The CRELD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from human Raji B lymphocytes, with targeted disruption of the CRELD1 gene. This engineered pool contains a heterogeneous array of loss-of-function alleles generated by CRISPR/Cas9-mediated gene disruption, offering a model that avoids clonal artifacts and preserves population-level variability for functional studies in B-cell biology and lymphoma.
The parental Raji cell line originates from a human Burkitt’s lymphoma and is characterized by its Epstein-Barr virus (EBV)-positive status, continuous proliferation, and expression of B-cell markers. As a B lymphocyte model, Raji cells are extensively used to study antibody production, immune response regulation, and the molecular underpinnings of lymphomagenesis. Their transformed phenotype and robust growth in suspension make them a tractable system for genetic manipulation and downstream functional assays, enabling dissection of gene functions that govern B-cell malignancies.
CRELD1 encodes a transmembrane protein with epidermal growth factor (EGF)-like domains that functions as a modulator of Notch receptor signaling and cell-cell adhesion. It is activated by Notch receptors and TGF-beta cues, and physically interacts with NOTCH1, NOTCH2, and integrins. CRELD1 regulates the Notch target genes HES1 and HEY1, and its signaling converges with the TGF-beta pathway through TGFBR1 and SMAD2/3 effectors. In adhesion networks, CRELD1 interacts with integrins such as ITGA4 and ITGB1, and cadherins like CDH1, thus linking extracellular adhesive contacts to intracellular cascades.
In Raji B cells, disruption of CRELD1 is predicted to impair Notch-dependent transcriptional responses, potentially affecting proliferation, differentiation, and microenvironmental interactions central to lymphomagenesis. Given the role of Notch signaling in B-cell development and lymphoma, this polyclonal knockout model offers a physiologically relevant system to dissect CRELD1 function in malignant B cells. It also permits exploration of crosstalk between Notch and TGF-beta pathways, relevant to B-cell lymphomas and developmental disorders such as atrioventricular septal defect and heterotaxy where CRELD1 mutations are found.
This product supports diverse applications including functional genomics of Notch signaling, drug target validation in lymphoma, and mechanistic studies of cell adhesion. Assays such as Western blotting, RT-qPCR, flow cytometry, cell adhesion assays, proliferation assays, and RNA-seq can be employed to analyze the consequences of CRELD1 loss. The polyclonal format enhances translational relevance by modeling the genetic heterogeneity of tumors. For further information, please contact Ascent Research.
