eIF2alpha (Phospho-Ser51) ELISA Kit (DEIA-XYA584)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
2 x 96T
Sample
cultured cells
Species Reactivity
Human, Mouse, Rat
Intended Use
The eIF2alpha (Phospho-Ser51) Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor eIF2alpha protein phosphorylation and expression profile in cells. The kit can be used for measuring the relative amounts of phosphorylated eIF2alpha in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on eIF2alpha phosphorylation.
Contents of Kit
1. 96-Well Cell Culture Clear-Bottom Microplate: 2 plates
2. 10x TBS: 24 mL
3. Quenching Buffer: 24 mL
4. Blocking Buffer: 50 mL
5. 10x Wash Buffer: 50 mL
6. 100x Anti-eIF2alpha (Phospho-Ser51) Antibody (Rabbit Polyclonal): 60 μL, red
7. 100x Anti-eIF2alpha Antibody (Rabbit Polyclonal): 60 μL, purple
8. 100x Anti-GAPDH Antibody (Mouse Monoclonal): 60 μL, green
9. HRP-Conjugated Anti-Rabbit IgG Antibody: 12 mL, glass
10. HRP-Conjugated Anti-Mouse IgG Antibody: 12 mL, glass
11. Primary Antibody Diluent: 12 mL
12. Ready-to-Use Substrate: 12 mL
13. Stop Solution: 12 mL
14. Crystal Violet Solution: 12 mL
15. SDS Solution: 24 mL
16. Adhesive Plate Seals: 4 seals
Storage
4°C/6 Months

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References


EIF2A promotes cell survival during paclitaxel treatment in vitro and in vivo

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

Authors: Chen, Lin; He, Jiang; Zhou, Jianhua; Xiao, Zhi; Ding, Nianhua; Duan, Yumei; Li, Wenzheng; Sun, Lun-Quan

The integrated stress response (ISR) is critical for cancer cell survival during stress stimuli and has been implicated in the resistance to cancer therapeutics, in which the mechanism, however, is poorly understood. Here, we showed that paclitaxel, the major chemotherapy drug for breast cancer, induced ISR and phosphorylated ser51 residue of EIF2S1 by EIF2AK3 and EIF2AK4. When exposed to paclitaxel, cancer cells activated the EIF2AK3/EIF2AK4-pEIF2S1-ATF4 axis and maintained redox homoeostasis by inducing expression of the major antioxidant enzymes HMOX1, SHMT2 and SLC7A11. Paclitaxel-mediated cell death was significantly increased following loss of ISR or ATF4 expression. This sensitizing effect could be partially rescued by Trolox, a ROS scavenger. We demonstrated that the alternative initiation factor EIF2A was essential for cancer cell survival after paclitaxel-mediated ISR both in vitro and in vivo. Moreover, patients with breast cancer exhibited higher ISR after chemotherapy, and the elevated mRNA levels of HMOX1, SHMT2 and EIF2A were correlated with poor prognosis. Collectively, our findings reveal a novel mechanism for paclitaxel resistance and suggest that targeting EIF2A combined with ISR agonist may be a potential treatment regimen to overcome drug resistance for breast cancer.

Pseudomonas toxin pyocyanin triggers autophagy: Implications for pathoadaptive mutations

AUTOPHAGY

Authors: Yang, Zhong-Shan; Ma, Lan-Qing; Zhu, Kun; Yan, Jin-Yuan; Bian, Li; Zhang, Ke-Qin; Zou, Cheng-Gang

Pseudomonas aeruginosa can establish life-long chronic infection in patients with cystic fibrosis by generating genetic loss-of-function mutations, which enhance fitness of the bacterium in the airways. However, the precise role of the pathoadaptive mutations in persistence in chronic airways infection remains largely unknown. Here we demonstrate that pyocyanin, a well-described P. aeruginosa virulence factor that plays an important role in the initial infection, promotes autophagy in bronchial epithelial cells. Disruption of phzM, which is required for pyocyanin biosynthesis, leads to a significant reduction in autophagy in Beas-2B cells and lung tissues. Pyocyanin-induced autophagy is mediated by the EIF2AK4/GCN2-EIF2S1/eIF2 alpha-ATF4 pathway. Interestingly, rats infected with the phzMD mutant strain have high mortality rate and numbers of colony-forming units, compared to those infected with wild-type (WT) P. aeruginosa PA14 strain, during chronic P. aeruginosa infection. In addition, the phzMD mutant strain induces more extensive alveolar wall thickening than the WT strain in the pulmonary airways of rats. As autophagy plays an essential role in suppressing bacterial burden, our findings provide a detailed understanding of why reduction of pyocyanin production in P. aeruginosa in chronic airways infections has been associated with better host adaptation and worse outcomes in cystic fibrosis.

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