The ID3 Knockout Jurkat Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal population derived from the Jurkat T-cell leukemia line, with disruption of the ID3 gene. This heterogeneous knockout pool provides a loss-of-function model for ID3 without clonal selection. Supplied as viable cells, it is immediately usable for expansion and functional assays. The polyclonal format minimizes clonal artifacts and is ideal for initial phenotypic screening and drug testing applications.
Jurkat cells are an immortalized human T lymphocyte line from acute T-cell leukemia, a mainstay for studies on T-cell receptor signaling, apoptosis, and oncogenic transformation. They are highly amenable to CRISPR/Cas9 genome editing and exhibit constitutive activation of pathways such as Notch, which is frequently altered in T-ALL. The ID3 knockout derivative thus leverages a well-characterized model for leukemogenesis and T-cell biology.
ID3 acts as a dominant-negative inhibitor of basic helix-loop-helix (bHLH) transcription factors by forming non-functional heterodimers with E proteins including E2A (TCF3), HEB (TCF12), and E2-2 (TCF4). This blocks E-box-mediated transcription of genes controlling differentiation, proliferation, and apoptosis. ID3 expression is induced downstream of Notch signaling through NICD/RBP-J-mediated activation and via TGF-??/Smad2/3. Additionally, Wnt pathway inputs influence ID3 levels. Consequently, ID3 knockout derepresses E protein activity, altering cell cycle and apoptosis gene expression, and thereby impacts T-cell fate decisions.
In Jurkat T-ALL cells, ID3 is often overexpressed, maintaining a differentiation block and survival advantage. CRISPR/Cas9-mediated ID3 knockout in this polyclonal population relieves suppression of E protein transcriptional programs, potentially restoring differentiation and sensitizing to apoptosis. Given the prominence of Notch1 mutations in T-ALL, this model is particularly suited for investigating crosstalk between oncogenic Notch and ID3-regulated networks. It also enables exploration of TGF-?? and Wnt contributions to leukemic growth and normal T-cell development.
This polyclonal ID3 knockout cell population supports diverse research applications including identification of ID3 target genes via RNA-seq or reporter assays, cell cycle and apoptosis analysis by flow cytometry, and co-immunoprecipitation of bHLH complexes. Functional studies may assess proliferation, drug sensitivity, and Notch signaling activity. The model is valuable for studying T-ALL pathogenesis and for screening therapeutic candidates. For detailed product specifications and support, contact Ascent Research.
