In Stock Cell Lines
Mus musculus (Mouse)
Large intestine (colon)
Adherent
The App Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited mouse colon carcinoma cell line with targeted disruption of the App gene. This model lacks amyloid precursor protein, a transmembrane glycoprotein involved in cell adhesion, neurite outgrowth, and synapse formation. App undergoes proteolytic processing by ??-, ??-, and ??-secretases to generate ??-amyloid peptides and an intracellular domain (AICD) that transcriptionally regulates targets through interactions with Fe65 and Tip60. The knockout line enables studies of Alzheimer??s disease amyloid processing, cancer cell adhesion and migration, and drug testing for ??-secretase inhibitors. It is particularly valuable in CT26 syngeneic tumor models for dissecting App??s role in tumor progression and immunotherapy responses.
FGFR4 Knockout A2780 Polyclonal Cells
Cat. No. ARG18356
LRP8 Knockout A549 Polyclonal Cells
Cat. No. ARG10343
BMP2 Knockout CAL27 Polyclonal Cells
Cat. No. ARG35353
GPNMB Knockout 143B Polyclonal Cells
Cat. No. ARG35668
AATK Knockout HAP1 Polyclonal Cells
Cat. No. ARG21533
GALNT11 Knockout AGS Polyclonal Cells
Cat. No. ARG2228
The App Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited knockout line derived from the mouse colon carcinoma cell line CT26.WT, featuring targeted disruption of the App gene. This loss-of-function model eliminates amyloid precursor protein expression through stable gene editing, enabling functional studies without transient gene silencing. The cell line retains parental CT26.WT properties and is validated for immediate use in research.
The parental CT26.WT line is an undifferentiated colon carcinoma model from BALB/c mice. Widely used in syngeneic tumor studies and immunotherapy, it exhibits rapid, immunogenic tumor growth and consistent kinetics. The epithelial tumor origin makes it suitable for examining oncogenic signaling and the influence of molecules like App on cancer cell behavior.
The App gene encodes a type I transmembrane glycoprotein processed by ??-secretase (ADAM10), ??-secretase (BACE1), and the ??-secretase complex (PSEN1, PSEN2, APH1, PEN2, NCSTN). Proteolysis yields ??-amyloid peptides (A??40, A??42) and the APP intracellular domain (AICD). AICD forms a transcriptional complex with Fe65 (APBB1) and Tip60, regulating expression of targets like neprilysin, GSK3??, and p53. App also interacts with Dab1, JIP1, Shc, and Grb2, connecting to Notch and Wnt/??-catenin pathways. In colon carcinoma, App may modulate adhesion, migration, and proliferation via Fe65-associated GSK3?? signaling.
Deleting App in CT26.WT creates a model to examine how amyloid precursor protein affects tumor cell adhesion, migration, and proliferation, processes critical in cancer progression. This knockout separates neuronal from epithelial functions of App, enabling focused study in a colon carcinoma context. Using the syngeneic CT26 platform, researchers can translate in vitro results to in vivo tumor growth and immunotherapy experiments in immunocompetent BALB/c mice, analyzing App-dependent changes in the tumor microenvironment.
The cell line supports Alzheimer??s research through Western blot analysis of APP fragments and ELISA quantification of A??40/42. Cancer biology applications include wound healing and proliferation assays to assess migration and growth, co-immunoprecipitation of Fe65 complexes, and immunofluorescence for APP localization. It is valuable for drug testing, such as ??-secretase inhibitor screening, and qPCR analysis of AICD target genes. It also enables study of the crosstalk between amyloidogenic processing and tumor cell signaling. This knockout model bridges neurobiology and oncology, offering a robust tool for diverse research. For further details, contact Ascent Research.
