The EBP Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the EBP gene in HEK293T cells. This heterogeneous pool carries diverse gene-disrupting edits, providing a robust loss-of-function model for the sterol ??8-??7 isomerase. The polyclonal format minimizes clonal artifacts and is optimized for bulk biochemical and functional studies.
HEK293T is a human embryonic kidney epithelial cell line transformed by adenovirus 5, expressing SV40 large T antigen. Its epithelial origin, high transfectability, and rapid growth make it a standard platform for studying membrane biology, signal transduction, and metabolism. The kidney epithelium background offers a non-hepatic context for cholesterol biosynthesis research.
EBP encodes the sterol ??8-??7 isomerase, an ER-resident enzyme that converts zymosterol to lathosterol, a key step in postsqualene cholesterol synthesis. EBP is regulated by SREBP-1 and SREBP-2 in response to cholesterol levels and insulin. It collaborates with DHCR7, SC5D, and NSDHL in the sterol pathway. Knockout leads to accumulation of ??8-sterols, disrupting membrane integrity and downstream production of cholesterol, vitamin D3, and steroid hormones.
In HEK293T cells, EBP loss impairs cholesterol biosynthesis, alters SREBP activation, and affects lipid droplet formation. This model mimics aspects of CDPX2 (Conradi-H??nermann syndrome), enabling study of skeletal dysplasia, ichthyosis, and cataract mechanisms. It allows exploration of cholesterol depletion on mTOR/SREBP signaling, apoptosis, and membrane receptor function in a human epithelial system.
Applications include cholesterol biosynthesis inhibitor screening, sterol profiling by GC-MS, filipin staining, and SREBP reporter assays. The polyclonal population supports RT-qPCR for pathway genes, immunofluorescence for enzyme localization, and metabolic assays for lipid synthesis. It is also suitable for phospho-signaling analysis and apoptosis studies under cholesterol depletion. For technical inquiries, contact Ascent Research.
