In Stock Cell Lines
Homo sapiens (Human)
Kidney
Adherent
The SENP2 Knockout HEK293T Cell Line is a CRISPR/Cas9-edited human cell line with SENP2 gene disruption, encoding the cysteine protease that deconjugates SUMO1, SUMO2, and SUMO3 from target proteins. This loss-of-function model enables researchers to dissect deSUMOylation dynamics and its impact on protein homeostasis, nuclear transport, and transcriptional regulation. Constructed in HEK293T epithelial cells, this platform supports studies of SUMO pathway signaling, including interactions with Mdm2, p53, and PML, and is suited for disease modeling of congenital heart defects, neural tube defects, and cancer. Applications range from substrate screening to apoptosis assays.
C8B Knockout HAP1 Polyclonal Cells
Cat. No. ARG22195
FRA10AC1 Knockout A2780 Polyclonal Cells
Cat. No. ARG18794
NT5C2 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG17274
PDGFRB Knockout THP-1 Polyclonal Cells
Cat. No. ARG7382
HSD17B11 Knockout NCI-H1299 Polyclonal Cells
Cat. No. ARG30766
CES2 Knockout Raji Polyclonal Cells
Cat. No. ARG1085
The SENP2 Knockout HEK293T Cell Line is a genetically modified human cell line in which CRISPR/Cas9-mediated genome editing has disrupted the SENP2 gene, creating a stable loss-of-function model for investigating deSUMOylation. This CRISPR/Cas9-edited knockout cell line enables researchers to dissect the biological consequences of SENP2 deficiency in a well-characterized cellular background, facilitating in-depth mechanistic and phenotypic analyses of SUMO pathway regulation.
The host cell line, HEK293T, is a derivative of human embryonic kidney epithelial cells transformed with adenovirus 5 DNA and stably expressing the SV40 large T antigen. Renowned for its high transfection efficiency and robust recombinant protein expression, this cell line is an ideal platform for functional genomics and biochemical studies. Its epithelial origin and nuclear architecture provide a physiologically relevant context for examining SUMO-dependent processes, particularly those governing nuclear transport and transcriptional control.
SENP2 encodes a cysteine protease that specifically deconjugates SUMO1, SUMO2, and SUMO3 from modified proteins, thereby reversing SUMOylation and modulating protein stability, subcellular localization, and transcriptional activity. It also processes full-length SUMO precursors into mature forms, a prerequisite for conjugation. SENP2 activity is regulated by the Sp1 transcription factor and oxidative stress, and it functions within a cycle involving the SAE1/SAE2 E1 activating enzyme, Ubc9 E2 conjugating enzyme, and PIAS family E3 ligases. Downstream deSUMOylation of substrates such as Mdm2, p53, c-Jun, and PML by SENP2 directly influences DNA damage responses, apoptosis, and cell cycle progression.
In HEK293T cells, the SENP2 knockout model provides a powerful tool to study SUMO-dependent nuclear dynamics and protein homeostasis. The cell line’s high-level protein expression aids in detecting subtle changes in SUMO conjugate profiles and facilitates the identification of novel SENP2 substrates. Given the involvement of SENP2 in congenital heart disease, neural tube defects, and cancer, this model is particularly valuable for dissecting disease-relevant SUMOylation defects and for screening compounds that modulate SENP2 activity.
This knockout cell line is designed for functional studies of deSUMOylation, investigation of SUMO-related regulatory mechanisms in gene expression and nuclear architecture, and disease modeling of SUMOylation defects. Researchers can utilize western blotting, immunofluorescence, co-immunoprecipitation, and SUMO pull-down assays to profile SUMO conjugate changes and identify SENP2 substrates, while reporter assays, cell cycle analysis, and apoptosis assays assess functional outcomes. For further technical details, please contact Ascent Research.
