The LMAN2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphocyte line, with targeted disruption of the LMAN2 gene. This product provides a loss-of-function model for investigating LMAN2 (also known as VIP36), an intracellular lectin critical for glycoprotein trafficking. The polyclonal pool harbors heterogeneous CRISPR/Cas9-mediated gene disruptions, ensuring a representative knockout effect without clonal selection. This format is ideal for studying the overall impact of LMAN2 ablation on cellular processes.
The Raji cell line is an Epstein-Barr virus-positive lymphoblastoid line established from Burkitt lymphoma. As B lymphocytes, Raji cells are central to humoral immunity and antibody production, exhibiting glycoprotein processing pathways relevant to immune function. The EBV-transformed background ensures robust proliferation and expression of viral modulators of trafficking, providing a pertinent context for studying LMAN2’s role in B-cell glycobiology and lymphoma.
LMAN2 encodes a transmembrane lectin that recognizes high-mannose type glycans on nascent glycoproteins in the endoplasmic reticulum (ER) and functions as a cargo receptor for anterograde transport to the Golgi apparatus. It forms complexes with LMAN1 (ERGIC-53) and MCFD2 to facilitate packaging of specific glycoprotein cargoes into COPII vesicles. LMAN2 expression is regulated downstream of ER stress pathways, with XBP1 acting as a key transcription factor. Knockout disrupts the selective transport of high-mannose glycoproteins, altering the cell surface glycoproteome. A critical downstream effect is impaired secretion of MMP-2, a protease involved in extracellular matrix remodeling and cancer cell migration, while other surface glycoproteins are also affected.
In Raji B lymphocytes, LMAN2 disruption provides a tool to explore glycoprotein trafficking defects in lymphoma biology. Due to high secretory activity for antibodies, impaired ER-to-Golgi transport may compromise immunoglobulin glycosylation and secretion, affecting humoral immunity. As LMAN2 has been linked to cancer cell migration and invasion via surface glycoprotein presentation and MMP-2 secretion, these knockout cells enable investigation in Burkitt lymphoma. The EBV-positive background further modulates glycoprotein processing, offering insights into viral-host trafficking interplay.
Applications include glycoprotein trafficking studies, ER-Golgi transport investigation, and lectin functional analysis in B lymphocytes. Assays such as Western blotting, RT-qPCR, immunofluorescence, and lectin blotting are used to confirm knockout and assess glycoprotein profiles. Migration and invasion assays evaluate the role in lymphoma cell motility, while flow cytometry quantifies surface glycoprotein changes. These cells also support research on ER stress pathways and glycoprotein secretion. For more information, please contact Ascent Research.
