The NTRK2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphocyte line, engineered to disrupt the NTRK2 gene encoding the TrkB receptor tyrosine kinase. This loss-of-function model eliminates functional TrkB expression, enabling detailed investigation of neurotrophin signaling in Burkitt lymphoma and other B-cell malignancies. As a polyclonal pool, the cells harbor diverse NTRK2 mutations, offering a robust system for gene function studies without clonal selection artifacts.
The Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphocyte model extensively utilized in immunological and oncological research. As a lymphoblastoid line, Raji cells maintain key characteristics of B-cell malignancies, including activated signaling and high proliferation, making it a standard platform for lymphomagenesis studies. TrkB expression in these cells has been associated with oncogenic processes and immune modulation, underscoring the relevance of this knockout for elucidating NTRK2 functions in lymphoproliferative diseases.
NTRK2 encodes the TrkB receptor, which upon binding brain-derived neurotrophic factor (BDNF) or neurotrophin-4/5 (NTF4/5), dimerizes and autophosphorylates. This activation recruits adaptor proteins SHC1, GRB2, and FRS2, initiating downstream cascades including RAS-MAPK (ERK1/2), PI3K-AKT-mTOR, and PLC??-mediated calcium/PKC signaling, with cross-talk to JAK/STAT pathways. Key downstream effectors include transcription factors CREB and NF-??B, which mediate survival and proliferation responses. Upstream regulators such as cAMP and calcium influx, along with interacting partners PTPN11/SHP2 and GAB1, modulate TrkB activity. Knockout of NTRK2 ablates this network, permitting targeted dissection of each signaling branch in B-cell contexts.
In Raji B lymphocytes, TrkB signaling promotes proliferation, survival, and chemoresistance, contributing to lymphomagenesis. This polyclonal knockout enables examination of how loss of TrkB affects lymphoma phenotypes such as cell cycle progression, apoptosis sensitivity, and migration. It also allows interrogation of neurotrophin crosstalk with B-cell receptor pathways or EBV latency programs, potentially uncovering therapeutic vulnerabilities in Burkitt lymphoma and other B-cell tumors. Additionally, the model supports screening of TrkB-targeted inhibitors.
Researchers can employ this NTRK2 knockout model in diverse experimental settings: western blotting for TrkB and phospho-ERK, RT-qPCR for knockdown validation, immunofluorescence for receptor localization, and flow cytometry for apoptosis detection using Annexin V/PI. Functional assays include cell proliferation (MTS/CCK-8), phospho-signaling arrays for MAPK/AKT, and drug sensitivity testing with TrkB inhibitors such as entrectinib. Co-immunoprecipitation of adaptor proteins and RNA-sequencing provide deeper mechanistic insights. This product is valuable for functional genomics of NTRK2 in lymphoid cancers, neurotrophin-mediated signaling in immune cells, and targeted therapy development. For further details, please contact Ascent Research.
