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APOE Gene-Engineered Cell Models Products

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Apolipoprotein E (APOE) critically regulates CNS lipid metabolism, synaptic stability, and amyloid-β clearance. The APOE4 allele remains the strongest genetic risk factor for late-onset Alzheimer's disease, driving Aβ aggregation and neuroinflammation through isoform-specific structural perturbations.

Our APOE-engineered isogenic models (E2/E3/E4) decode allele-dependent pathologies: astrocytic lipid dysregulation, impaired microglial phagocytosis, and neuronal cholesterol misprocessing. These systems enable targeted interrogation of APOE4's pathogenic cascades—tau hyperphosphorylation via disrupted LRP1 signaling, lysosomal dysfunction, and therapeutic evaluation. Current strategies prioritize conformation-stabilizing ligands, APOE2-boosting CRISPR, and splice-switching antisense oligonucleotides. Contact us to explore your project and get a quote!

View our APOE model categories below or click to access our product list immediately.

Featured APOE Gene-Engineered Cell Model Categories

We encourage you to check out our categories of APOE gene-engineered cell models and see how they can enhance your research efforts.

Model Category Description
APOE Isoform Models These models allow for the study of the distinct effects of different APOE isoforms (E2, E3, and E4) on cellular function, amyloid-beta processing, and neurotoxicity.
APOE Mutation Models Study the impact of specific APOE mutations associated with various neurological disorders, providing insights into disease mechanisms. Rare APOE mutations (R142G: familial AD; H62R: cerebral amyloid angiopathy) exhibit allele-specific pathologies. R142G disrupts hinge-domain salt bridges, causing lipid helix destabilization and Aβ42 oligomerization. H62R impairs LDLR binding, inducing vascular amyloidosis via TGF-β suppression. CRISPR-isogenic models enable mutation-specific therapeutic exploration—antisense nucleotide correction, structural chaperones—while mapping neurovascular dysfunction cascades.
APOE Knock-Out Models Elucidate the fundamental role of APOE by examining cellular phenotypes in the absence of functional APOE protein.
APOE Knock-In Models Precisely introduce specific APOE variants into the endogenous APOE locus, providing a physiologically relevant context for studying subtle alterations in APOE function.
APOE Tagged Cell Lines Facilitate protein localization, interaction studies, and purification with our range of APOE cell lines expressing tagged proteins (e.g., GFP, FLAG).

Features of Our APOE Gene-Engineered Cell Models

Creative Biolabs' APOE gene-engineered cell models are designed to provide you with:

  • Accurate Disease Modeling: Precisely replicate specific APOE mutations and their relevant impact on disease pathogenesis.
  • Targeted Drug Discovery Tools: Effective platforms for screening potential therapeutic compounds and assessing their efficacy in modulating APOE-related pathways.
  • Mechanistic Insights: Powerful tools to dissect the detailed mechanisms by which APOE variants contribute to disease, leading to a deeper understanding of disease processes.

Advantages of Our APOE Gene-Engineered Cell Models

When you choose Creative Biolabs for your APOE research, you gain access to:

  • Unparalleled Depth, Flexibility, and Translational Relevance: Our models go beyond simple disease replication, capturing the nuances of APOE dysfunction for more meaningful research and insights.
  • Compatibility with Advanced Imaging Techniques: Compatibility with cutting-edge imaging techniques enables precise visualization of dynamic processes and protein interactions.
  • Robust Platforms for High-Throughput Screening: Efficient tools to evaluate the effectiveness of potential therapeutic compounds.
  • Custom Model Generation Services: Tailored cell models designed to meet your specific research objectives.
A picture presents Aβ-independent roles for apoE in Alzheimer's disease pathology. (OA Literature)Fig.1 Schematic overview of Aβ-independent roles for apoE in Alzheimer's disease pathology.1

APOE Mechanisms in AD and Other Related Diseases

Apolipoprotein E (APOE) orchestrates multifaceted roles in the central nervous system, extending beyond lipid transport to critically influence the pathogenesis of Alzheimer's disease (AD) and related neurological disorders. Distinct APOE isoforms, particularly APOE4, significantly modulate amyloid-beta (Aβ) metabolism and clearance, with APOE4 exhibiting a less efficient capacity in this crucial process compared to APOE3 and APOE2. This differential impact on Aβ accumulation is a cornerstone in AD development.

Furthermore, APOE's influence transcends amyloid pathology, engaging with tau protein phosphorylation, synaptic integrity, neuroinflammation, and even cerebral amyloid angiopathy. The intricate interplay between APOE isoforms and these diverse mechanisms underscores the complexity of neurodegenerative pathways. Investigating these nuanced interactions holds immense potential for unveiling novel therapeutic strategies aimed at mitigating the devastating effects of AD and associated conditions.

FAQs

  • How can APOE Gene-Engineered Cell Models improve the accuracy of my research?
    Creative Biolabs' cellular platforms afford investigators a genetically defined milieu, thereby abrogating confounding variables inherent in endogenous APOE expression and yielding enhanced accuracy and reproducibility. Researchers are invited to engage with us to delineate specific investigative requirements and ascertain the capacity of our models to optimize their studies.
  • What repertoire of APOE isoforms is accessible within Creative Biolabs' cell model portfolio?
    Our portfolio includes the full spectrum of APOE variants (E2, E3, E4), with extended capabilities for generating mutation-specific cellular systems. Researchers may commission precise genetic edits - single-nucleotide polymorphisms, domain deletions, or patient-derived alleles—through CRISPR/Cas9-mediated homology-directed repair. For protocol optimization guidance or isoform characterization data (western blot validation, lipid uptake assays), our technical team provides experimental design consultation.
  • Are Creative Biolabs' APOE Gene-Engineered Cell Models suitable for drug screening?
    Indeed, these models are optimally suited for both high-throughput and targeted pharmacological screening assays. Their inherent reliability and physiological fidelity render them invaluable tools for the identification of prospective therapeutic entities. Inquiries regarding application-specific protocols and the integration of our cell models into drug discovery workflows are welcome.
  • What quality control measures are in place to ensure the accuracy of the cell models?
    We deploy stringent quality assurance protocols, encompassing genotyping, protein expression profiling, and functional validation assays, to confirm the fidelity of APOE gene editing and the sustained viability of the cell lines. Comprehensive documentation detailing our validation processes is available upon request.
  • How do your APOE Gene-Engineered Cell Models compare to traditional cell models?
    Traditional cellular models exhibit overexpression artifacts and non-physiological APOE secretion profiles, fundamentally limiting the mechanistic resolution of isoform-specific effects. Our isogenic systems maintain endogenous promoter regulation and lipid-binding domain structural fidelity, enabling precise dissection of ε2/ε3/ε4-dependent lipid trafficking anomalies and microglial phagocytic dysfunction. Collaborative access is available for comparative validation studies against humanized APOE-TR mouse models or high-content compound screening platforms.

Creative Biolabs empowers your neurological disease research with advanced tools. Our APOE Gene-Engineered Cell Models provide a robust platform to unravel the complexities of APOE isoforms and their role in how diseases develop. Contact our team to explore these models and discuss your unique project requirements.

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Reference

  1. Husain, Mohammed Amir, Benoit Laurent, and Mélanie Plourde. "APOE and Alzheimer's disease: from lipid transport to physiopathology and therapeutics." Frontiers in neuroscience 15 (2021): 630502. Distributed under Open Access License CC BY 4.0, without modification.