Genome-edited Cells
Ascites
The IRF1 Knockout Ramos Cell Line is a CRISPR/Cas9-edited knockout cell line generated from human Burkitt's lymphoma-derived Ramos B lymphocytes. By disrupting the IRF1 gene, this model enables loss-of-function analysis of a key transcription factor that mediates interferon signaling and immune activation. IRF1 responds to upstream signals including IFNG, IFNA, TNF, and IL-1 via STAT1 and NF-kappaB, and regulates downstream effectors such as HLA class I molecules, CIITA, and OAS1. This knockout cell line is therefore suited for studies of interferon responses, antigen presentation, tumor suppression, and apoptosis in B-cell contexts, with applications in lymphoma research and immunology.
BLZF1 Knockout K562 Polyclonal Cells
Cat. No. ARG20327
FPGT Knockout HT29 Polyclonal Cells
Cat. No. ARG13841
IRAK4 Knockout Hela Polyclonal Cells
Cat. No. ARG37298
DTWD2 Knockout MES-OV Polyclonal Cells
Cat. No. ARG39941
LPL Knockout Hela Polyclonal Cells
Cat. No. ARG7805
Mouse Natural Killer (NK) Cell Medium
Cat. No. ARM0592
The IRF1 Knockout Ramos Cell Line is a CRISPR/Cas9-edited knockout cell line that provides a loss-of-function model for the IRF1 gene in human B lymphocytes. This gene-disrupted cell line enables targeted investigation of IRF1-dependent processes without the need for sustained drug selection or transient silencing.
The Ramos cell line, derived from a human Burkitt’s lymphoma, is a widely used model for B-cell receptor signaling, apoptosis, and interferon responses. Its B lymphocyte identity supports studies of humoral immunity, including antibody production and antigen presentation, making it relevant for both basic immunology and lymphoma research.
IRF1 encodes a transcription factor activated by interferons (IFNG, IFNA, IFNB), TNF, IL-1, and TLR ligands through upstream mediators STAT1 and NF-kappaB. Upon activation, IRF1 binds ISRE elements to regulate genes involved in antiviral defense (OAS1, PKR), antigen presentation (HLA-A, HLA-B, HLA-C, CIITA, TAP1, PSMB9), chemokine signaling (CXCL10), and apoptosis/cell cycle arrest (CASP1, CDKN1A). IRF1 interacts with cofactors such as STAT1, NF-kappaB p65, IRF8, and histone acetyltransferases (CBP, EP300, PCAF) to orchestrate transcription. Its activity is integrated within JAK-STAT and NF-kappaB pathways, where JAK1/JAK2 phosphorylate STAT1/STAT2, leading to IRF9 complex formation, and IKK/RelA and TBK1/IRF3/IRF7 modules converge. Negative regulation by PIAS1 and SOCS1 ensures tight control.
Disrupting IRF1 in Ramos cells abolishes a central node of interferon signaling, impairing ISRE-driven gene expression and downstream immune functions. This knockout line allows dissection of how IRF1 loss affects B-cell receptor signaling, apoptosis, and antigen presentation, and provides a system to study IRF1’s tumor-suppressive roles in lymphomagenesis, particularly its promotion of cell cycle arrest and apoptosis.
Applications include investigating interferon signaling pathways, tumor suppressor mechanisms, immune modulation, and antigen presentation in B cells. Typical validation techniques include Western blotting, RT-qPCR, RNA-seq, flow cytometry, interferon stimulation assays, ChIP-qPCR, co-immunoprecipitation, and drug sensitivity studies. For further information or to discuss specific experimental applications, please contact Ascent Research.
