The MAP4K1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population derived from the Raji B lymphocyte line. This product features targeted disruption of MAP4K1, encoding HPK1, resulting in a mixed population of cells with loss-of-function edits. The polyclonal nature avoids clonal bias, providing a robust model for studying MAP4K1 function. This tool is intended for investigations of B-cell receptor signaling, lymphoma biology, and immune regulation without the need for single-cell cloning.
The Raji cell line originates from a human Burkitt lymphoma and serves as a classic B lymphocyte model. These cells express surface BCR, CD19, CD20, and retain functional signaling modules. Their transformed phenotype permits continuous culture while preserving key B-cell functions like antibody production and antigen presentation. Raji cells are extensively used to dissect B-cell signaling, oncogenic mechanisms, and immune responses, offering a lymphomagenic background highly relevant for studying negative regulators of lymphocyte activation.
MAP4K1 (HPK1) is a serine/threonine kinase that negatively regulates lymphocyte receptor signaling. Following BCR engagement, Src-family kinases phosphorylate HPK1, which then phosphorylates the adaptor BLNK. This recruits inhibitory molecules, dampening downstream JNK and NF-??B cascades. Specifically, HPK1 attenuates JNK (MAPK8) activity, reducing c-Jun phosphorylation and AP-1 transactivation. Interactors like SLP-76, GRB2, LAT, 14-3-3 proteins, and PP2A facilitate its regulatory role. Thus, HPK1 acts as a checkpoint that limits BCR-driven immune activation, proliferation, and survival.
In Raji cells, MAP4K1 knockout removes a key negative feedback brake on BCR signaling. This is expected to enhance JNK and NF-??B pathway outputs after stimulation, boosting transcriptional programs controlled by c-Jun, AP-1, and NF-??B. The model likely exhibits altered proliferation, apoptosis, and effector functions, mirroring aspects of lymphoma or autoimmunity. It enables functional assessment of HPK1 loss in B-cell biology and provides insight into how dysregulated signaling contributes to B-cell malignancies.
Research applications include BCR stimulation assays with phospho-JNK analysis, NF-??B reporter assays, Western blotting, RT-qPCR, and flow cytometry. The cells facilitate immune checkpoint research, drug target validation, and immunotherapy studies. Proliferation and apoptosis assays can quantify functional consequences of HPK1 loss. This polyclonal knockout product is a versatile resource for dissecting HPK1-dependent signaling networks. For further technical details, contact Ascent Research.
