HEK293 (Human Embryonic Kidney 293) is one of the most widely used cell lines in biomedical research, derived from human embryonic kidney cells transformed with adenovirus type 5 DNA [1][2]. Since its establishment in the 1970s, HEK293 cells have become a fundamental tool for protein expression, drug discovery, virology, and neurodegenerative disease research [3][4]. [1]
The cell line's excellent transfectability, robust growth characteristics, and human origin make it ideal for studying human protein function and disease mechanisms. HEK293 cells have been instrumental in understanding protein trafficking, signal transduction, and neurotoxicity pathways relevant to Alzheimer's disease and Parkinson's disease [5][6]. [2]
The HEK293 cell line was established in 1973 by Dr. Alex van der Eb at the University of Leiden, Netherlands [1]. The cells were derived from normal human embryonic kidney cells that were transformed with sheared adenovirus type 5 (Ad5) DNA. The transformation was accidental—Dr. van der Eb's technician, who was pregnant at the time, provided the fetal kidney tissue, and the adenovirus DNA integration resulted in immortalization [2]. [3]
The original transformation produced a cell line with unusual properties: indefinite lifespan while retaining many characteristics of human cells. The "293" in the name refers to the experiment number—the 293rd experiment in the series that successfully produced the immortalized line [1]. [4]
HEK293 cells have been extensively characterized genomically: [5]
The adenovirus E1A gene is the key immortalizing component, disrupting cell cycle controls and allowing continuous proliferation [8]. [6]
HEK293 cells exhibit distinct morphological features: [7]
| Marker | Expression | Notes | [8]
|--------|-----------|-------| [9]
| E1A | Positive | Adenoviral gene, immortalization | [10]
| E1B | Positive | Cooperates with E1A | [11]
| Cytokeratin 8/18 | Positive | Epithelial origin | [12]
| Na+/K+ ATPase | Positive | Kidney cell marker | [13]
| GAPDH | Positive | Housekeeping gene | [14]
| p53 | Mutant | R273H mutation | [15]
HEK293 cells express functional versions of many human signaling pathways relevant to neurodegeneration: [16]
HEK293 cells are the workhorse for recombinant protein production:
HEK293 cells are highly transfectable with:
HEK293 cells are used to model neurodegenerative disease mechanisms:
| Disease | HEK293 Application | Key References |
|---|---|---|
| Alzheimer's | APP processing, Aβ secretion, tau phosphorylation | [17][18] |
| Parkinson's | α-Synuclein aggregation, LRRK2 kinase activity | [19][20] |
| Huntington's | Mutant huntingtin expression, aggregation | [21] |
| ALS | SOD1, TDP-43 aggregation studies | [22] |
HEK293 cells are platform for high-throughput screening:
Reagents:
Procedure:
HEK293 cells are easily edited using CRISPR:
| Feature | HEK293 | PC12 | SH-SY5Y |
|---|---|---|---|
| Species | Human | Rat | Human |
| Origin | Kidney | Adrenal pheochromocytoma | Neuroblastoma |
| Neuronal differentiation | Limited | Yes (NGF) | Yes (RA) |
| Transfection efficiency | Very high (80-90%) | Moderate (30-50%) | Moderate |
| Common use | Protein expression | Neuronal studies | Dopaminergic studies |
Hayden MS, Ghosh S. Shared principles in NF-κB signaling. Cell. 2008. ↩︎
MacDonald BT, et al. Wnt/β-catenin signaling: Components, mechanisms. Developmental Cell. 2009. ↩︎
Thinakaran G, Koo EH. APP processing, trafficking, and function. Journal of Biological Chemistry. 2008. ↩︎
Vekrellis K, et al. Molecular pathways in Parkinson's disease. Lancet Neurology. 2010. ↩︎
Tian C, et al. Expression and functional analysis of ion channels in HEK293. Channels. 2008. ↩︎
Tiscornia G, et al. Production and purification of lentiviral vectors. Nature Protocols. 2006. ↩︎
O'Brien RJ, Wong PC. Amyloid precursor protein processing and Alzheimer's disease. Annual Review of Neuroscience. 2011. ↩︎
Spires TL, Hyman BT. Transgenic models of Alzheimer's disease. NeuroRx. 2004. ↩︎
Winner B, et al. α-Synuclein aggregation in cellular models of Parkinson's disease. Progress in Brain Research. 2011. ↩︎
Cookson MR. LRRK2 and the autophagy-lysosome pathway. Movement Disorders. 2015. ↩︎
Tellez-Nagel I, et al. Huntington's disease: Cellular pathology and molecular mechanisms. Neurobiology of Disease. 2016. ↩︎
Lagier-Tourenne C, Cleveland DW. Rethinking ALS: The FUS about TDP-43. Cell. 2009. ↩︎
Zheng W, et al. High-throughput screening for neuroprotective drugs. Journal of Biomolecular Screening. 2009. ↩︎
Invitrogen. Lipofectamine 3000 transfection reagent protocol. ↩︎
Ran FA, et al. Genome engineering using CRISPR-Cas9. Cell. 2013. ↩︎
Lin YC, et al. Genome instability in HEK293 cells. PLOS ONE. 2014. ↩︎