In Stock Cell Lines
Mus musculus (Mouse)
Skin
Adherent
The Ifnar1 Knockout B16-F10 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the highly metastatic mouse melanoma B16-F10 line, with disruption of the Ifnar1 gene encoding the type I interferon receptor subunit IFNAR1. This model ablates interferon-alpha/beta signaling, blocking downstream activation of JAK1, TYK2, STAT1, STAT2, and IRF9-mediated ISG expression. Derived from C57BL/6 mice, B16-F10 cells form an aggressive syngeneic tumor model widely used in metastasis and immunotherapy research. The Ifnar1 knockout variant enables investigation of interferon-dependent immune evasion, tumor progression, and therapeutic response, with applications in signaling analysis, in vivo tumor studies, and immune cell coculture assays.
AQP6 Knockout HAP1 Polyclonal Cells
Cat. No. ARG21880
ABCB10 Knockout CaSki Polyclonal Cells
Cat. No. ARG35894
ABL2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG37827
LRRC75A Knockout Hela Polyclonal Cells
Cat. No. ARG7719
NFKB1 Knockout HCT116 Polyclonal Cells
Cat. No. ARG7199
Rabbit Aortic Smooth Muscle Cells
Cat. No. ARP0681
The Ifnar1 Knockout B16-F10 Cell Line is a CRISPR/Cas9-edited knockout cell line derived from the C57BL/6 mouse melanoma B16-F10 line, featuring disruption of the Ifnar1 gene encoding the type I interferon receptor subunit IFNAR1. This loss-of-function model eliminates type I interferon responsiveness, providing a defined genetic background for studying interferon signaling in melanoma biology.
The parental B16-F10 cell line is a widely used highly metastatic melanoma model in syngeneic C57BL/6 mice, forming primary tumors and spontaneous metastases. It serves as an essential platform for investigating metastasis mechanisms and evaluating immunotherapies, including immune checkpoint inhibitors.
IFNAR1, in complex with IFNAR2, is activated by type I interferons IFN-?? and IFN-?? and downstream of pattern recognition receptor agonists such as poly(I:C). Ligand-bound receptor activates JAK1 and TYK2 kinases, which phosphorylate STAT1 and STAT2. These STATs assemble with IRF9 to form the ISGF3 complex, which translocates to the nucleus and binds ISRE elements, inducing interferon-stimulated genes (ISGs) like Mx1, Oas1, and Ifit1. This pathway underpins antiviral defense, immunomodulation, and upregulation of MHC class I. Disruption of Ifnar1 abolishes this signaling, blocking ISG expression and reducing interferon-driven MHC class I presentation, a trait that may facilitate tumor immune evasion.
In the B16-F10 context, Ifnar1 knockout allows dissection of how melanoma cells exploit interferon signaling defects to escape immune detection. The model is valuable for examining the role of type I interferon in tumor progression, metastasis, and response to immunotherapy. It enables direct testing of tumor cell-intrinsic interferon effects separate from host immune signaling.
Researchers can employ this cell line for western blotting of IFNAR1 and phosphorylated STAT1 to verify pathway inactivation, flow cytometry for surface MHC class I, and qPCR or RNA-seq to assess ISG induction. In vivo syngeneic tumor models permit analysis of growth kinetics and metastasis, while coculture assays reveal altered interactions with T cells and NK cells. The model also supports development of IFNAR1-targeted therapies and viral infection studies. For further inquiries, contact Ascent Research.
