CISD1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Burkitt’s lymphoma B cell line Raji. This product consists of a heterogeneous mixture of Raji B lymphocytes carrying targeted disruptions in the CISD1 gene, generated without single-cell cloning, thereby retaining the genetic diversity inherent to polyclonal knockout models. The population is suitable for bulk functional assays where averaged loss-of-function effects are studied, avoiding clonal artifacts. As a suspension culture, these cells maintain the EBV-positive phenotype of parental Raji cells, enabling straightforward handling in standard lymphocyte culture conditions.
The Raji cell line is a widely used model for B cell malignancies, originally established from a patient with Burkitt’s lymphoma. These B lymphocytes exhibit lymphoblast morphology, grow in suspension, and are positive for Epstein-Barr virus (EBV). Raji cells recapitulate key features of aggressive B cell lymphomas, including rapid proliferation and altered mitochondrial metabolism, making them a relevant host for studying mitochondrial protein function. The EBV-positive status also provides a context for examining virus?Chost interactions that may influence mitochondrial dynamics.
CISD1 encodes an outer mitochondrial membrane protein that plays a critical role in iron-sulfur cluster transfer and the regulation of oxidative phosphorylation and redox homeostasis. It is transcriptionally regulated by PPAR?? and responsive to cellular iron levels and oxidative stress. CISD1 interacts with CISD2 and other mitochondrial outer membrane proteins involved in iron-sulfur cluster biogenesis, such as ferredoxin and iron-sulfur cluster scaffold proteins. Mechanistically, CISD1 functions upstream of oxidative phosphorylation complexes, modulates reactive oxygen species (ROS) production, and influences AMPK signaling, thereby coupling mitochondrial electron transport to metabolic and apoptotic pathways.
In Raji B lymphocytes, disruption of CISD1 is expected to alter iron-sulfur cluster transfer, leading to impaired oxidative phosphorylation and dysregulated ROS levels. Given the high metabolic demands of lymphoma cells, loss of CISD1 may trigger metabolic reprogramming, reduce mitochondrial respiratory capacity, and sensitize cells to oxidative stress-induced apoptosis. This model allows investigation of how mitochondrial redox control influences proliferation and survival in B cell malignancies, potentially identifying vulnerabilities exploitable in lymphoma therapy.
This polyclonal knockout cell population is particularly suited for functional analysis of CISD1 in mitochondrial biology and its role in B cell lymphoma metabolic reprogramming. Researchers can employ Western blotting to confirm CISD1 protein disruption, measure oxygen consumption rates to assess oxidative phosphorylation, detect ROS levels, and perform apoptosis and proliferation assays. Moreover, global gene expression profiling by RNA-seq facilitates exploration of downstream transcriptomic changes. The cells serve as a tool for drug target validation in type 2 diabetes and cancer, where CISD1 is implicated in metabolic dysregulation. For additional information, please contact Ascent Research.
