The C1QBP Knockout HEK293T Polyclonal Cells are a polyclonal knockout cell population created via CRISPR/Cas9-mediated gene disruption in HEK293T cells. This loss-of-function model enables the study of the multifunctional C1QBP protein (p32/gC1qR). The polyclonal pool provides a heterogeneous mixture of edited cells, suitable for robust functional genomics without single-cell cloning.
HEK293T cells are human embryonic kidney cells transformed with adenovirus 5 DNA and expressing SV40 large T antigen, facilitating high transfection efficiency and episomal replication. This cell line is widely used for protein expression, viral packaging, and signal transduction studies, making it an ideal host for investigating complement and mitochondrial pathways.
C1QBP is a multicompartmental protein that functions as a receptor for C1q via its globular heads (C1qA, C1qB, C1qC) and modulates the classical complement pathway through SERPING1, influencing C3 and CD59. In mitochondria, C1QBP binds TFAM, interacts with PRKCD, and regulates mitochondrial translation, oxidative phosphorylation, and intrinsic apoptosis. Upstream, TNF-alpha and NF-kB upregulate C1QBP transcription, while hypoxia and phorbol esters modulate its activity. Downstream, C1QBP activates MAPK1/3 (ERK1/2) and NF-kB, promoting PTGS2 (COX-2) and MMP9 expression, and engages AKT signaling. C1QBP also interacts with HIV-1 Tat, linking it to host?Cpathogen dynamics.
In HEK293T cells, C1QBP knockout enables dissection of its roles in complement activation, mitochondrial function, and signaling. The high transfection efficiency allows introduction of reporters like NF-kB dual-luciferase for real-time pathway monitoring. Mitochondrial function can be assessed by metabolic flux assays, and cancer phenotypes such as proliferation, migration, and apoptosis can be evaluated. The knockout also supports host?Cpathogen studies, including HIV-1 Tat interactions.
Researchers can employ these cells in assays such as complement deposition, Seahorse mitochondrial stress tests, western blotting, RT-qPCR, immunofluorescence, co-immunoprecipitation, cell proliferation, apoptosis, migration, and NF-kB dual-luciferase reporter assays. This model supports research in complement biology, mitochondrial disorders, cancer, autoimmune diseases, and viral pathogenesis. For further information, please contact Ascent Research.
