The MTMR2 Knockout Raji Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population specifically designed for loss-of-function investigation of the MTMR2 gene. This heterogeneous pool of edited Raji B lymphocytes provides a robust experimental system that minimizes clonal artifacts while enabling comprehensive functional analyses of MTMR2-dependent processes. The polyclonal format ensures broad representation of editing outcomes, making it suitable for pooled screens and population-level assays.
The host Raji cell line is a well-characterized human B lymphocyte derived from an EBV-positive Burkitt lymphoma, retaining lymphoblastoid properties and key immunological functions such as antibody secretion and antigen presentation. As a model for adaptive immunity and B-cell malignancies, Raji cells are extensively employed in studies of oncogenic signaling, endosomal dynamics, and immune response mechanisms.
MTMR2 encodes a phosphoinositide phosphatase that specifically dephosphorylates PI(3)P and PI(3,5)P2, lipids essential for endosomal maturation and autophagy. MTMR2 activity is regulated by upstream factors including the transcription factors EGR2 and SOX10, and is embedded within the PI3K-AKT pathway. The protein interacts with scaffold components MTMR5/SBF1, MTMR13/SBF2, FIG4, and VAC14 to form complexes that modulate lipid turnover. Downstream, MTMR2 controls the localization of PI(3)P effectors EEA1 and Hrs, the PI(3,5)P2 effector TRPML1, and mTORC1 activity, thereby coordinating autophagic flux. Loss of MTMR2 leads to substrate accumulation, disrupting endosomal trafficking and autophagy, with implications for VPS34, BECN1, ULK1, and ATG protein networks.
In the Raji B lymphocyte context, this knockout model permits dissection of PI(3)P-dependent endosomal sorting during antigen processing and antibody production. Given its lymphoma origin, the model is particularly suited to exploring the interplay between oncogenic signaling and autophagy, where dysregulated autophagy influences lymphoma cell survival and drug sensitivity. It also enables investigation of how MTMR2 loss recapitulates aspects of Charcot-Marie-Tooth type 4B1 neuropathy and myopathy at the cellular level, offering insights into immune cell-specific requirements for endosomal homeostasis.
Typical applications encompass western blotting and immunofluorescence for endosome/autophagosome markers, PI(3)P lipid quantification, LC3-GFP reporter assays for autophagy flux, and flow cytometry for apoptosis profiling. The model supports drug screening for phosphatase activators, RT-qPCR analysis of downstream targets, and drug sensitivity studies. For further information, please contact Ascent Research.
