The CAVIN1 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of the caveolar coat protein CAVIN1. This product provides a genetically heterogeneous pool of HEK293T cells carrying targeted disruptions of the CAVIN1 gene, eliminating the need for single-cell cloning and enabling rapid deployment in loss-of-function experiments. The knockout is generated using CRISPR/Cas9-mediated gene disruption, resulting in a population-level CAVIN1 deficiency suitable for biochemical and cell-based assays.
The parental HEK293T cell line is a human embryonic kidney epithelial line widely used for recombinant protein expression and viral vector production. Derived from HEK293 cells by stable integration of SV40 large T antigen, it promotes episomal replication of plasmids containing the SV40 origin. This makes HEK293T highly transfectable and transducible, facilitating lentivirus and AAV production, as well as transient and stable protein expression. Its robust growth and well-characterized proteome provide a consistent background for knockout studies.
CAVIN1 is an essential component of the caveolar coat complex, cooperating with caveolin-1, -2, and -3 to induce membrane curvature and stabilize caveolae. It directly interacts with EHD2, filamin A, and actin to organize caveolar domains and link them to the cytoskeleton. CAVIN1 serves as a signaling scaffold by recruiting and modulating Src family kinases, eNOS, and the insulin receptor. Upstream regulators include PPAR?? agonists, insulin, TGF-??, and mechanical stress. Downstream, CAVIN1 propagates signals through PI3K/Akt, MAPK/ERK, and RhoA pathways, and regulates cholesterol efflux via ABCA1. These interactions place CAVIN1 at the nexus of lipid metabolism, mechanotransduction, and growth factor signaling.
In HEK293T cells, which express endogenous CAVIN1 and form functional caveolae, the polyclonal knockout disrupts caveolar architecture and associated signaling platforms. This system is valuable for studying acute signaling downstream of the insulin receptor, Src, and eNOS, as well as caveolae-dependent endocytosis and cholesterol homeostasis. Because CAVIN1 interacts with dysferlin and TGF-?? pathway components, the knockout cells also model muscular dystrophy-associated and fibrotic signaling. The loss of CAVIN1 enables screening for caveolar function modulators and validation of protein?Cprotein interactions within the caveolar coat.
Applications include caveolae biology, metabolic research, and lipodystrophy modeling, using cholesterol uptake assays, phospho-signaling western blotting, and caveolae internalization assays. In cancer research, these cells are employed in migration and invasion assays to examine caveolar roles in metastasis and Src-driven oncogenesis. The knockout population is also suitable for drug screening targeting caveolar dysfunction, with readouts such as immunofluorescence-based caveolin localization, RNA-seq transcriptional profiling, and insulin-stimulated Akt phosphorylation. For further information, please contact Ascent Research.
