosis resistance. The Jurkat background facilitates study of HERC4-dependent effects on pathways like NF-??B and MAPK, critical in immune function and oncogenesis. The polyclonal population captures phenotypic heterogeneity, offering a realistic model for cellular responses.
Typical applications include investigating HERC4 function in ubiquitin-proteasome dynamics, T cell biology, and cancer models. Standard assays include Western blot and RT-qPCR for knockout confirmation, proteasome activity and ubiquitination assays, cell proliferation (MTS/MTT), apoptosis (Annexin V), and flow cytometry for cell cycle analysis. This tool is also suitable for drug target validation of ubiquitin ligases in leukemia. For additional information, please contact Ascent Research.
