The FKBP8 Knockout Raji Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte line, featuring targeted disruption of the FKBP8 gene. This loss-of-function model provides a reproducible pool of edited cells for investigating FKBP8-dependent regulatory networks without the selection of a single-cell clone. The polyclonal format captures a range of allelic disruptions, enabling robust loss-of-function studies while maintaining the genetic heterogeneity inherent to polyclonal populations, making it suitable for examining FKBP8-mediated processes in a biologically relevant context.
Raji cells are a well-characterized human Burkitt lymphoma-derived B lymphocyte line that is Epstein?CBarr virus (EBV)-positive, carries a p53 mutation, and bears a c-Myc translocation, hallmark features of aggressive B-cell malignancy. Widely employed in immunology and cancer research, these suspension-adapted cells serve as a model for lymphomagenesis, viral oncogenesis, and B-cell receptor signaling. Their dysregulated proliferation and survival pathways, combined with defined genetic lesions, create a stringent backdrop for evaluating the functional impact of FKBP8 ablation on disease-relevant signaling circuits.
FKBP8 encodes a peptidyl-prolyl cis-trans isomerase that functions as an endogenous inhibitor of mTOR kinase, directly binding mTOR and blocking its activation on lysosomal surfaces, thereby suppressing mTORC1 downstream signaling. This activity is counter-regulated by mTORC1 itself, as well as by ER stress and p53. FKBP8 also targets Bcl-2 to mitochondria, promoting anti-apoptotic responses, and modulates autophagy through physical interaction with Beclin-1. Consequently, FKBP8 loss influences phosphorylation of S6K and 4E-BP1, alters Bcl-2 localization, and rebalances autophagic flux. The protein interacts with a network of factors including mTOR, Bcl-2, Bcl-xL, calcineurin, Hsp90, and FKBP38, embedding it within key nodes of growth and death pathways.
In the Raji cellular context, which harbors a non-functional p53 and overexpressed c-Myc, FKBP8 knockout is expected to perturb the balance between mTOR-driven proliferation and stress responses. The dual role of FKBP8 as an mTOR inhibitor and mitochondrial guardian suggests that its deletion may sensitize cells to mTORC1 hyperactivity, modulate apoptosis under genotoxic or ER stress, and dysregulate autophagy, all of which are critical in Burkitt lymphoma pathogenesis. This model thus offers a unique platform to dissect how FKBP8 integrates oncogenic and tumor-suppressive signals in EBV-driven B-cell transformation.
This polyclonal knockout cell population supports a broad array of biochemical and functional assays, including western blot, RT-qPCR, S6K phosphorylation analysis, annexin V apoptosis detection, LC3-based autophagy flux measurement, co-immunoprecipitation of FKBP8-associated complexes, cell viability profiling, and rapamycin sensitivity testing. Experimental applications range from elucidating mTOR regulation in B-cell lymphoma and examining crosstalk between apoptosis and autophagy to screening drug sensitivity and probing EBV oncogenesis. For detailed product information and support, please contact Ascent Research.
