The CRTC1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji human B lymphocyte cell line. This product provides a heterogeneous pool of cells carrying targeted disruptions in the CRTC1 gene, enabling loss-of-function studies in a B-cell lymphoma background. The polyclonal format preserves population-level diversity while eliminating wild-type CRTC1 expression, making it suitable for biochemical and functional assays without clonal expansion artifacts.
Raji is an Epstein-Barr virus (EBV)-positive Burkitt lymphoma B-cell line originally isolated from an 11-year-old male. These lymphoblastoid cells are widely employed as a model for B-cell biology, immunological investigations, and oncogenic mechanisms underlying Burkitt lymphoma. Raji cells exhibit robust proliferation and are amenable to various genetic manipulations and downstream assays, making them a practical host for examining gene function in mature B lymphocytes.
CRTC1 (CREB-regulated transcription coactivator 1) functions as a cAMP-responsive transcriptional coactivator that binds to and enhances the activity of CREB (cAMP response element-binding protein). Under basal conditions, CRTC1 is phosphorylated by the salt-inducible kinases SIK1/SIK2 and AMPK, promoting its binding to 14-3-3 proteins and cytoplasmic sequestration. Activation of cAMP/PKA signaling or calcineurin-mediated dephosphorylation triggers CRTC1 nuclear translocation, where it interacts with CREB and the coactivators CBP/p300 to drive transcription of downstream targets. Key CRTC1 target genes include G6PC and PCK1 (gluconeogenic enzymes), the circadian regulators PER1 and PER2, and neuronal factors such as BDNF, reflecting its roles in energy homeostasis, circadian rhythms, and neuronal function. CRTC1 is also recognized as an oncogenic fusion partner in mucoepidermoid carcinoma, where it forms a CRTC1-MAML2 fusion that aberrantly activates CREB target genes.
In the Raji B-cell lymphoma background, this polyclonal knockout model enables dissection of CRTC1-dependent transcriptional programs in lymphoid cells, including potential cross-talk between CREB/CRTC1 signaling and oncogenic pathways. Because CRTC1 integrates metabolic and hormonal cues, its disruption in Raji cells permits exploration of how AMPK and SIK kinases, calcineurin, and cAMP/PKA contribute to B-cell proliferation, survival, and metabolic adaptation. This system is particularly valuable for studying non-canonical roles of CRTC1 outside classical gluconeogenic tissues and for evaluating its contribution to B-cell lymphoma pathogenesis.
Researchers can employ this polyclonal knockout population for a range of experimental applications including Western blotting and RT-qPCR to confirm CRTC1 ablation, CREB luciferase reporter assays to measure CREB transcriptional activity, and cAMP stimulation coupled with immunocytochemistry to monitor CRTC1 nuclear translocation. Functional studies of cell proliferation, metabolic flux, and transcriptome-wide changes via RNA-seq can uncover CRTC1-dependent pathways in B-lymphoma. This model is also suitable for small-molecule screens targeting CRTC1 regulatory kinases, calcineurin, or CREB interaction. For further technical specifications, pricing, and ordering information, please contact Ascent Research.
