GABARAPL2 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated from the Raji B lymphoblast cell line, carrying a targeted disruption of the GABARAPL2 gene. This loss-of-function model enables the investigation of autophagy-related processes in a human B lymphocyte context, providing a valuable tool for studying autophagosome maturation, selective autophagy, and lysosomal degradation pathways.
The Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphoblast line, widely used as an in vitro model for B cell biology, lymphoma pathogenesis, and immune cell function. Raji cells exhibit robust proliferation and are amenable to various biochemical and cell-based assays, including transfection, immunofluorescence, and flow cytometry, making them suitable for autophagy studies in a hematological malignancy background.
GABARAPL2 (GABA type A receptor-associated protein-like 2) is a ubiquitin-like protein of the LC3/GABARAP family that plays a critical role in autophagosome formation, maturation, and fusion with lysosomes. Upon autophagy induction, GABARAPL2 is conjugated to phosphatidylethanolamine on autophagosomal membranes, a process regulated by the ATG12-ATG5-ATG16L1 complex and ATG3/ATG7 conjugation systems. GABARAPL2 functions downstream of the ULK1 kinase complex and Beclin-1/VPS34-mediated initiation, and its expression is transcriptionally regulated by TFEB, a master regulator of lysosomal biogenesis, in response to mTORC1 and AMPK signaling. The protein interacts directly with autophagy receptors such as p62/SQSTM1 and NBR1 to mediate selective autophagy of ubiquitinated cargo, and it facilitates autophagosome-lysosome fusion via interactions with Syntaxin 17 and LAMP1/2. Dysregulation of GABARAPL2 has been implicated in impaired autophagic flux, contributing to cancer cell survival, neurodegeneration, and host responses to infection.
In Raji B cells, the GABARAPL2 polyclonal knockout population provides a physiologically relevant system to dissect autophagy-dependent mechanisms in B lymphocyte homeostasis, antigen presentation, and lymphomagenesis. EBV-transformed B cells rely on autophagy for metabolic adaptation and viral latency, and disruption of GABARAPL2 may perturb these processes, offering insights into tumorigenic signaling and potential therapeutic vulnerabilities. The polyclonal nature of this knockout product preserves genetic heterogeneity while ensuring robust loss-of-function at the population level, facilitating studies that require pooled cell analysis rather than clonal artifacts.
This knockout model is tailored for a range of experimental applications, including autophagy research in B lymphocytes, investigation of drug resistance mechanisms, and screening for autophagy modulators. Researchers can employ Western blotting to monitor LC3-II lipidation and p62 degradation, immunofluorescence to visualize LC3 puncta formation, and flow cytometry with autophagy-specific dyes to assess autophagic flux. Additional assays such as RT-qPCR for autophagy gene expression, transmission electron microscopy for ultrastructural analysis of autophagosomes, and cell viability assays following treatment with chemotherapeutic agents or autophagy inhibitors are highly applicable. The GABARAPL2 Knockout Raji Polyclonal Cells thus serve as a versatile platform for basic and translational studies in cancer, neurodegenerative disorders, and infectious diseases. For further technical details, please contact Ascent Research.
