The BASP1 Knockout Jurkat Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of Jurkat T lymphoblasts, designed to disrupt the BASP1 gene and ablate functional protein expression. This polyclonal format preserves editing diversity, reducing clonal artifacts and enabling robust loss-of-function studies under near-physiological knockout conditions. The cells are optimal for high-throughput or pooled screening applications.
Derived from an acute T cell leukemia patient, the Jurkat host cell line is a suspension culture of CD4-positive T lymphoblasts. These cells retain key signaling pathways for T cell activation, apoptosis, and proliferation, making them a principal model for leukemia biology, T cell receptor signaling, and cancer pharmacology. Jurkat cells are easily transfectable and compatible with diverse molecular and cell-based assays.
BASP1 operates as a transcriptional co-repressor for Wilms?? tumor protein 1 (WT1) by recruiting histone deacetylase 1 (HDAC1) to target gene promoters, thereby silencing transcription. In parallel, BASP1 binds calmodulin in a calcium-dependent manner and interacts with phosphatidylinositol 4,5-bisphosphate (PIP2) and filamentous actin, linking calcium influx and protein kinase C (PKC) signals to actin filament assembly. Consequently, BASP1 integrates WT1-mediated transcriptional repression and calcium-dependent cytoskeletal regulation, positioning it within the WT1-BASP1-HDAC1 complex and the Ca2+-calmodulin-BASP1-actin axis.
In Jurkat cells, BASP1 knockout allows dissection of WT1-mediated gene regulatory networks in T cell leukemia, where WT1 is frequently dysregulated. Loss of BASP1 derepresses WT1 target genes, likely affecting programs of differentiation and apoptosis. Concurrently, disruption of BASP1-calmodulin-actin signaling may impair actin remodeling required for immune synapse formation and leukemic cell migration. Thus, this model supports integrated analysis of transcriptional and cytoskeletal contributions to leukemia pathology.
This polyclonal knockout cell population is suitable for Western blotting and RT-qPCR to confirm BASP1 ablation and downstream target changes, co-immunoprecipitation to assess WT1-HDAC1 complex integrity, immunofluorescence for actin cytoskeletal architecture, flow cytometry for apoptosis and surface marker analysis, and drug sensitivity assays for leukemia therapeutic screening. RNA-seq can reveal global transcriptomic alterations. For additional technical information or collaboration, please contact Ascent Research.
