This product provides a CRISPR/Cas9-edited polyclonal Raji cell population carrying targeted disruption of the LATS1 gene. The mixed knockout pool enables loss-of-function studies without the influence of clonal selection artifacts.
Raji cells are a human B lymphocyte line derived from Burkitt lymphoma, a highly aggressive non-Hodgkin lymphoma. They grow in suspension and exhibit lymphoblastoid morphology. Raji cells express surface IgM and maintain Epstein-Barr virus (EBV) latent proteins, features that have established this line as a workhorse in immunology and cancer research, particularly for B cell signaling and transformation studies.
LATS1 encodes a serine/threonine kinase central to the Hippo tumor suppressor pathway. Upon activation by MST1/STK4 and MST2/STK3, scaffolded by SAV1 and MOB1A/B, LATS1 phosphorylates YAP1 and TAZ. This phosphorylation promotes 14-3-3 binding, leading to cytoplasmic sequestration or ubiquitin-mediated proteasomal degradation of YAP/TAZ, thereby inhibiting TEAD-dependent transcription of growth-promoting genes such as CTGF and CYR61. Consequently, LATS1 restricts cell proliferation and promotes apoptosis. Upstream inputs include NF2/Merlin, KIBRA, and RASSF1A, while downstream targets also include AMOT family proteins.
In Raji B cells, LATS1 loss may dysregulate growth control, offering a model to study Hippo pathway involvement in B cell lymphomagenesis. The EBV-positive background permits investigation of crosstalk between viral latency and Hippo signaling. Since Raji cells are suspension-adapted, they facilitate high-throughput analyses, and loss of LATS1 may influence B cell receptor responses, apoptosis, and drug sensitivity.
Typical applications include Western blotting for LATS1, p-LATS1, YAP, and p-YAP to confirm pathway alteration. RT-qPCR for CTGF and CYR61 assesses YAP/TAZ transcriptional output. Immunofluorescence reveals YAP localization shifts. Co-immunoprecipitation probes LATS1 interactions with MOB1 or YAP. Flow cytometry quantifies cell cycle and apoptosis changes. Functional assays such as colony formation, migration, and invasion, as well as transcriptomic profiling and drug sensitivity screening, can be performed. For additional information, please contact Ascent Research.
