FAT1 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line. This product provides a heterogenous pool of cells carrying targeted disruptions in the FAT1 gene, enabling loss-of-function studies without clonal selection. The polyclonal format preserves biological variability and is well-suited for functional genomics, drug screening, and pathway analysis. Researchers can use these cells to interrogate FAT1-dependent mechanisms in hematopoietic malignancy models with robust reproducibility.
The parental Raji cell line originates from an Epstein?CBarr virus (EBV)-positive Burkitt??s lymphoma and represents a widely used suspension lymphoblastoid model of mature B lymphocytes. Raji cells constitutively exhibit malignant B-cell features, including high proliferative capacity and immunoglobulin expression, making them ideal for studying B-cell receptor signaling, apoptosis regulation, and oncogenic pathways. Their suspension growth facilitates high-throughput applications and scalable experimental designs.
FAT1 encodes an atypical cadherin that senses intercellular contact and transduces signals primarily through the Hippo pathway. Extracellularly, it engages in calcium-dependent homophilic and heterophilic interactions with DCHS1. Intracellularly, FAT1 recruits the scaffold protein SAV1 and the kinases MST1 and LATS1, which form a core kinase cassette that phosphorylates and inactivates the transcriptional co-activators YAP and TAZ. This phosphorylation promotes cytoplasmic retention and degradation, thereby inhibiting expression of pro-proliferative and anti-apoptotic targets. Additionally, FAT1 intersects with Wnt signaling by modulating ??-catenin stability and contributes to actin cytoskeleton reorganization through regulators such as ENA/VASP. Upstream, FAT1 expression is itself subject to ??-catenin/TCF-dependent transcriptional regulation, establishing feedback control.
In Raji B lymphocytes, FAT1 is thought to function as a tumor suppressor, and its disruption may relieve Hippo-mediated inhibition of YAP/TAZ, enhancing cell survival and proliferation. Loss of FAT1 can also alter adhesion properties and cytoskeletal dynamics, potentially affecting B-cell homing and metastatic behavior. This knockout model therefore offers a physiologically relevant system to dissect how FAT1 coordinates contact-dependent growth control in B-cell malignancies and to evaluate its impact on chemosensitivity and immune evasion.
Typical applications include investigating FAT1-mediated Hippo signaling in lymphoma, performing drug sensitivity assays with agents such as doxorubicin and etoposide, and assessing apoptosis or cell-cycle changes via flow cytometry. Researchers can measure YAP/TAZ phosphorylation status by Western blotting, quantify target gene expression using RT-qPCR or RNA-seq, and map protein interactions through co-immunoprecipitation of endogenous partners like MST1 or ??-catenin. Phospho-signaling arrays further enable hypothesis-driven exploration of crosstalk between FAT1 and parallel pathways. For additional technical details or to discuss your experimental needs, please contact Ascent Research.
