GPATCH11 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Jurkat T lymphoblast line. These cells carry a targeted disruption of the GPATCH11 gene, resulting in loss of functional protein expression. The polyclonal format preserves genetic heterogeneity inherent to CRISPR editing, suitable for population-level functional studies. This loss-of-function model enables investigation of GPATCH11 roles in T cell biology without requiring clonal expansion.
The Jurkat cell line is an immortalized human T lymphoblast line derived from a patient with acute T cell leukemia. It is widely used to study T lymphocyte signaling, leukemia biology, and apoptosis. Jurkat cells express functional T cell receptors (TCRs) and downstream signaling components, enabling analysis of pathways such as NFAT, NF-??B, and AP-1. Their genetic tractability and well-characterized transcriptome make them an ideal host for gene editing studies of RNA processing and splicing.
GPATCH11 is a G-patch domain-containing protein predicted to function as an RNA-binding protein involved in pre-mRNA splicing. The G-patch domain mediates interactions with DEAD-box RNA helicases, notably DHX15, a component of the U5 snRNP and spliceosome. GPATCH11 is thought to regulate spliceosome assembly or catalytic activity, influencing alternative splicing and transcriptome output. While its upstream regulators and downstream targets remain uncharacterized, the protein??s association with core splicing machinery positions it as a modulator of RNA metabolism. Functional studies in Jurkat knockout cells may clarify how GPATCH11-dependent splicing events coordinate gene expression programs critical for lymphocyte function.
In Jurkat T cells, splicing regulation is linked to activation, proliferation, and apoptosis. Dysregulation of mRNA splicing is common in leukemias, and splicing factors are potential therapeutic targets. Disrupting GPATCH11 in a polyclonal Jurkat population allows investigation of its contributions to T cell growth, viability, and signaling under basal and stimulated conditions. This model is valuable for dissecting DEAD-box helicase-associated splicing in leukemia pathogenesis. The polyclonal format retains the mutational spectrum from CRISPR editing, enabling pooled knockout phenotyping that may better reflect tumor heterogeneity than single-cell clones.
The GPATCH11 Knockout Jurkat Polyclonal Cells are designed for functional genomic and biochemical assays. They can be used for RNA-seq to identify splicing alterations and transcriptome changes upon GPATCH11 loss, alongside RT-qPCR and western blotting for target validation and protein-level analysis. Flow cytometry enables evaluation of surface markers, cell cycle, and apoptosis. Proliferation and apoptosis assays allow direct phenotypic comparison to wild-type Jurkat cells. These applications support investigations into RNA processing in immune cells, splicing-dependent cancer mechanisms, and functional characterization of unstudied splicing regulators. For additional information, please contact Ascent Research.
