The GATA6 Knockout Raji Polyclonal Cells consist of a polyclonal population of Raji human B lymphocytes subjected to CRISPR/Cas9-mediated disruption of the GATA6 gene. This product provides a pooled knockout model that abolishes GATA6 transcriptional function without clonal isolation, enabling loss-of-function studies in a heterogeneous genetic background.
Raji cells are an EBV-positive lymphoblastoid B cell line derived from a Burkitt??s lymphoma patient, growing in suspension. They serve as a well-established model for B-cell lymphoma, immune signaling, and therapeutic screening, offering a relevant context to study oncogenic and tumor-suppressive mechanisms in lymphoid malignancies.
GATA6 is a zinc-finger transcription factor that governs cell fate, differentiation, and proliferation through context-dependent tumor-suppressive or oncogenic activities. It is activated by upstream signals including BMP4, Wnt ligands, TGF-??, and PI3K/AKT cascades. GATA6 operates within transcriptional complexes incorporating FOG1/ZFPM1 and FOG2/ZFPM2 coregulators, and interacts with GATA4, NKX2-5, SP1, and SMAD proteins. In Wnt signaling, GATA6 cooperates with TCF/LEF factors; in TGF-?? pathways, it engages SMAD complexes. Its direct downstream targets encompass HNF4A, MUC2, p21/CDKN1A, Cyclin D1, BCL2 family members, and E-cadherin, linking GATA6 to cell cycle control and apoptosis.
In Raji lymphoma cells, disruption of GATA6 eliminates its transcriptional output, perturbing gene networks that regulate proliferation and survival??notably those involving p21/CDKN1A, Cyclin D1, and BCL2 family genes. This perturbation allows dissection of GATA6??s role in B-cell receptor and NF-??B pathways, aiding in the understanding of its contribution to lymphomagenesis.
The polyclonal knockout cells are suitable for functional genomics, including RNA-seq-based target gene identification and ChIP-qPCR validation of GATA6 genomic occupancy. They facilitate drug response profiling via MTT/XTT proliferation and Annexin V apoptosis assays, as well as flow cytometric assessment of B-cell markers (CD19, CD20) and colony formation studies. The model supports mechanistic investigations into GATA6-mediated tumor suppression and gene editing technology optimization. For additional information, please contact Ascent Research.
