HEK 293

Cat.No.: CSC-6980J

Species: Homo sapiens (Human)

Source: Kidney

Morphology: Adherent fibroblastoid cells growing as monolayer

Culture Properties: Adherent

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Cat.No.
CSC-6980J
Description
The cells express the transforming gene of adenovirus 5. Adenovirus 5 DNA from both the right and left ends of the viral genome are present. The line is excellent for titrating human adenoviruses. The cell line does not adhere to the substrate when left at room temperature for any length of time. The cells will reattach to the flask over a period of several days in culture at 37°C. The cells express an unusual cell surface receptor for vitronectin composed of the integrin beta-1 subunit and the vitronectin receptor alpha-v subunit.
Species
Homo sapiens (Human)
Source
Kidney
Recommended Medium
Dulbecco's modified Eagle's medium with 4.5 g/L glucose 90%; fetal bovine serum, 10%
Culture Properties
Adherent
Morphology
Adherent fibroblastoid cells growing as monolayer
Storage
Liuqid Nitrogen, -180°C
Shipping
Dry ice
Synonyms
HEK293; Hek293; HEK-293; HEK/293; HEK;293; 293; 293 HEK; 293 Ad5; Graham 293; Graham-293; Human Embryonic Kidney 293
Citation Guidance
If you use this products in your scientific publication, it should be cited in the publication as: Creative Bioarray cat no. If your paper has been published, please click here to submit the PubMed ID of your paper to get a coupon.

The Human Embryonic Kidney 293 (HEK293) cell line stands as one of the most widely adopted and thoroughly validated mammalian expression systems in modern biomedical research. Originally established in 1973 by Alex van der Eb and Frank Graham at Leiden University through stable transfection of normal human fetal kidney cells with sheared adenovirus type 5 DNA, HEK293 cells have since become an indispensable platform across academic, biotechnology, and biopharmaceutical settings - second only to HeLa cells in global research utilization.

A defining strength of HEK293 cells lies in their exceptional transfection efficiency, readily accepting foreign genetic material via a broad spectrum of chemical, physical, and viral delivery methods, significantly reducing experimental turnaround compared to alternative cell lines such as CHO. As a human-origin cell line, HEK293 cells are uniquely capable of performing complex human-like post-translational modifications (PTMs) - including glycosylation, phosphorylation, and γ-carboxylation - ensuring that recombinant proteins are produced with authentic biological activity and structural fidelity that non-human systems fundamentally cannot replicate.

HEK293 cells exhibit rapid proliferation, robust adaptability to both adherent and suspension culture formats, and proven compatibility with serum-free media, enabling scalable protein production under GMP-aligned conditions. Their consistent, batch-to-batch reproducibility makes them an ideal model for receptor signaling studies, viral vector manufacturing, drug screening, toxicology assessment, and the production of therapeutic proteins.

Furthermore, the versatile HEK293 cell family - including the widely used HEK293T variant expressing the SV40 Large T antigen for enhanced episomal replication - offers researchers flexible, fit-for-purpose solutions across transient and stable expression paradigms.

VPS35 Deficiency Markedly Reduces the Proliferation of HEK293 Cells

The retromer protein complex is involved in various physiological processes, especially endosomal trafficking, and its dysregulation has been linked to Alzheimer's disease and Parkinson's disease, as well as VPS35 knockout (KO), causing early embryonic lethality.

To investigate the effects of VPS35 loss, we used CRISPR/Cas9 to generate VPS35 KO human embryonic kidney 293 (HEK293) cells. We analyzed changes in retromer component expression, cell proliferation, apoptosis, and mitochondrial dynamics using Western blotting, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and confocal microscopy.

The results showed that VPS35 KO significantly reduced cell proliferation and decreased expression of VPS29 and VPS26, both essential for retromer complex assembly. Compared to control cells, KO cells exhibited elevated levels of cleaved caspase-3, poly(ADP-ribose) polymerase, cytochrome C, and p21, while the expression of Ki-67, CDK4, and cyclin D was reduced. Additionally, VPS35 deletion also promoted mitochondrial fragmentation, associated with increased expression of mitochondrial fission-related proteins. These findings suggest that VPS35 plays a critical role in cell growth and survival by modulating apoptosis, mitochondrial dynamics, and cell cycle progression.

Endogenous protein levels in VPS35 KO HEK293 cells were analyzed via Western blotting using antibodies against the indicated proteins.

Fig. 1. VPS35 deficiency leads to activation of apoptotic signaling and cycle-related proteins (Lee, Sujin, et al., 2026).

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