The KIDINS220 Knouckout HT29 Polyclonal Cells product consists of a CRISPR/Cas9?edited polyclonal cell population in which the KIDINS220 gene is disrupted. This polyclonal knockout model avoids clonal isolation, maintaining a heterogeneous genetic background that more closely mimics complex tumor biology, and is suitable for loss?of?function studies.
The parental HT29 line originates from a primary colorectal adenocarcinoma of a 44?year?old Caucasian female. These well?differentiated epithelial cells are a standard model for studying intestinal epithelial biology, colorectal cancer progression, and therapeutic responses. HT29 cells can be induced to differentiate into enterocyte?like cells, providing a unique system to examine signaling in both progenitor and differentiated states.
KIDINS220 is a scaffold protein that orchestrates neurotrophin receptor signaling. It forms complexes with TrkA, TrkB, and p75NTR, and upon stimulation by NGF, BDNF, or NT?3, recruits adaptors CRK, SHC, and Grb2. This assembly propagates signals to ERK1/2, AKT, and PLC??1, and also influences JNK and NF???B pathways. Additionally, KIDINS220 interacts with RhoG and ???tubulin, linking neurotrophin input to Rho GTPase?driven cytoskeletal changes. Through these interactions, KIDINS220 regulates key processes such as cell proliferation, survival, differentiation, and migration.
In colorectal cancer, KIDINS220 has been implicated in enhancing invasive potential, possibly via Rho GTPase?mediated actin reorganization and focal adhesion dynamics. The KIDINS220?knockout HT29 polyclonal cells enable delineation of this scaffold??s specific contribution to malignant phenotypes in an epithelial context. Moreover, the differentiation capacity of HT29 allows investigation of KIDINS220 function in both undifferentiated and differentiated intestinal cells, shedding light on its dual roles in cancer progression and tissue homeostasis.
This tool is ideal for functional assays such as phospho?ERK1/2, phospho?AKT, and phospho?JNK immunoblotting following neurotrophin stimulation; co?immunoprecipitation to confirm disrupted KIDINS220?Trk interactions; and Boyden chamber or scratch?wound assays to quantify migration and invasion. NF???B luciferase reporter measurements and immunofluorescence localization studies are also readily performed. The polyclonal nature of the product ensures population?level reproducibility and facilitates drug screening campaigns focused on neurotrophin?dependent pathways in colorectal cancer. For additional technical support, please contact Ascent Research.
