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.
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 |
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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). |
Creative Biolabs' APOE gene-engineered cell models are designed to provide you with:
When you choose Creative Biolabs for your APOE research, you gain access to:
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.
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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