The ATRN Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, designed to disrupt the ATRN gene encoding attractin. This loss-of-function model serves as a robust tool for investigating ATRN-dependent pathways in a colorectal cancer background. The polyclonal population provides a heterogeneous knockout pool that reflects diverse editing events, enabling functional studies without the constraints of single-cell clonal expansion.
HT-29 is an established human colorectal adenocarcinoma cell line with epithelial morphology, extensively used in cancer biology research. It retains characteristics of intestinal epithelial cells, making it a relevant model for studying colorectal cancer signaling, tumor progression, and drug responses. HT-29 cells express key components of the melanocortin and cAMP pathways, providing a physiologically relevant context for dissecting ATRN-mediated functions.
ATRN encodes attractin, a transmembrane glycoprotein that acts as an accessory receptor for AGRP and alpha-MSH, modulating melanocortin receptor activity. ATRN interacts with MC1R and MC4R, and its engagement influences downstream signaling through cAMP and PKA, ultimately regulating transcription factors such as CREB. Disruption of ATRN is known to perturb melanocortin signaling, resulting in altered cAMP production and impaired cell adhesion, reflecting its roles in energy homeostasis and immune modulation. Additionally, ATRN functions downstream of AGRP and alpha-MSH, while its downstream effects converge on PKA-mediated phosphorylation cascades.
In HT29 cells, ATRN knockout provides a valuable model to study the intersection of melanocortin signaling and colorectal cancer biology. Given HT29??s origin from colorectal adenocarcinoma, this knockout system allows researchers to explore how ATRN loss impacts tumor cell adhesion, proliferation, and response to apoptotic stimuli. The polyclonal nature reflects the genetic heterogeneity often observed in tumors, making it suitable for evaluating drug sensitivity and signaling redundancy in a population context.
Typical applications of this knockout model include investigating melanocortin pathway dynamics via cAMP assays, assessing cell adhesion changes through adhesion assays, and measuring downstream gene expression by RT-qPCR and Western blotting. Immunofluorescence can localize signaling components, while functional studies can examine how AGRP, alpha-MSH, or synthetic ligands modulate the knockout phenotype. This product is ideal for colorectal cancer signaling research, drug screening, and pathway validation. For further information, please contact Ascent Research.
