The GLRX3 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population derived from the Raji B lymphocyte line, in which the GLRX3 gene has been disrupted to ablate its expression. This polyclonal knockout pool is generated without single-cell cloning, thereby retaining population-level heterogeneity while eliminating functional GLRX3 protein. The cells serve as a versatile loss-of-function model for investigating the molecular functions of GLRX3 in human B cell contexts, particularly in relation to redox regulation, iron-sulfur cluster biogenesis, and signal transduction pathways.
The parental Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt??s lymphoma-derived B lymphocyte model that is extensively utilized in immunology and cancer research. Raji cells exhibit characteristic features of transformed B cells, including constitutive activation of survival pathways and latent EBV gene expression, making them a relevant system for studying B cell malignancies, viral oncology, and lymphocyte biology. Their robust growth in suspension culture and well-characterized signaling networks facilitate reproducible experimental assays.
GLRX3 (glutaredoxin 3) is a multifunctional oxidoreductase crucial for redox homeostasis and cytosolic iron-sulfur (Fe-S) cluster biogenesis. It scaffolds Fe-S cluster assembly via interactions with Anamorsin (CIAO1), ABCB7, GLRX2, and TXN. GLRX3 also directly binds and modulates protein kinase C theta (PKC??), influencing downstream signaling. Regulated by oxidative stress, Nrf2, NF-??B, and AP-1, GLRX3 itself governs PKC??, PRMT1, JNK, NF-??B, and Bcl-2 family activity, thereby integrating redox signals with kinase cascades that control proliferation and apoptosis.
In Raji B lymphocytes, GLRX3 knockout likely impairs Fe-S cluster processes and PKC??-mediated signal transduction. PKC?? is key in B cell receptor (BCR) signaling and NF-??B activation; thus, its disruption may attenuate BCR-driven survival and proliferation. Loss of redox regulation could sensitize cells to oxidative stress and alter apoptosis via JNK and Bcl-2 pathways. This model aids dissection of redox-oncogenic signaling intersections in B cell lymphomas and drug resistance mechanisms.
This product supports functional B cell studies, lymphoma research, and Fe-S cluster biogenesis analysis. It enables exploration of PKC?? signaling, redox gene regulation, and apoptosis control. Assays include western blotting, RT-qPCR, flow cytometry, immunofluorescence, co-IP, reporter assays, oxidative stress tests, and drug sensitivity screening. For more information, contact Ascent Research.
