The PARK2-encoded E3 ubiquitin ligase orchestrates mitochondrial quality control (via FUNDC1-mediated mitophagy), proteostasis (20S proteasome assembly), and cell cycle regulation (p21 degradation). Dysfunctional PARK2 variants drive pathologies spanning early-onset Parkinson's (dopaminergic mitophagy failure) to lung adenocarcinoma (p53/MDM2 dysregulation). Our isogenic models—CRISPR-edited KO, OE, and disease-associated mutants in iPSC-derived neurons/astrocytes—enable mechanistic studies of Lewy body aggregation (phase-separated mimetics), ferroptosis susceptibility, and context-dependent oncogenic signaling. Integrated biosensors (mt-Keima for mitophagy flux) and high-content screening platforms support targeted therapeutic development. To explore tailored PARK2 models for your neurodegeneration or cancer research, contact our neuroscience team for collaborative solutions.
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Explore our diverse selection of PARK2 gene-engineered cell models, tailored to meet a wide range of research needs. Each category is designed to provide you with specific tools to investigate the multifaceted roles of the PARK2 gene in Parkinson's disease.
Creative Biolabs' PARK2 Gene-Engineered cell models stand out for several reasons:
Feature | Description |
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Precise Genetic Modification | We use advanced gene-editing technologies, like CRISPR-Cas9, to introduce specific PARK2 alterations with high accuracy, minimizing off-target effects. |
Disease Relevance | Our models faithfully replicate key aspects of PARK2-linked Parkinson's disease, closely mimicking the cellular and molecular changes associated with the disease. |
Versatility | We offer a broad spectrum of models, including knockout, knock-in, and overexpression, to suit diverse research objectives and experimental designs. |
When you choose Creative Biolabs, you benefit from:
Problems in the PARK2 gene are a main cause of autosomal recessive Parkinson's disease (PD). Parkin must work correctly for mitophagy. Mitophagy is a key process in cells. It removes damaged mitochondria selectively. When PARK2 does not work, this quality control fails. This leads to a buildup of bad mitochondria. Neurons then become damaged. This contributes to how PD develops. While PARK2 is mainly linked to PD, new research suggests more. It may play a role in other brain diseases. It seems to affect mitochondrial health. It also influences protein breakdown pathways. Elucidating the precise mechanistic underpinnings of its contribution to these related disorders remains an active and evolving domain of scientific inquiry.
At Creative Biolabs, we are dedicated to providing you with the highest quality PARK2 gene-engineered cell models and services to accelerate your research. Reach out to us today via email at info@creative-biolabs.com or submit an online inquiry to learn more about how our PARK2 gene-engineered cell model products can advance your studies.
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