Species Reactivity
Human; Mouse; Rat
Intended Use
The PEK/PERK Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor PEK/PERK protein expression profile in cells. The kit can be used for measuring the relative amounts of PEK/PERK in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on PEK/PERK.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 1 Plates
2. 10x TBS: 24 mL (10x), Clear
3. Quenching Buffer: 24 mL (1x), Clear
4. Blocking Buffer: 50 mL (1x), Clear
5. 10x Wash Buffer: 50 mL (10x), Clear
6. 100x Anti-PEK/PERK Antibody (Rabbit Polyclonal): 60 μL (100x), Purple
7. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL (100x), Green
8. HRP-Conjugated Anti-Rabbit IgG Antibody: 6 mL (1x), Glass
9. HRP-Conjugated Anti-Mouse IgG Antibody: 6 mL (1x), Glass
10. Primary Antibody Diluent: 12 mL (1x), Clear
11. Ready-to-Use Substrate: 12 mL (1x), Brown
12. Stop Solution: 12 mL (1x), Clear
13. Crystal Violet Solution: 6 mL (1x), Glass
14. SDS Solution: 24 mL (1x), Clear
15. Adhesive Plate Seals: 4 Seals
Citations
Publication ()
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Aspirin ameliorates cerebral infarction through regulation of TLR4/NF‑κB‑mediated endoplasmic reticulum stress in mouse model
Xin Wang, Bin Shen, Dezhou Sun, Xiangyu Cui
Applications: ELISA
Reactive species: Mouse
"Abstract: Cerebral infarction is a cerebrovascular disease caused by local brain ischemic necrosis or softening, which is associated with diabetes, obesity, hypertension and rheumatic heart arrhythmia. Previous studies have indicated that aspirin is a potential oral anticoagulant in the treatment of cerebral ischemic stroke. However, the potential mechanism mediated by aspirin in cerebral infarction therapy is not well understood. The present study analyzed the therapeutic effects of aspirin on cerebral infarction and investigated the underlying molecular mechanism of aspirin-ameliorated benefits for thrombolysis. The results demonstrated that aspirin inhibited inflammation and apoptosis of cerebrovascular endothelial cells in a mouse model of cerebral infarction. Aspirin treatment suppressed toll-like receptor (TLR)4 and nuclear factor (NF)-κB expression in cerebrovascular endothelial cells."
Article snippet: The expression of PERK (cat. no DEIA-XYA1959; Creative Diagnostics, USA). 
Figure 1. Aspirin inhibited the protein expression levels of PERK. 
Figure 2. The relative activities of PERK and eIF2α.
COA
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