ANKRD26 Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HT29 human colorectal adenocarcinoma cell line, providing a loss-of-function model for the ANKRD26 gene. This polyclonal pool results from CRISPR/Cas9-mediated gene disruption, offering a heterogeneous knockout background for robust functional studies.
The HT29 parental cell line, established from a human colorectal adenocarcinoma, is a widely characterized epithelial tumor model exhibiting adherent growth, tumorigenic properties, and the ability to form differentiated glandular structures. HT29 cells retain key colorectal cancer oncogenic mutations, including those in APC and KRAS, and display constitutive activation of WNT and MAPK pathways, making them a relevant system for investigating colorectal carcinoma biology, metastasis, and therapeutic responses.
ANKRD26 encodes an ankyrin repeat domain-containing protein that acts as a central regulator of megakaryocyte differentiation and platelet production. Biochemically, ANKRD26 functions within the thrombopoietin (THPO)/MPL signaling network, where THPO binding to MPL activates JAK2 and STAT3. ANKRD26 physically interacts with Src family kinases, SH2 domain-containing adaptors, and cytoskeletal linker proteins, facilitating crosstalk with integrin ??IIb/??3 and focal adhesion kinase (FAK). Through these interactions, ANKRD26 modulates cytoskeletal dynamics and the MAPK/ERK signaling cascade, influencing processes such as adhesion, migration, and proliferation.
Within the HT29 colorectal cancer context, disruption of ANKRD26 is expected to disturb cytoskeletal organization and integrin-mediated adhesion, leading to altered cell motility and invasive behavior. The convergence of THPO/MPL/Src and MAPK/ERK pathways suggests that ANKRD26 loss may also affect cell cycle progression and proliferation. This model is instrumental for evaluating the potential tumor-suppressive or oncogenic functions of ANKRD26 in colorectal cancer and for exploring its role in epithelial tumor progression. Moreover, it offers a tractable system to study signaling events underlying ANKRD26-related thrombocytopenia.
Researchers can apply these polyclonal knockout cells in a range of assays, including cell proliferation (e.g., real-time imaging or colorimetric methods), transwell migration and invasion assays, western blotting for phospho-Src (Tyr416) and FAK (Tyr397), immunofluorescence staining for F-actin, RT-qPCR analysis of megakaryocytic or epithelial markers, and flow cytometry for cell cycle phases. Such approaches support functional genomics screens, drug sensitivity testing, and mechanistic studies of ANKRD26-dependent signaling. For additional information, pricing, or to request a quote, please contact Ascent Research.
