The PBXIP1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte line (Homo sapiens). This model features targeted disruption of PBXIP1, a gene encoding a multi-domain scaffold protein that integrates signals from major oncogenic pathways. The polyclonal format captures a spectrum of editing alleles within a bulk cell population, enabling robust functional studies without the selection biases inherent in monoclonal isolates. Each vial is cryopreserved to support reproducible experimental setups.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B lymphocyte model. It retains hallmark features of aggressive B-cell malignancies, including constitutively active NF-??B signaling, MYC dysregulation, and PI3K pathway engagement. Grown in suspension, Raji cells are widely adopted for lymphoma biology research, providing a disease-relevant context to examine genes such as PBXIP1 that influence B-cell survival and transformation.
PBXIP1 (pre-B-cell leukemia transcription factor-interacting protein 1) functions as a cytoplasmic and nuclear scaffold that physically bridges PBX1 with key signaling effectors, including ??-catenin and ERK1/2. Upstream, PBXIP1 integrates signals from activated EGF/EGFR, TGF-?? receptors, and the kinases MEK1/2 and AKT. It directly interacts with ??-catenin, p85 PI3K, PREP1, estrogen receptor alpha, and N-CoR, assembling transcriptional regulatory complexes. Through these interactions, PBXIP1 promotes the expression of oncogenic targets such as c-Myc, cyclin D1, and MMP9, thereby coordinating cell cycle progression, migration, and apoptosis resistance across WNT/??-catenin, PI3K/AKT, and MAPK/ERK pathways.
Within the Raji Burkitt lymphoma background, endogenous PBXIP1 likely sustains aberrant proliferative and survival signaling. Its knockout impairs the formation of PBX1?C??-catenin transcriptional complexes and reduces downstream activation of TCF/LEF target genes. This disruption is expected to attenuate PI3K/AKT/mTOR and MEK/ERK cascades, revealing pathway dependencies that may be exploited therapeutically. The model provides a physiologically relevant system for probing PBXIP1??s role in B-cell malignancies and has translational implications given the gene??s involvement in breast, lung, and brain cancers.
Typical research applications of these polyclonal PBXIP1 knockout Raji cells include functional dissection of oncogenic pathway crosstalk in B-cell lymphoma, validation of PBXIP1 as a potential drug target, and investigation of apoptosis and proliferation control. Researchers can employ techniques such as Western blotting for protein analysis, RT-qPCR for transcriptional profiling, flow cytometry for surface marker or cell cycle evaluation, MTT-based viability measurements, Annexin V apoptosis assays, co-immunoprecipitation to assess protein complexes, and RNA-seq for global gene expression changes. For further technical inquiries or to explore custom applications, please contact Ascent Research.
