The PATL1 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-mediated gene-disrupted population derived from the Raji B lymphocyte line, targeting the PATL1 locus to eliminate functional protein expression. This polyclonal knockout pool provides a heterogeneous loss-of-function model for studying PATL1-dependent processes without clonal selection, enabling robust investigation of mRNA decay and translational control in a human B-cell context. The product is supplied as a validated polyclonal population and is suitable for a broad range of functional assays requiring PATL1 deficiency.
The Raji host cell line is an Epstein-Barr virus-immortalized lymphoblastoid cell line originating from Burkitt lymphoma. As a model of human B lymphocytes, Raji cells are extensively used in immunology and cancer research to examine humoral immunity, B-cell activation, proliferation, and lymphomagenesis. Their rapid growth and well-characterized signaling landscape make them an ideal chassis for probing post-transcriptional regulatory mechanisms, particularly those governing mRNA stability and translation during immune responses.
PATL1 functions as an mRNA decapping activator, a scaffold that recruits the decapping complex??comprising DCP1A, DCP2, and EDC4??to target mRNAs, facilitating removal of the 5?? cap and subsequent 5??-to-3?? exonucleolytic decay by XRN1. It also interacts with the LSM1-7 complex, UPF1, and Argonaute2 (AGO2), linking decapping to nonsense-mediated decay and microRNA-mediated silencing. Upstream, PATL1 is regulated by cellular stress pathways including mTOR and MAPK/ERK signaling, while downstream its activity globally influences mRNA half-lives and translational output, thereby modulating the balance between translation and degradation in cytoplasmic RNA granules.
In Raji B cells, PATL1 knockout disrupts processing body (P-body) formation and alters the decay kinetics of mRNAs involved in cell cycle control, apoptosis, and immune signaling. Given that B lymphocytes rely on precise gene expression changes during antigen responses, impaired PATL1 function may disturb activation thresholds and proliferation, offering a model for studying RNA dysfunction in B-cell malignancies. This system is also relevant to broader pathological contexts where PATL1-linked neurodevelopmental disorders, breast cancer, and colorectal cancer implicate aberrant mRNA turnover in disease progression.
Researchers can employ these knockout cells in mRNA stability assays using actinomycin D chase, RT-qPCR quantification of specific decay substrates, polysome profiling to assess translational efficiency, and RNA sequencing to map transcriptome-wide changes. Immunofluorescence staining for P-body markers such as DCP1A and GW182 allows visualization of granule dynamics, while flow cytometry facilitates analysis of B-cell surface markers and viability. Additional applications include western blotting for downstream effectors and co-immunoprecipitation to validate protein interactions. For technical specifications and ordering information, please contact Ascent Research.
