eEF2K (Phospho-Ser366) ELISA Kit (DEIA-XYA574)

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, Rat
Intended Use
The eEF2K (Phospho-Ser366) Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor eEF2K protein phosphorylation and expression profile in cells. The kit can be used for measuring the relative amounts of phosphorylated eEF2K in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on eEF2K 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-eEF2K (Phospho-Ser366) Antibody (Rabbit Polyclonal): 60 μL, red
7. 100x Anti-eEF2K 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


A novel method to identify protein kinase substrates: eEF2 kinase is phosphorylated and inhibited by SAPK4/p38 delta

EMBO JOURNAL

Authors: Knebel, A; Morrice, N; Cohen, P

We have developed a method of general application for identifying putative substrates of protein kinases in cell extracts. Using this procedure, we identified the physiological substrates of several mitogen-activated protein kinase kinases and an authentic substrate of stress-activated protein kinase (SAPK) 2a/p38. A 120 kDa protein was detected in skeletal muscle extracts that was phosphorylated rapidly by SAPK4/p386, but poorly by SA-PK2/p38, SA-PK3/p38 gamma, SAPK1/JNK or extracellular signal-regulated kinase 2 (ERK2). It was purified and identified as eukaryotic elongation factor 2 kinase (eEF2K). SAPK4/p38 delta phosphorylated eEF2K at Ser359 in vitro, causing its inactivation. eEF2K became phosphorylated at Ser359 and its substrate eEF2 became dephosphorylated (activated) when KB cells were exposed to anisomycin, an agonist that activates all SAPKs, including SAPK4/p38 delta. The anisomycin-induced phosphorylation of Ser359 was unaffected by SB 203580, U0126 or rapamycin, and was prevented by overexpression of a catalytically inactive SA-PK4/p38 delta mutant, suggesting that SAPK4/p38 delta may mediate the inhibition of eEF2K by this stress. The phosphorylation of eEF2K at Ser359 was also induced by insulin-like growth factor-1. However, this was blocked by rapamycin, indicating that Ser359 is targeted by at least two signalling pathways.

Comparative Genome of GK and Wistar Rats Reveals Genetic Basis of Type 2 Diabetes

PLOS ONE

Authors: Liu, Tiancheng; Li, Hong; Ding, Guohui; Wang, Zhen; Chen, Yunqin; Liu, Lei; Li, Yuanyuan; Li, Yixue

The Goto-Kakizaki (GK) rat, which has been developed by repeated inbreeding of glucose-intolerant Wistar rats, is the most widely studied rat model for Type 2 diabetes (T2D). However, the detailed genetic background of T2D phenotype in GK rats is still largely unknown. We report a survey of T2D susceptible variations based on high-quality whole genome sequencing of GK and Wistar rats, which have generated a list of GK-specific variations (228 structural variations, 2660 CNV amplification and 2834 CNV deletion, 1796 protein affecting SNVs or indels) by comparative genome analysis and identified 192 potential T2D-associated genes. The genes with variants are further refined with prior knowledge and public resource including variant polymorphism of rat strains, protein-protein interactions and differential gene expression. Finally we have identified 15 genetic mutant genes which include seven known T2D related genes (Tnfrsf1b, Scg5, Fgb, Sell, Dpp4, Icam1, and Pkd2l1) and eight high-confidence new candidate genes (Ldlr, Ccl2, Erbb3, Akr1b1, Pik3c2a, Cd5, Eef2k, and Cpd). Our result reveals that the T2D phenotype may be caused by the accumulation of multiple variations in GK rat, and that the mutated genes may affect biological functions including adipocytokine signaling, glycerolipid metabolism, PPAR signaling, T cell receptor signaling and insulin signaling pathways. We present the genomic difference between two closely related rat strains (GK and Wistar) and narrow down the scope of susceptible loci. It also requires further experimental study to understand and validate the relationship between our candidate variants and T2D phenotype. Our findings highlight the importance of sequenced-based comparative genomics for investigating disease susceptibility loci in inbreeding animal models.

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