The ANKRD1 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human ANKRD1 gene. This product provides a loss-of-function model in the widely used HEK293T host background, enabling investigation of ANKRD1-dependent signaling and cellular processes. The polyclonal format reflects a heterogeneous mixture of edited cells generated through CRISPR/Cas9-mediated gene disruption, without isolation of single-cell clones. This population-level knockout approach preserves the natural cellular context and is suitable for diverse functional assays where clonal variation is not a primary concern.
The host cell line, HEK293T, is a well-established derivative of human embryonic kidney HEK293 cells that stably expresses the SV40 large T antigen. This property permits episomal replication of plasmids containing the SV40 origin, enhancing transient protein expression and lentiviral production. HEK293T cells are a preferred tool for high-efficiency viral propagation, protein overproduction, and reporter-based assays. Their robust growth, ease of transfection, and well-characterized signaling milieu make them an ideal background for studying gene function with CRISPR tools.
ANKRD1 (also known as cardiac ankyrin repeat protein, CARP) encodes a transcription cofactor that functions as a repressor or activator in muscle and non-muscle lineages. It lies downstream of mechanosensitive and growth factor inputs, including TGF-??1, YAP/TAZ, MRTF-A/SRF, and mechanical stretch. ANKRD1 interacts with YAP1, TEAD, SRF, MYOD, TGF-??1, and the giant sarcomeric protein titin, modulating transcription of cardiac troponin I, myosin light chain 2, ??-actin, matrix metalloproteinases, and the pro-apoptotic factor p53. Through these associations, ANKRD1 couples biomechanical stress to gene expression programs governing muscle differentiation, hypertrophy, and apoptosis.
In the HEK293T epithelial context, ANKRD1 overexpression has been linked to TGF-??-driven epithelial-mesenchymal transition signatures, but its knockout may disrupt TGF-?? and Hippo pathway crosstalk, altering SMAD2/3 and YAP/TAZ activity. ANKRD1 loss can attenuate stress-responsive transcription, modify cell adhesion dynamics, and shift proliferation rates, providing a platform to dissect how ANKRD1 represses or activates target genes depending on mechanical and chemical inputs. The polyclonal knockout population thus offers a functional model to explore ANKRD1??s role in non-muscle cells.
These polyclonal knockout cells enable studies of ANKRD1 in muscle differentiation and hypertrophy, TGF-??/Hippo crosstalk, cardiac stress responses, and drug screening for cardiomyopathies. They are validated for assays such as western blotting, RT-qPCR, luciferase reporters for SRF or YAP/TAZ, YAP immunofluorescence, and adhesion or proliferation assays. For additional details or to request a quote, please contact Ascent Research.
