In Stock Cell Lines
Homo sapiens (Human)
Kidney
Adherent
The RNF213 Knockout HEK293T Cell Line is a CRISPR/Cas9-edited knockout cell line lacking the E3 ubiquitin ligase RNF213, a key regulator of NF-??B signaling that mediates I??B?? degradation and VEGF expression. This model is relevant for Moyamoya disease research, ubiquitination pathway analysis, and angiogenesis studies. Based on the highly transfectable HEK293T epithelial host, the line is ideal for NF-??B reporter assays, VEGF ELISA, tube formation, and wound healing migration assays, supporting comprehensive analysis of RNF213??s role in vascular biology, lipid metabolism, and Moyamoya disease.
KIAA1191 Knockout K562 Polyclonal Cells
Cat. No. ARG20762
AIFM2 Knockout HEK293T Polyclonal Cells
Cat. No. ARG25637
CCL14 Knockout HAP1 Polyclonal Cells
Cat. No. ARG43161
CDKN1A Knockout MES-OV Polyclonal Cells
Cat. No. ARG6455
Rat Osteoblast Medium
Cat. No. ARM0313
Human Leptomeningeal Pericyte Medium
Cat. No. ARM0093
The RNF213 Knockout HEK293T Cell Line is a CRISPR/Cas9-edited knockout cell line featuring disruption of the human RNF213 gene in the HEK293T epithelial host. This loss-of-function model provides a stable platform for investigating RNF213-dependent mechanisms in cellular signaling, protein ubiquitination, and angiogenesis. The cell line is suitable for a wide range of downstream analyses, including gene rescue and pathway interrogation.
HEK293T is a human embryonic kidney cell line transformed with adenovirus type 5 DNA and expressing SV40 large T antigen, resulting in high transfection efficiency and robust protein production. Its epithelial origin makes it a convenient system for studying cell migration, barrier function, and signaling pathways relevant to disease. The cell line??s ease of manipulation and well-characterized background support reliable and reproducible experiments across diverse research areas.
RNF213 encodes an E3 ubiquitin ligase that activates NF-??B signaling by promoting ubiquitin-dependent degradation of I??B??, thereby liberating NF-??B p65 to drive transcription of downstream targets such as VEGF. Its activity is modulated by upstream stimuli including interferon-gamma, NF-??B, and hypoxia, and it interacts with filamin A and caveolin-1 to influence actin cytoskeleton remodeling. Consequently, loss of RNF213 disrupts NF-??B?Cmediated gene expression and cytoskeletal dynamics, linking it to vascular homeostasis and Moyamoya disease.
In the HEK293T background, this knockout cell line enables precise dissection of RNF213 function without endogenous interference. The high transfectability of the host facilitates complementation studies and reporter assays, allowing rapid assessment of mutant RNF213 variants or small-molecule modulators. Furthermore, the epithelial context supports investigations into RNF213??s roles in cell motility, inflammatory responses, and metabolic regulation.
Key research applications include dissecting Moyamoya disease mechanisms through analysis of NF-??B signaling dysregulation and impaired angiogenesis, studying RNF213-mediated ubiquitination using ubiquitination assays and co-immunoprecipitation of interacting partners such as filamin A and caveolin-1, and exploring lipid droplet biology with lipid droplet staining. The cell line supports functional assessments via NF-??B reporter assays, VEGF ELISA, tube formation, and wound healing migration assays, complemented by western blotting and RT-qPCR for target validation. For additional product details or to initiate a purchase, please reach out to Ascent Research.
