The EPHA2 Knockout Raji Polyclonal Cells consist of a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with targeted disruption of the EPHA2 gene. This loss-of-function model provides a genetically diverse system for investigating EPHA2-dependent signaling in a human B-cell background, avoiding clonal selection artifacts. Quality-controlled for viability and growth, these cells are ready for use in biochemical, cell biological, and pharmacological assays.
The Raji parental line originates from an EBV-positive Burkitt??s lymphoma patient and carries the t(8;14) translocation leading to constitutive MYC overexpression. As a suspension-adapted B-lymphocyte model, Raji is widely employed in studies of B-cell biology, lymphomagenesis, and antibody-dependent cellular cytotoxicity. Endogenous EPHA2 expression permits direct evaluation of knockout-mediated changes in adhesion, migration, and survival.
EPHA2 encodes a receptor tyrosine kinase that mediates ephrin-A?Cdriven bidirectional signaling. Upon ephrin-A1 (EFNA1) or ephrin-A5 (EFNA5) binding, the receptor autophosphorylates and activates SRC kinase and focal adhesion kinase (FAK/PTK2), as well as the GRB2?CSOS?CRAS cascade that signals through RAF, MEK, and ERK (MAPK1/3). EPHA2 also stimulates PI3K?CAKT pathway and Rho GTPases (RAC1, RHOA) via VAV exchange factors. Important interaction partners include SHC1, PTPN11 (SHP2), integrin ??1 (ITGB1), and ANKS1A, which couple receptor activity to cytoskeletal reorganization and cell adhesion.
In Raji B cells, EPHA2 governs ephrin-A?Cmediated cell repulsion and adhesion, processes implicated in lymphoma cell homing and dissemination. Knockout of EPHA2 disrupts these repulsive cues, enabling precise dissection of the receptor??s role in B-cell malignancy. This model supports analysis of EPHA2-specific contributions to PI3K?CAKT and MAPK/ERK pathway activation, as well as Rho GTPase-driven cytoskeletal remodeling, clarifying how ephrin-A signaling modulates B-cell behavior.
Typical research applications encompass functional investigation of EPHA2 in B-cell lymphoma, validation of EPHA2 inhibitors, and screening for pathway modulators. The polyclonal knockout cells are compatible with ephrin-A1 stimulation for phospho-tyrosine profiling, Western blotting, flow cytometry, Transwell migration/invasion, ephrin-A1?Ccoated adhesion assays, co-immunoprecipitation, phospho-RTK arrays, and caspase-3/7 apoptosis assays. For additional technical information or to discuss your project needs, please contact Ascent Research.
