The BEND3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in which the BEND3 gene is disrupted in the Jurkat T-cell line. This loss-of-function model enables investigation of BEND3-mediated transcriptional repression in T cell acute lymphoblastic leukemia (T-ALL) without relying on clonal isolates, providing a heterogeneous system suitable for pooled functional genomics and signaling studies.
Jurkat is an immortalized T lymphocyte line derived from a 14-year-old male with T-ALL, widely used to study T cell signaling and leukemogenesis. Constitutively activated Notch1 signaling, driven by mutations in NOTCH1 or FBXW7, renders these cells dependent on Notch target gene expression, making Jurkat an ideal host for interrogating regulators such as BEND3 that modulate Notch transcriptional output.
BEND3 is a BEN domain-containing transcriptional repressor that binds DNA and recruits corepressor complexes like SIN3A-HDAC and NuRD. In the Notch pathway, BEND3 directly interacts with RBPJ to silence target genes including HES1, MYC, and DLL1. NOTCH1 activation and SOX2 can regulate BEND3 function, relieving repression and enabling context-specific gene expression crucial for cell proliferation and differentiation.
In Jurkat cells, knockout of BEND3 results in derepression of Notch targets such as HES1 and MYC, capturing a key regulatory mechanism in T-ALL. This polyclonal knockout model allows dissection of how loss of BEND3-dependent silencing reshapes the Notch-driven transcriptional program and may expose therapeutic vulnerabilities in cancers with aberrant Notch signaling.
Applications include functional genomics screens, compound screening for Notch modulators, and mechanistic studies of transcriptional repression. Compatible techniques include Western blotting, RT-qPCR, RNA-seq, ChIP-qPCR, Notch reporter assays, flow cytometry, proliferation, apoptosis, and drug sensitivity assays. For further information, contact Ascent Research.
