PARK2 Human

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the progressive loss of dopaminergic neurons in the substantia nigra, a region of the brain that plays a key role in movement control . Mutations in the PARK2 gene are one of the genetic causes of Parkinson’s disease, particularly in cases of autosomal recessive juvenile Parkinsonism .

PARK2 is an element in a multiprotein E3 ubiquitin ligase complex, which mediates the targeting of substrate proteins for proteasomal degradation . This process is essential for maintaining cellular homeostasis and preventing the accumulation of toxic proteins that can lead to cell death. Alterations in the PARK2 gene can disrupt this process, leading to the accumulation of damaged proteins and contributing to the development of Parkinson’s disease .

Human recombinant PARK2 is a laboratory-produced version of the natural protein. It is created using recombinant DNA technology, which involves inserting the human PARK2 gene into bacterial or mammalian cells to produce the protein in large quantities. This recombinant protein is used in research to study the function of PARK2 and its role in Parkinson’s disease, as well as to develop potential therapeutic strategies .

Research on PARK2 has provided valuable insights into the molecular mechanisms underlying Parkinson’s disease. Studies have shown that PARK2 mutations can lead to mitochondrial dysfunction, oxidative stress, and impaired protein clearance, all of which contribute to the degeneration of dopaminergic neurons . Understanding these mechanisms is crucial for developing targeted therapies that can slow or halt the progression of the disease.

In addition to its role in Parkinson’s disease, PARK2 has been implicated in other neurodegenerative disorders and cancers, making it a significant target for biomedical research .