ALMS1 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma line, featuring a targeted disruption of the ALMS1 gene. This loss-of-function model enables the study of ALMS1-dependent processes in a well-characterized epithelial cancer background. The polyclonal format captures a diverse range of edited alleles, providing a representative population-level knockout phenotype suitable for functional screening and pathway analysis.
HT29 is a widely used human colon adenocarcinoma cell line with epithelial morphology, serving as a robust model for colorectal cancer biology. These cells retain key signaling networks relevant to tumorigenesis and metabolic regulation, making them an appropriate host for investigating the intersection of ciliary protein function and oncogenic pathways. The HT29 background supports high-throughput applications and is amenable to standard transfection, imaging, and biochemical assays.
ALMS1 encodes a large centrosomal and basal body protein that organizes ciliogenesis and intracellular trafficking. It is transcriptionally regulated by RFX factors and responds to cilia-dependent signals. ALMS1 forms complexes with ??-actinin, myosin, IFT88, and other centrosomal components to coordinate ciliary assembly and Hedgehog signaling. Its disruption impairs the formation and maintenance of primary cilia, leading to defective Hedgehog pathway transduction, altered cell cycle progression, and dysregulation of downstream targets such as IFT particle proteins and cell cycle regulators.
In the HT29 adenocarcinoma context, ALMS1 knockout disrupts the ciliary signaling axis implicated in cancer cell proliferation, migration, and metabolic adaptability. Given the links between ALMS1 mutations and Alstr?m syndrome??a ciliopathy characterized by obesity, type 2 diabetes, and dilated cardiomyopathy??this model provides a unique tool for exploring how ciliary defects contribute to both rare genetic disorders and epithelial tumor biology. The loss of ALMS1 function in colorectal cancer cells may reveal crosstalk between centrosome duplication, ciliary maintenance, and tumor metabolic reprogramming.
Researchers can employ these polyclonal knockout cells in a variety of experimental settings, including immunofluorescence for ciliary markers (acetylated tubulin, ARL13B), Western blotting for signaling effectors, flow cytometric analysis of cell cycle changes, and glucose uptake assays to assess metabolic consequences. The model is also suitable for migration/invasion studies and RT-qPCR profiling of ciliary gene expression. Altogether, this system supports applications in ciliopathy disease modeling, oncogenic signaling interrogation, and metabolic disorder research. For detailed technical inquiries or to discuss potential applications, please contact Ascent Research.
