The PANK4 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji cell line, targeting the PANK4 gene (Homo sapiens). This product consists of a heterogeneous pool of cells with CRISPR/Cas9-mediated disruption of PANK4, enabling loss-of-function studies in a B lymphocyte background. The knockout cells retain the essential phenotypic characteristics of the parental Raji line while lacking functional PANK4 protein, providing a robust model for investigating the gene’s roles in signaling and metabolism.
Raji cells are a suspension-adapted human Burkitt lymphoma line, widely used as a model for B cell malignancies. These EBV-positive lymphoblasts express surface markers CD19 and CD20, and they originate from a patient with Burkitt lymphoma. The Raji line is extensively characterized for studies of B cell biology, antigen presentation, and EBV-mediated oncogenesis. Their stable growth in culture and tumorigenic potential in vivo make them a practical host for gene editing and functional assays, including xenograft tumor models.
PANK4 is a member of the pantothenate kinase family that, despite lacking enzymatic activity, functions as a critical scaffold protein for AKT signaling. It directly interacts with AKT1 and the catalytically active pantothenate kinases PANK1, PANK2, and PANK3, facilitating AKT phosphorylation and activation. PANK4 operates downstream of growth factor receptors and PI3K, and may be transcriptionally regulated by NF-??B, to drive downstream phosphorylation of PDK1, AKT, mTORC1, and S6K, ultimately upregulating Cyclin D1 and BCL2. Through this scaffold function, PANK4 couples coenzyme A biosynthesis to the PI3K/AKT/mTOR pathway, thereby promoting cell proliferation and survival.
In the Raji B lymphoma background, PANK4 knockout significantly attenuates oncogenic PI3K/AKT/mTOR signaling, reduces cellular coenzyme A levels, and impairs tumorigenic potential. This model thus establishes a direct mechanistic link between coenzyme A metabolism and B cell malignancy. The loss-of-function phenotype is particularly relevant for investigating metabolic regulation of apoptosis and cell cycle progression, as well as for dissecting the scaffold function of PANK4 independent of its paralogs. Researchers can use these cells to explore how metabolic nodes interface with canonical oncogenic pathways in lymphomagenesis.
Typical research applications include investigating the role of PANK4 in B cell lymphoma biology, probing crosstalk between coenzyme A metabolism and AKT signaling, and validating PANK4 as a therapeutic target. The polyclonal knockout cells are suitable for a range of assays such as western blotting and RT-qPCR for PANK4 expression, LC-MS?Cbased CoA quantification, phospho-AKT flow cytometry, proliferation and apoptosis assays, soft agar colony formation, and xenograft tumor models. Co-immunoprecipitation experiments can map altered protein interactions in the absence of PANK4. For further details or to discuss custom applications, please contact Ascent Research.
