MAP4 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the Raji B lymphocyte line. This product provides a heterogeneous pool of cells harboring loss-of-function mutations in the MAP4 locus, enabling functional studies of microtubule-associated protein 4 in a malignant B-cell background. The knockout strategy employs Cas9 nuclease and target-specific guide RNAs to ablate MAP4 expression across the population, generating a robust model for investigating microtubule dynamics in lymphoma biology.
The Raji cell line was originally established from a Burkitt lymphoma patient and is characterized by Epstein-Barr virus (EBV) positivity and expression of hallmark B-cell surface markers. As a lymphoblastoid cell line, Raji cells retain features of cancerous B lymphocytes and are widely employed in cancer research, particularly for studying oncogenic signaling, apoptosis, and drug responses. Their rapid proliferation and well-defined karyotype make them a suitable substrate for genetic manipulation and phenotypic screening.
MAP4 encodes a ubiquitously expressed microtubule-stabilizing protein that binds directly to tubulin and promotes polymerization, thereby regulating cytoskeletal architecture. During interphase, MAP4 maintains microtubule integrity, while in mitosis, its activity is modulated by phosphorylation events mediated by CDK1/cyclin B and Aurora A kinase. This phosphorylation reduces MAP4??s affinity for microtubules, facilitating the dynamic instability required for proper mitotic spindle assembly and chromosome segregation. MAP4 also interacts with kinesin motor proteins and other microtubule-associated factors, positioning it at a critical node between cytoskeletal regulation and cell cycle progression. Disruption of MAP4 thus perturbs mitotic fidelity and may influence cell proliferation and sensitivity to microtubule-targeting agents.
In the Raji B-cell lymphoma context, MAP4 loss offers a valuable loss-of-function model to dissect how microtubule stability impacts malignant lymphocyte biology. Aberrant microtubule dynamics are implicated in cancer cell division and survival, and MAP4??s role in mitosis makes it a potential determinant of response to chemotherapeutics such as vinca alkaloids and taxanes. Researchers can use this knockout to examine whether MAP4 deficiency alters mitotic progression, induces mitotic catastrophe, or modifies the efficacy of spindle poisons in a lineage-relevant system.
This polyclonal knockout product is suited for applications including Western blotting to confirm MAP4 ablation and tubulin expression, immunofluorescence analysis of microtubule networks, flow cytometric cell cycle profiling, and proliferation assays in the presence of microtubule inhibitors. It enables high-throughput drug sensitivity screens and mechanistic studies of mitotic regulation in B-cell malignancies. For comprehensive product details, technical support, or ordering information, please contact Ascent Research.
