ARMC6 Knockout HEK293T Polyclonal Cells constitute a CRISPR/Cas9-mediated loss-of-function model targeting the human ARMC6 gene in the HEK293T background. This polyclonal population, generated by transient transfection of Cas9 and guide RNA expression vectors, contains a heterogeneous mix of genetic disruptions, enabling rapid functional studies without single-cell cloning. The product is supplied as a ready-to-use knockout pool suitable for transient and pooled screening applications, providing a robust system to interrogate ARMC6-dependent phenotypes.
The host cell line, HEK293T, is a widely used derivative of human embryonic kidney HEK293 cells that stably expresses the SV40 large T-antigen. This enables episomal replication of plasmids containing the SV40 origin of replication, resulting in high-level protein expression from transfected constructs. HEK293T cells exhibit an adherent epithelial morphology and are extensively employed for transient transfection, lentiviral production, and functional genomics screens. Their robust growth and ease of genetic manipulation make them an ideal chassis for studying signaling pathways and protein?Cprotein interactions.
ARMC6 (Armadillo repeat-containing protein 6) is a putative scaffold protein characterized by multiple armadillo repeat domains that mediate protein?Cprotein interactions. In the canonical Wnt/??-catenin pathway, extracellular Wnt ligands such as Wnt3a engage Frizzled (FZD) receptors and Dishevelled (DVL) to regulate the destruction complex containing AXIN and APC. This cascade stabilizes cytoplasmic ??-catenin (CTNNB1), which translocates to the nucleus and partners with TCF/LEF transcription factors (e.g., TCF7L2) to activate target genes including AXIN2, MYC, and CCND1. ARMC6 is predicted to facilitate assembly of signaling complexes at the level of ??-catenin or its nuclear effectors; its knockout disrupts Wnt-dependent transcriptional programs, thereby impairing cell cycle progression and proliferation.
In the HEK293T background, Wnt/??-catenin signaling is functionally intact, with modest basal activity that can be readily stimulated. ARMC6 knockout in these cells provides a physiologically relevant model to dissect the protein??s role in transmitting or modulating Wnt signals. Disruption of ARMC6 is expected to attenuate expression of Wnt target genes, perturb downstream cell cycle regulators, and potentially sensitize cells to apoptosis. Given the involvement of aberrant Wnt signaling in colorectal cancer and other malignancies, this model serves as a valuable tool for investigating druggable nodes within the pathway and for defining the ARMC6 interactome in an epithelial context.
Typical applications include functional characterization of ARMC6 via luciferase reporter assays (e.g., TOPFlash/FOPFlash), quantitative immunoblotting for active ??-catenin, and RT-qPCR profiling of Wnt target genes. Cell proliferation and apoptosis can be assessed using MTS/BrdU incorporation and caspase-3/7 activation kits, respectively. Co-immunoprecipitation coupled with mass spectrometry enables identification of ARMC6-binding partners, while Boyden chamber or scratch-wound assays can evaluate effects on cell migration and invasion. This polyclonal knockout product is well-suited for pooled CRISPR screens, drug target validation studies, and pathway dissection in cancer cell biology. For further details or to inquire about customization options, please contact Ascent Research.
