NEK3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the human Raji Burkitt lymphoma B lymphocyte line. This gene-edited product targets disruption of the NEK3 gene, encoding a serine/threonine kinase involved in cytoskeletal organization and cell cycle progression. The polyclonal format provides a heterogeneous cell pool, avoiding artifacts from single-clone selection, and is ideal for robust loss-of-function investigations in suspension cultures.
The Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma model extensively used in B-cell malignancy, virology, and immunology research. As a mature B lymphocyte, it expresses relevant surface markers and signaling machinery. The EBV genome enables studies of viral latency-host interactions. Combining this background with NEK3 knockout allows dissection of kinase-dependent pathways in transformed B cells, facilitating analysis of proliferation, survival, and cytoskeletal dynamics in lymphoma.
NEK3, a NIMA-related serine/threonine kinase, operates downstream of the prolactin receptor (PRLR) and JAK2/STAT5 signaling. Upon prolactin binding, NEK3 is activated and phosphorylates paxillin and VAV2, which then coordinate Rac1-mediated actin reorganization and cell motility. The kinase also interacts with GRB2 and participates in microtubule regulation, connecting prolactin cues to broader cytoskeletal remodeling. In Raji B lymphocytes, NEK3 likely integrates signals to control cell shape and cell cycle transitions. CRISPR/Cas9-mediated disruption of NEK3 is expected to impair PRLR-dependent phosphorylation events, attenuating prolactin-induced cytoskeletal changes and potentially affecting proliferation and migration.
This NEK3 knockout Raji model is a powerful system to study prolactin signaling in B-cell malignancies. Prolactin and its receptor influence lymphocyte function and lymphoma progression; NEK3 may mediate PRLR effects on actin dynamics crucial for B-cell migration and immune synapse formation. The model enables dissection of NEK3-specific roles in PRLR pathways, providing insight into kinase-dependent mechanisms relevant to prolactin-sensitive cancers including breast cancer and Burkitt lymphoma. The polyclonal nature avoids clonal expansion biases.
Typical applications include prolactin stimulation assays with phospho-STAT5 and phospho-Akt detection via Western blot or flow cytometry, proliferation and migration assays to quantify NEK3-dependent phenotypes, and immunofluorescence for cytoskeletal markers. This tool is suited for drug screening targeting the PRLR-JAK2-STAT5-NEK3 axis or exploring NEK3 in immune cell trafficking. The model also supports investigation of crosstalk between prolactin and other oncogenic pathways in lymphoma. For further details or to request a quote, please contact Ascent Research.
