The FLT3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line. These human suspension cells carry a targeted disruption of the FLT3 gene, resulting in loss of functional FLT3 receptor tyrosine kinase expression. This polyclonal pool serves as a versatile loss-of-function model for investigating FLT3-dependent signaling without the clonal selection bias associated with single-cell-derived lines.
The Raji cell line originates from an EBV-positive Burkitt lymphoma patient and is widely used as a model for B-cell malignancies and immune regulation. These suspension-adapted B lymphoblastoid cells retain key features of antigen-presenting cells and are capable of robust proliferation. Their EBV-transformed status provides a reproducible genetic background for studying oncogenic signaling, and the cells?? lymphoid origin makes them particularly relevant for examining pathways involved in hematopoietic development and leukemogenesis.
FLT3 is a receptor tyrosine kinase activated by FLT3 ligand (FL) and hematopoietic cytokines. Ligand binding induces dimerization and autophosphorylation, recruiting adaptor proteins GRB2, GAB2, SHC, and PTPN11, along with the ubiquitin ligase CBL. This initiates downstream signaling via the PI3K-AKT-mTOR axis, the RAS-RAF-MEK-ERK MAPK pathway, and the JAK-STAT module, with STAT5 serving as a key transcriptional effector. These signals upregulate targets such as BCL2 and cyclin D1, promoting cell survival and proliferation. FLT3 integrates external cues to fine-tune hematopoietic cell fate decisions.
In the Raji B-cell background, FLT3 signaling sustains growth and inhibits apoptosis. CRISPR/Cas9-mediated FLT3 disruption ablates PI3K/AKT, MAPK/ERK, and JAK/STAT pathway activation, impairing proliferation and survival. These polyclonal knockout cells serve as an isogenic system to isolate FLT3-specific contributions from EBV-driven oncogenic signals, enabling study of compensatory networks and identification of therapeutic vulnerabilities.
These cells are suitable for Western blotting of phosphorylated FLT3 and downstream effectors, flow cytometry for FLT3 surface expression, and proliferation or apoptosis assays. They are also used in drug sensitivity profiling with FLT3 inhibitors such as quizartinib and midostaurin, functional characterization of FLT3 mutations via rescue experiments, transcriptomic analysis by RNA-seq, and co-immunoprecipitation studies of signaling complexes. Typical applications include dissecting FLT3 signaling in B-cell malignancies, preclinical drug screening, and hematopoietic development research. For technical details or bulk inquiries, please contact Ascent Research.
