Exploration of the Role of Necroptosis in Stroke

Necroptosis may be triggered by a variety of triggers, including cytokines of the TNF family, reactive oxygen species, activated TLR, and certain pathogens. Take TNF-α as an example, necroptosis binds to death receptors in the cell membrane when triggered. Once activated, these receptors bind to the bridging proteins TRADD and TRAF2, leading to downstream activation of RIP kinases. The present study has confirmed that necroptosis does occur in the pathologic process of stroke, but the relationship between necroptosis and the pathological process of stroke is unclear. Ace Therapeutics provides a comprehensive service to explore the role of necroptosis in stroke. We provide in vitro and in vivo models of necroptosis and stroke to evaluate the role of aberrant expression of target proteins in necroptosis. In addition, we detect necroptosis by testing the integrity of the plasma membrane, cellular inclusions, and mitochondrial membrane potential.

Exploration of the Role of Necroptosis in Stroke

Exploration of the Role of Initiation of Necroptosis in Stroke

The first step in triggering necroptosis is to initiate necroptosis. Proteins such as apoptosis proteins are known to be associated with the initiation of necroptosis, but the associated mechanisms of action are poorly understood. Therefore, Ace Therapeutics offers a comprehensive service to explore how the initiation of necroptosis affects the pathological process of stroke.

  • We use protein microarrays, PCR microarrays, and other assays to identify differential genes or proteins in the pathway of necroptosis as target proteins.
  • We detect expression levels, localization, and activity changes of target proteins by qPCR, western blotting, and ELISA assays.
  • We determine the mode of action of target proteins by protein interactions such as yeast two-hybrid assay, plasmon resonance assay, fluorescence energy transfer assay, and immunoprecipitation assay.

Exploration of the Role of Execution of Necroptosis in Stroke

The occurrence of necrophagia induces inflammation and other activities and thus regulates the pathological process of stroke. The pseudokinase MLKL may act as the primary executor of necroptosis. Phosphorylation of RIP1 and RIP3 induces necroptosis to form necrosome. However, current studies are not thorough on the execution process of necroptosis. Ace Therapeutics provides comprehensive expertise to study the role of the necroptotic process in stroke.

In addition, Ace Therapeutics offers a one-stop scientific service to explore the role of necroptosis in stroke in a scientific and accurate manner. If you would like to learn more about our services, please feel free to contact us.

  1. Jun-Long, H., et al., Necroptosis signaling pathways in stroke: From mechanisms to therapies. Curr Neuropharmacol, 2018. 16(9): p. 1327-1339.
  2. Hribljan, V., et al., Necroptosis is one of the modalities of cell death accompanying ischemic brain stroke: From pathogenesis to therapeutic possibilities. Croat Med J, 2019. 60(2): p. 121-126.
All of our services are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.
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