The CTDSP1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in the human Raji B lymphocyte background, engineered for loss-of-function studies of the CTDSP1 gene. This product provides a heterogeneous knockout model in which target-gene disruption is generated via CRISPR/Cas9, enabling researchers to investigate the functional consequences of CTDSP1 ablation without assumptions of clonal homogeneity. The polyclonal format captures population-level effects and is well-suited for pooled functional genomics, signaling studies, and drug response profiling.
The Raji host cell line is an EBV-positive B lymphoblastoid line originally derived from a patient with Burkitt lymphoma, a highly aggressive B-cell malignancy. Raji cells are a widely used model system for studying B-cell biology, lymphomagenesis, and EBV-driven transformation. They exhibit robust growth in suspension culture and are amenable to a wide range of molecular and cellular assays, making them an appropriate background for interrogating the roles of tumor suppressors and signaling regulators in lymphoma.
CTDSP1 encodes a CTD small phosphatase that specifically dephosphorylates serine-5 of the RNA polymerase II C-terminal domain, leading to transcriptional repression of REST-target genes. CTDSP1 is a key component of the REST corepressor complex, interacting with REST, SIN3A, CoREST, and HDAC1/2 to silence neuronal gene expression in non-neuronal cells. Additionally, CTDSP1 functions as a tumor suppressor by dephosphorylating SMAD2 and SMAD3, thereby inhibiting TGF-beta signaling. This dual role positions CTDSP1 at the intersection of REST-mediated transcriptional regulation and TGF-beta pathway suppression, with downstream effects on cell cycle and proliferation.
In the context of Raji cells, CTDSP1 knockout provides a powerful tool to explore the interplay between REST-dependent gene silencing and TGF-beta tumor-suppressive signaling in B-cell lymphoma. Loss of CTDSP1 expression is often associated with promoter hypermethylation in various cancers, including lymphomas, neuroblastoma, glioma, colorectal and breast cancers. The knockout model facilitates investigation of epigenetic silencing mechanisms and the impact of restoring CTDSP1 function. Moreover, because Raji cells are EBV-positive, this model can be used to study how viral latency and oncogenic signaling intersect with host transcriptional regulation.
This polyclonal knockout population is suitable for a broad range of applications, including screening for small molecules that reactivate epigenetically silenced tumor suppressors, assessing TGF-beta and REST signaling dynamics via phospho-SMAD2/3 analysis and RNA-seq, and evaluating drug sensitivity in Burkitt lymphoma models. Researchers can employ assays such as Western blotting for CTDSP1 and its targets, RT-qPCR for REST target gene expression, ChIP-qPCR for occupancy analyses, immunofluorescence, flow cytometry, and proliferation or apoptosis assays. These experiments support mechanistic studies in cancer biology, immunology, and drug discovery. For more information, please contact Ascent Research.
