Exploration of the Role of Autophagy in Stroke

The exact role of autophagy in stroke is ambiguous, and current studies on the role of autophagy in stroke are not uniform and vary widely from one another. To provide a more accurate and scientific understanding of the role of autophagy in stroke, Ace Therapeutics offers a comprehensive service to facilitate your research exploring the role of autophagy in the development of stroke.

Exploration of the Role of Initiation of Autophagy in Stroke

The initiation of autophagy is influenced by many factors. The findings suggest that stroke episodes initiate the autophagic pathway through the activation of AMPK to activate the ULK1 kinase complex.

• We have established in vitro and in vivo models through techniques such as drug administration and genetic manipulation to investigate the effects of proteins related to autophagy initiation on stroke pathology, starting from proteins related to autophagy initiation such as mTOR, AMPK, and ULK1/2.
• We validate the effect of autophagy initiation-related proteins on autophagy initiation in stroke pathology by detecting the activity of related proteins and downstream signaling pathway proteins while monitoring the autophagic process in real-time.

Exploration of the Role of Autophagy Pathway in Stroke

The initiation of autophagy is followed by successive steps of vesicle nucleation, vesicle elongation, and fusion and degradation. In response to the complex role of the autophagic homeostatic process on neurons disrupted by stroke, Ace Therapeutics provides an exhaustive service to explore the role of autophagy in the stroke process.

To explore the role of proteins associated with the autophagic process, such as Beclin-1, vacuolar protein sorting 34 (VPS34), VPS15, and ATG14L for vesicle nucleation, ATG12-ATG5-ATG16L and ATG8 (LC3)-phosphatidylethanolamine (PE) for vesicle elongation, SNARE syntaxin 17, PLEKHM1 and Atg14 proteins for fusion and degradation, and the signaling pathways downstream of the above processes, we provide various protein assay services.

• ELISA, western blotting, immunohistochemistry, and reporter gene assays for the determination of specific proteins
• PCR array for quantitative analysis of multiple genes related to a specific pathway or mechanism of action

Exploration of the Role of Termination of Autophagy in Stroke

Due to the deleterious effects of autophagy on the stroke process in some cases, we need to gain insight into the mechanisms of autophagy termination in order to better exploit the relevant pathways for the development of new therapies. In this regard, Ace Therapeutics offers a comprehensive service to explore the role of autophagy termination in the stroke process.

• On the one hand, we can induce the termination of autophagy through drug administration, such as autolysosomal products, ULK-targeted inhibitors, and VSP34 inhibitors, and then detect changes in the relevant signaling pathways through quantitative protein assays and quantitative gene expression assays.
• On the other hand, in vitro and in vivo stroke models with gene deletion were established by genetic manipulation, and the related signaling pathway changes were detected by quantitative protein assays and quantitative gene expression assays.

We have a complete autophagic process monitoring technology. If you would like to learn more about our services, please feel free to contact us.

• Observation of autophagosome formation with transmission electron microscopy
• Observing GFP-LC3 fusion protein to trace autophagy formation with fluorescence microscopy
• Western blotting for LC3 and p62 protein expression
• Keima protein-based autophagy evaluation
• Autophagy-related protein localization techniques

1. Shi, Q., et al., The role of autophagy in the pathogenesis of ischemic stroke. Curr Neuropharmacol, 2021. 19(5): p. 629-640.
2. Mo, Y., et al., Autophagy and inflammation in ischemic stroke. Neural Regen Res, 2020. 15(8): p. 1388-1396.