[pThr202/Tyr204] Erk1/2 ELISA Kit (DEIA6371)

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

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Size
96T
Sample
cell lysates
Species Reactivity
N/A
Intended Use
The [pThr202/Tyr204] Erk1/2 ELISA kit is a complete kit for the quantitative determination of pERK in cell lysates.
Contents of Kit
1. ERK Microtiter Plate
2. pERK Antibody, 10 mL
3. Assay Buffer 21, 100 mL
4. pERK Conjugate, 10 mL
5. Wash Buffer Concentrate, 100 mL
6. pERK Standard
7. TMB Substrate
8. Stop Solution 2, 10 mL
9. CD Cell Lysis Buffer 2, 100 mL
10. pERK Assay Layout Sheet, 1 each
11. Plate Sealer, 3 each
Storage
All components of this kit, except the pERK Standard, are stable at 4°C until the kit's expiration date. The pERK Standard must be stored at or below -20°C. For more detailed information, please download the following document on our website.
Sensitivity
2.67 pg/mL

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References


Influenza A Virus Infection of Human Respiratory Cells Induces Primary MicroRNA Expression

JOURNAL OF BIOLOGICAL CHEMISTRY

Authors: Buggele, William A.; Johnson, Karen E.; Horvath, Curt M.

The cellular response to virus infection is initiated by recognition of the invading pathogen and subsequent changes in gene expression mediated by both transcriptional and translational mechanisms. In addition to well established means of regulating antiviral gene expression, it has been demonstrated that RNA interference (RNAi) can play an important role in antiviral responses. Virus-derived small interfering RNA (siRNA) is a primary antiviral response exploited by plants and invertebrate animals, and host-encoded microRNA (miRNA) species have been clearly implicated in the regulation of innate and adaptive immune responses in mammals and other vertebrates. Examination of miRNA abundance in human lung cell lines revealed endogenous miRNAs, including miR-7, miR-132, miR-146a, miR-187, miR-200c, and miR-1275, to specifically accumulate in response to infection with two influenza A virus strains, A/Udorn/72 and A/WSN/33. Known antiviral response pathways, including Toll-like receptor, RIG-I-like receptor, and direct interferon or cytokine stimulation did not alter the abundance of the tested miRNAs to the extent of influenza A virus infection, which initiates primary miRNA transcription via a secondary response pathway. Gene expression profiling identified 26 cellular mRNAs targeted by these miRNAs, including IRAK1, MAPK3, and other components of innate immune signaling systems.

Autophagy and KRT8/keratin 8 protect degeneration of retinal pigment epithelium under oxidative stress

AUTOPHAGY

Authors: Baek, Ahruem; Yoon, Soojin; Kim, Jean; Baek, Yu Mi; Park, Hanna; Lim, Daehan; Chung, Hyewon; Kim, Dong-Eun

Contribution of autophagy and regulation of related proteins to the degeneration of retinal pigment epithelium (RPE) in age-related macular degeneration (AMD) remain unknown. We report that upregulation of KRT8 (keratin 8) as well as its phosphorylation are accompanied with autophagy and attenuated with the inhibition of autophagy in RPE cells under oxidative stress. KRT8 appears to have a dual role in RPE pathophysiology. While increased expression of KRT8 following autophagy provides a cytoprotective role in RPE, phosphorylation of KRT8 induces pathologic epithelial-mesenchymal transition (EMT) of RPE cells under oxidative stress, which is mediated by MAPK1/ERK2 (mitogen-activated protein kinase 1) and MAPK3/ERK1. Inhibition of autophagy further promotes EMT, which can be reversed by inhibition of MAPK. Thus, regulated enhancement of autophagy with concurrent increased expression of KRT8 and the inhibition of KRT8 phosphorylation serve to inhibit oxidative stress-induced EMT of RPE cells as well as to prevent cell death, suggesting that pharmacological manipulation of KRT8 upregulation through autophagy with combined inhibition of the MAPK1/3 pathway may be attractive therapeutic strategies for the treatment of AMD.

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