In Stock Cell Lines
Mus musculus (Mouse)
Large intestine (colon)
Adherent
The Rfx5 Knockout CT26 Cell Line is a CRISPR/Cas9-edited knockout cell line with targeted disruption of the Rfx5 gene in the murine CT26 colon carcinoma background. Rfx5 encodes a critical subunit of the RFX complex, which cooperates with CIITA, RFXAP, and RFXANK to drive MHC class II expression downstream of IFNG/JAK/STAT signaling. Knockout of Rfx5 abrogates MHC class II induction, thereby impairing CD4+ T cell-mediated anti-tumor immunity. This model is applied in tumor immunology, immunotherapy development, and bare lymphocyte syndrome research. Representative assays include flow cytometry for MHC class II, CD4+ T cell co-cultures, cytokine profiling, and in vivo tumor studies in BALB/c mice.
ASB15 Knockout HAP1 Polyclonal Cells
Cat. No. ARG21929
NOTCH2 Knockout HT29 Polyclonal Cells
Cat. No. ARG14512
BAG6 Knockout Raji Polyclonal Cells
Cat. No. ARG21351
JAK1 Knockout A549 Polyclonal Cells
Cat. No. ARG23142
BCL7B Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG31333
DPM1 Knockout Hela Polyclonal Cells
Cat. No. ARG39661
The Rfx5 Knockout CT26 Cell Line is a CRISPR/Cas9-edited knockout cell line featuring a targeted disruption of the Rfx5 gene in the murine CT26 colon carcinoma background. Rfx5 encodes a critical subunit of the regulatory factor X (RFX) complex, a master transcriptional regulator of major histocompatibility complex class II (MHC class II) gene expression and adaptive immunity. This cell line serves as a genetically defined model to dissect the role of Rfx5-dependent antigen presentation in tumor biology and immune surveillance.
The CT26 cell line was derived from a chemically induced colon carcinoma in a BALB/c mouse and is widely used as a syngeneic tumor model in cancer immunotherapy and tumor immunology. These immunogenic cells upregulate MHC class II upon interferon-gamma (IFNG) stimulation via the JAK-STAT-IRF1-CIITA pathway, enabling CD4+ T cell activation. Consequently, CT26 provides an optimal background for studying the interplay between MHC class II-dependent antigen presentation and anti-tumor immunity.
Rfx5 is a DNA-binding subunit of the RFX complex, together with RFXAP and RFXANK, which cooperates with CIITA to drive MHC class II transcription. IFNG receptor engagement activates JAK1/JAK2, leading to STAT1 phosphorylation and induction of IRF1 and CIITA. CIITA then recruits the RFX complex and NF-Y to MHC class II promoters and the CD74 gene. Disruption of Rfx5 abrogates this enhanceosome, eliminating expression of MHC class II alleles (e.g., H2-Aa, H2-Eb) and CD74, thereby impairing CD4+ T cell-mediated immune responses.
In CT26 cells, Rfx5 knockout abolishes IFNG-induced MHC class II surface expression, preventing tumor cell recognition by CD4+ T cells. This mimics bare lymphocyte syndrome type II and provides a platform to investigate immune evasion through MHC class II downregulation. The model enables dissection of CD4+ T cell-specific contributions to tumor rejection, checkpoint blockade efficacy, and tumor microenvironment, while facilitating study of alternative antigen cross-presentation pathways.
This knockout cell line is validated for flow cytometry, western blotting for RFX5, phospho-STAT1, and CIITA, and RT-qPCR for MHC class II and CD74 transcripts. Co-culture with CD4+ T cells and cytokine profiling (e.g., IL-2, IFNG) assess functional antigen presentation. In vivo syngeneic tumor implantation in BALB/c mice enables monitoring of tumor growth, immune infiltration, and immunotherapy responses. The Rfx5 Knockout CT26 Cell Line serves as a versatile tool for preclinical immuno-oncology research. For further information, please contact Ascent Research.
