The FSTL3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphoblastoid line, designed to disrupt the FSTL3 gene and generate a loss-of-function model. This polyclonal format provides a heterogeneous pool of edited cells, reflecting diverse knockout outcomes and enabling bulk functional analyses without clonal isolation. The product is intended for researchers investigating FSTL3 biology in a B lymphocyte context, with utility in signal transduction studies, cancer research, and drug development.
Raji cells are an Epstein-Barr virus (EBV)-positive Burkitt??s lymphoma-derived suspension line widely employed as a model for B cell malignancies and immunological research. These lymphoblastoid cells exhibit type III EBV latency and MYC translocations, driving high proliferation. Their human origin and lymphoid lineage make them particularly suitable for studying TGF-beta superfamily signaling, apoptosis, and oncogenic transformation.
FSTL3 encodes a secreted glycoprotein that binds and inhibits activin A, myostatin, and GDF11, preventing their interaction with the type II receptor ACVR2B and thereby suppressing SMAD2/3 phosphorylation. In the knockout, loss of FSTL3 relieves this inhibition, enhancing SMAD2/3 activation and altering transcription of downstream targets such as CDKN1A (p21), CCND1 (cyclin D1), and MYC. FSTL3 is regulated by TGFB1, HIF1A, and IL6, and it interacts with FST. Key components of the signaling cascade include receptors TGFBR1/ACVR1, SMAD4, and the inhibitory SKI/SnoN proteins, forming a tightly controlled network.
In Raji cells, FSTL3 knockout disrupts the local TGF-beta/activin signaling balance, potentially hyperactivating the pathway and impacting proliferation and apoptosis. This model is relevant for dissecting FSTL3’s role in lymphoma biology, where TGF-beta signals can have tumor-suppressive or oncogenic effects depending on context. The combination of FSTL3 loss with EBV latency programs provides a unique system to study virus?Chost interactions in B cell transformation.
Applications include Western blot analysis of phospho-SMAD2, RT-qPCR measurement of CDKN1A, CCND1, and MYC expression, and flow cytometry for apoptosis and cell cycle profiling. RNA-seq can reveal transcriptome-wide changes, and drug sensitivity assays with TGF-beta inhibitors can explore resistance mechanisms. This polyclonal knockout pool is suitable for functional genomics screens and pathway interrogation in lymphoma research. For further information, please contact Ascent Research.
