In Stock Cell Lines
Mus musculus (Mouse)
Large intestine (colon)
Adherent
The B3gnt3 Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited murine colon carcinoma cell line with disruption of B3GNT3, a glycosyltransferase extending poly-N-acetyllactosamine chains. B3GNT3, regulated by Wnt/??-catenin and TGF-??, modifies integrin ??1 and E-cadherin glycosylation, affecting FAK signaling. This model in CT26.WT enables investigation of glycosylation in tumorigenesis and immune evasion. Applications include glycan profiling by flow cytometry, adhesion and migration assays, and syngeneic tumor studies. It interacts with B4GalT1, LARGE, and dystroglycan, and influences FUT and ST3GAL enzymes. Ideal for cancer glycobiology and immuno-oncology research.
ACBD6 Knockout HGC-27 Polyclonal Cells
Cat. No. ARG29399
AGK Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30260
HMGN3 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG31646
GPR107 Knockout SK-HEP-1 Polyclonal Cells
Cat. No. ARG32496
CR2 Knockout CaSki Polyclonal Cells
Cat. No. ARG9868
CLIC4 Knockout AGS Polyclonal Cells
Cat. No. ARG2316
The B3gnt3 Knockout CT26.WT Cell Line is a CRISPR/Cas9-edited knockout cell line in which the B3gnt3 gene has been disrupted in the murine CT26.WT colon carcinoma epithelial cell line. This loss-of-function model enables dissection of B3GNT3-catalyzed glycan modifications in cancer cell biology without endogenous gene interference. It provides a defined background to investigate how B3GNT3-dependent glycosylation alters adhesion and migration.
CT26.WT originates from a chemically induced colon carcinoma in BALB/c mice. This tumorigenic epithelial cell line is extensively employed in immuno-oncology research, especially for syngeneic models with intact immune systems. Its aggressive in vitro and in vivo growth and well-characterized behavior make it an ideal host for evaluating gene disruption effects on tumor progression and therapeutic response.
B3GNT3 functions as a glycosyltransferase that catalyzes beta-1,3-GlcNAc addition to galactose, extending poly-N-acetyllactosamine chains. This enzyme operates in glycosphingolipid biosynthesis, O-glycan processing, and N-glycan processing. Transcriptionally regulated by SP1 and activated by Wnt/??-catenin and TGF-?? pathways, B3GNT3 modifies adhesion receptors like integrin ??1 and E-cadherin, consequently modulating focal adhesion kinase (FAK) signaling. It interacts with B4GalT1, LARGE, and dystroglycan. Downstream glycan effects involve FUT enzymes, ST3GAL sialyltransferases, and B4GALT1.
In CT26.WT cells, B3gnt3 disruption permits interrogation of how poly-N-acetyllactosamine synthesis contributes to tumorigenic behavior. As B3GNT3 is overexpressed in colorectal, gastric, and pancreatic cancers, this knockout is highly relevant for dissecting its role in progression. Loss of B3GNT3 is predicted to alter glycosylation of integrins and cadherins, thereby impairing adhesion, migration, and anti-apoptotic pathways. Because CT26.WT is a syngeneic model, this line is ideal for studying glycosylation-dependent immune evasion and immunotherapy responses.
Researchers can employ flow cytometry with lectins to profile surface glycans, adhesion and migration assays to measure functional outcomes, and western blotting to detect glycosylated integrins. RNA-seq can reveal transcriptional networks impacted by B3GNT3 loss. In vivo syngeneic xenograft studies assess tumor growth, metastasis, and immunotherapy response. This line facilitates screening of glycan-dependent drug sensitivities. For further information or to discuss custom applications, contact Ascent Research.
