The NOMO1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted population derived from the Raji B lymphocyte cell line. This product provides a polyclonal knockout model with targeted disruption of the NOMO1 gene, enabling loss-of-function studies without clonal selection. The heterogeneous pool retains the genetic diversity of the original editing event, offering a robust platform for investigating NOMO1-dependent processes in a lymphoid cellular context.
The Raji parental cell line originates from an Epstein-Barr virus (EBV)-positive Burkitt lymphoma patient, representing a well-characterized model for B cell physiology, lymphomagenesis, and immune response. These suspension-adapted B lymphocytes are widely used to study B cell receptor signaling, apoptosis regulation, and sensitivity to chemotherapeutic agents, providing a disease-relevant background for exploring NOMO1 function in hematological malignancies.
NOMO1 encodes a transmembrane protein that functions as a negative regulator of Nodal signaling, a subset of the transforming growth factor-beta (TGF-beta) superfamily. Mechanistically, NOMO1 retains Nodal receptor components??including NODAL, CRIPTO, and ACVR2A??within the endoplasmic reticulum, preventing their trafficking to the cell surface and subsequent ligand-induced phosphorylation of SMAD2/3. This sequestration blocks downstream transcriptional activation of targets such as Lefty and Pitx2. NOMO1 acts in concert with NCLN (Nicalin) as part of the ER membrane complex, modulating protein folding and quality control. Its activity is influenced by upstream stimuli, including NODAL and BMP ligands, as well as ER stress signals, positioning NOMO1 at the intersection of developmental signaling and proteostasis.
In the Raji B cell background, NOMO1 knockout provides a unique tool to dissect the crosstalk between Nodal/TGF-beta pathways and lymphomagenesis. Given the role of TGF-beta in immune surveillance and B cell homeostasis, disruption of its antagonist may alter proliferation, survival, or drug sensitivity. This model enables researchers to examine how ER-retention mechanisms govern receptor availability, influencing downstream phospho-SMAD2/3 levels and the expression of oncogenic or tumor-suppressive targets.
Researchers can employ these polyclonal knockout cells in functional assays: Western blotting for SMAD2/3 phosphorylation and RT-qPCR for Nodal target genes (Lefty, Pitx2) assess signaling; immunofluorescence reveals receptor localization; flow cytometry monitors B cell surface markers. Apoptosis and drug sensitivity studies apply. This model supports studies of developmental signaling in cancer, ER proteostasis, and therapeutic targets in B cell malignancies. For more information, contact Ascent Research.
