The CELF1 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphoblast line, designed to disrupt the CELF1 gene. This heterogeneous loss-of-function model preserves the inherent genetic diversity of polyclonal editing, enabling robust, unbiased investigation of CELF1-dependent post-transcriptional regulation without the constraints of clonal selection. The product is supplied as a pool of edited cells, each carrying CRISPR-mediated gene disruption, and is optimized for immediate use in downstream functional assays.
Raji cells are an Epstein-Barr virus (EBV)-positive B lymphoblast line originating from a Burkitt’s lymphoma patient. They grow in suspension, maintain characteristic B-cell surface markers, and are extensively employed in immunology and oncology research as a physiologically relevant model for B-cell malignancies. Their transformed phenotype, well-defined signaling networks, and susceptibility to EBV-driven modulation make them an ideal host for studying oncogenic processes, apoptosis, and RNA biology in lymphoid cancers.
CELF1 is an RNA-binding protein that orchestrates alternative splicing, mRNA stability, and translation of numerous transcripts, directly controlling the expression of pivotal cell cycle and survival regulators such as the cyclin-dependent kinase inhibitor p21 (CDKN1A) and the anti-apoptotic factor Mcl-1 (MCL1). Its activity is modulated by upstream signals including ERK phosphorylation, p53, c-Myc, NF-??B, and miR-23b, and it engages in molecular interactions with splicing factors (e.g., hnRNP H, EWSR1) and the translation initiation complex component eIF4E. Through these interactions, CELF1 integrates cues from the MAPK/ERK and MYC pathways to fine-tune post-transcriptional gene expression networks that govern proliferation and apoptosis.
In the Raji B-lymphoblast background, disruption of CELF1 is predicted to dysregulate its downstream targets, including p21 and Mcl-1, thereby altering cell cycle progression and apoptotic thresholds. Given CELF1??s involvement in cancer-relevant signaling cascades such as ERK and its role in lymphomagenesis, this polyclonal knockout model offers a powerful tool to examine how loss of CELF1-mediated RNA processing affects B-cell transformation, survival, and response to therapeutic interventions. The pooled population captures a spectrum of editing outcomes, facilitating phenotypic analyses that reflect the complexity of polyclonal tumor cell populations.
This model supports a wide range of research applications, including the study of RNA processing alterations in B-cell malignancies using RNA-seq and RNA immunoprecipitation to track transcriptome-wide splicing and stability changes. Complementary techniques such as Western blotting, RT-qPCR, and flow cytometry enable validation of protein-level effects, while proliferation and apoptosis assays dissect the functional consequences of CELF1 knockout. Reporter assays further allow monitoring of translational control mechanisms. The polyclonal knockout cells are also suited for drug target validation and functional genomics screens. For additional details or custom inquiries, please contact Ascent Research.
