The FAM8A1 Knockout Raji Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population for loss-of-function analysis of FAM8A1 in a human B lymphocyte context. This product consists of a heterogeneous pool of Raji cells with targeted disruptions at the FAM8A1 locus, enabling population-level functional studies while preserving cellular diversity. The polyclonal format avoids clonal selection artifacts and offers a practical model for investigating apoptotic signaling.
Raji cells are a human Burkitt’s lymphoma B lymphocyte line that is EBV-positive and expresses high levels of CD19, CD20, and CD37. As a model of mature B-cell malignancy, Raji retains key pathways of adaptive immunity, including antibody production and antigen presentation. The p53 tumor suppressor network, frequently altered in lymphomas, is partially functional in these cells, making them relevant for studying p53-dependent apoptosis.
FAM8A1 is a p53-inducible pro-apoptotic protein that promotes mitochondrial outer membrane permeabilization. Upon activation by DNA damage kinases (ATM, ATR) or oncogenic stress, p53 transcriptionally upregulates FAM8A1, which translocates to mitochondria via the TOMM complex. There, it interacts with BCL-2 family members, facilitating BAX/BAK activation, cytochrome c release, and subsequent caspase-9 and caspase-3 cleavage. This cascade executes the intrinsic apoptosis pathway, positioning FAM8A1 as a direct effector linking p53 to mitochondrial cell death in response to genotoxic insults.
In B-cell lymphomas, resistance to apoptosis often arises from p53 pathway inactivation or overexpression of anti-apoptotic BCL-2 proteins. FAM8A1 knockout in Raji cells enables dissection of its specific contribution to mitochondrial apoptosis in a lymphoma background. This model can clarify how loss of this p53 target influences sensitivity to DNA-damaging agents or BH3 mimetics, and how EBV-driven survival signals intersect with the apoptotic machinery. It is particularly useful for exploring therapeutic strategies aimed at restoring apoptosis in B-cell malignancies.
Typical applications include western blotting and RT-qPCR to validate FAM8A1 knockout and assess downstream apoptotic markers, flow cytometry to quantify mitochondrial membrane potential and caspase activation, and immunofluorescence to monitor cytochrome c release. Drug sensitivity assays with chemotherapeutics or targeted BCL-2 inhibitors can identify resistance mechanisms dependent on FAM8A1. This cell product supports functional genomics and drug discovery efforts targeting apoptosis in lymphoma. For additional technical support, please contact Ascent Research.
