In Stock Cell Lines
Mus musculus (Mouse)
Large intestine (colon)
Adherent
The Gng4 Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited murine colon carcinoma model with targeted disruption of Gng4, encoding the G protein gamma-4 subunit. As part of the G?¦? complex, Gng4 regulates key effectors such as PLC?? and PI3K??, thereby modulating MAPK/ERK and Akt pathways critical in colorectal cancer progression. This knockout cell line enables detailed study of GPCR-mediated signaling in tumor biology, supporting proliferation, migration, second messenger, and drug screening assays. It is a valuable tool for dissecting Gng4-dependent mechanisms in immuno-oncology and cancer research.
LZIC Knockout A2780 Polyclonal Cells
Cat. No. ARG18349
CREB3L2 Knockout HT29 Polyclonal Cells
Cat. No. ARG13973
DGCR6L Knockout Hela Polyclonal Cells
Cat. No. ARG8709
HDDC3 Knockout MES-OV Polyclonal Cells
Cat. No. ARG24513
MAD1L1 Knockout AGS Polyclonal Cells
Cat. No. ARG3240
P2RX4 Knockout Raji Polyclonal Cells
Cat. No. ARG1496
The Gng4 Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited knockout cell line derived from murine CT26.WT colon carcinoma, featuring targeted disruption of the Gng4 gene. Gng4 encodes the gamma-4 subunit of heterotrimeric G proteins, a component of the G?¦? dimer that mediates signal transduction from G protein-coupled receptors (GPCRs). This loss-of-function model allows precise interrogation of G protein ?¦? subunit function in colorectal cancer signaling.
The CT26.WT host cell line is a wild-type murine colon carcinoma model established from a BALB/c mouse, widely recognized for its utility in immuno-oncology and cancer biology research. It displays aggressive tumorigenic and metastatic properties, making it a valuable tool for studying colorectal adenocarcinoma progression and for evaluating therapeutic interventions in a syngeneic context.
Gng4 forms part of the G?¦? signaling complex, which dissociates from G?? subunits (e.g., G??i, G??q) upon GPCR activation. This complex directly regulates effectors including PLC??, PI3K??, adenylyl cyclase, and GIRK channels, thereby modulating downstream cascades such as MAPK/ERK, PI3K/Akt, and cAMP/PKA pathways. Interactions with RGS proteins further tune signal dynamics. Through these networks, Gng4 influences cellular responses like proliferation, migration, and ion flux.
In the CT26.WT background, knockout of Gng4 provides a means to dissect the contribution of the ??4 subunit to colorectal cancer cell behavior. Since MAPK/ERK and Akt pathways are frequently dysregulated in colorectal tumors, this model is particularly suited for investigating how G?¦?-dependent signaling supports oncogenic phenotypes. It also enables studies on the interplay between GPCR signaling and tumor microenvironment interactions.
This cell line supports a range of experimental applications, including RT-qPCR and Western blotting for knockout confirmation, proliferation and migration assays to measure phenotypic outcomes, and cAMP and calcium flux measurements to assess second messenger signaling. Phospho-ERK/Akt analysis by flow cytometry or immunoblotting monitors downstream pathway activity. The model is also suitable for drug screening, RNA-seq transcriptomic profiling, and immune-tumor interaction studies in syngeneic mice. For further information or custom inquiries, please contact Ascent Research.
