The HTT Knockout HT29 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout population targeting the huntingtin (HTT) gene in the HT29 human colorectal adenocarcinoma cell line. This loss-of-function model facilitates the study of HTT’s roles in non-neuronal contexts, including intracellular trafficking, transcriptional regulation, and cell survival. The polyclonal format provides a heterogeneous mix of edited alleles, suitable for pooled functional analyses without single-cell cloning.
HT29 cells, derived from a human colorectal adenocarcinoma, display an adherent epithelial morphology and serve as a classic intestinal epithelial model. Widely used in cancer biology, these cells retain features such as inducible differentiation and are employed to investigate proliferation, apoptosis, and migration. Their robust growth and genetic tractability make them an ideal host for studying gene function in colorectal cancer.
Huntingtin is a large scaffold protein that organizes vesicle trafficking via interactions with HIP1, HAP1, and kinesin/dynactin complexes. It is activated by AKT phosphorylation and proteolytically processed by caspases and calpains. Downstream, HTT promotes BDNF transcription through REST/NRSF nuclear translocation and supports mitochondrial function. In signaling, HTT engages in endocytosis (clathrin/HIP1), autophagy (mTOR/ULK1), apoptosis (caspase-3), and neurotrophin pathways (BDNF/TrkB).
In HT29 colorectal cancer cells, HTT knockout allows dissection of its non-neuronal functions, particularly in survival and apoptosis. HTT??s interaction with p53 and caspases positions it at a key node for cell death decisions, while its roles in autophagy and endocytosis may influence tumor progression. This model enables exploration of HTT’s impact on epithelial integrity, motility, and drug response, bridging neural and peripheral disease research.
This polyclonal knockout model supports diverse assays, including western blotting, proliferation/apoptosis analyses, immunofluorescence, and motility assays. It is ideal for drug screening to identify HTT modulators with relevance to Huntington??s disease, and for investigating HTT-dependent vulnerabilities in colorectal cancer. Co-immunoprecipitation and transcriptional profiling can further map altered signaling networks. For technical inquiries, please contact Ascent Research.
