EGR1/2 ELISA Kit

Name: EGR1/2 ELISA Kit
SKU: DEIA-XYA581
Rating: 5 (1 reviews)

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

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COA

SDS

Datasheet

Sample

Cultured cells

Species Reactivity

Human, Mouse, Rat

Detection Method

Cell-Based ELISA

Intended Use

The EGR1/2 Cell-Based ELISA Kit is a convenient, lysate-free, high throughput and sensitive assay kit that can monitor EGR1/2 protein expression profile in cells. The kit can be used for measuring the relative amounts of EGR1/2 in cultured cells as well as screening for the effects that various treatments, inhibitors (ie. siRNA or chemicals), or activators have on EGR1/2.

Contents of Kit

1. 96-Well Cell Culture Clear-Bottom Microplate, 1 Plate
2. 10× TBS, 24 ml (10×), Stability after first use: 1 month at 4°C
3. Quenching Buffer, 24 ml (1×), Stability after first use: 1 month at 4°C
4. Blocking Buffer, 50 ml (1×), Stability after first use: 1 month at 4°C
5. 15× Wash Buffer, 50 ml (15×), Stability after first use: 1 month at 4°C
6. 100× Anti- EGR1/2 Antibody, 60 μl (100×), Stability after first use: 1 month at 4°C
7. 100× Anti-GAPDH Antibody, 60 μl (100×), Stability after first use: 1 month at 4°C
8. HRP-Conjugated Anti-Rabbit IgG Antibody, 6 ml (1×), Stability after first use: 1 month at 4°C
9. HRP-Conjugated Anti-Mouse IgG Antibody, 6 ml (1×), Stability after first use: 1 month at 4°C
10. Primary Antibody Diluent, 12 ml (1×), Stability after first use: 1 month at 4°C
11. Ready to Use Substrate, 12 ml (1×), Stability after first use: 1 month at 4°C
12. Stop Solution, 12 ml (1×), Stability after first use: 1 month at 4°C
13. Crystal Violet Solution 6 ml (1×), Stability after first use: 1 month at 4°C
14. SDS Solution, 24 ml (1×), Stability after first use: 1 month at 4°C
15. Adhesive Plate Seals, 2 Seals, Stability after first use: 1 month at 4°C

Storage

Storage: 4°C
Expiration: 6 months from receipt

Citations

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Certificate of Analysis

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Customer Reviews

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Increased expression of EGR1 and KLF4 by polysulfide via activation of the ERK1/2 and ERK5 pathways in cultured intestinal epithelial cells

BIOMEDICAL RESEARCH-TOKYO

Authors: Arakaki, Kaoru; Uehara, Ayako; Higa-Nakamine, Sayomi; Kakinohana, Manabu; Yamamoto, Hideyuki

Abstract

Sodium trisulfide (Na2S3) releases hydrogen polysulfide (H2Sn) and is useful for the investigation of the effects of H2Sn on the cell functions. In the present study, we first examined the effects of Na2S3 on the gene expression of IEC-6 cells, a rat intestinal epithelial cell line. Microarray analysis and reverse transcription-polymerase chain reaction analysis revealed that Na2S3 increased the gene expression of early growth response 1 (EGR1) and Kruppel-like transcription factor 4 (KLF4). It was interesting that U0126, an inhibitor of the activation of extracellular signal-regulated kinase 1 (ERK1), ERK2, and ERK5, inhibited the Na2S3-induced gene expression of EGR1 and KLF4. Na2S3 activated ERK1 and ERK2 (ERK1/2) within 15 min. In addition to ERK1/2, Na2S3 activated ERK5. We noticed that the electrophoretic mobility of ERK5 was decreased after Na2S3 treatment. Phos-tag analysis and in vitro dephosphorylation of the cell extracts indicated that the gel-shift of ERK5 was due to its phosphorylation. The gel-shift of ERK5 was inhibited completely by both U0126 and ERK5-IN-1, a specific inhibitor of ERK5. From these results, we concluded that the gel-shift of ERK5 was induced through autophosphorylation by activated ERK5 after Na2S3 treatment. The present study suggested that H2Sn affected various functions of intestinal epithelial cells through the activation of the ERK1/2 and ERK5 pathways.

EGR1 recruits TET1 to shape the brain methylome during development and upon neuronal activity

NATURE COMMUNICATIONS

Authors: Sun, Zhixiong; Xu, Xiguang; He, Jianlin; Murray, Alexander; Sun, Ming-an; Wei, Xiaoran; Wang, Xia; McCoig, Emmarose; Xie, Evan; Jiang, Xi; Li, Liwu; Zhu, Jinsong; Chen, Jianjun; Morozov, Alexei; Pickrell, Alicia M.; Theus, Michelle H.; Xie, Hehuang

Abstract

Life experience can leave lasting marks, such as epigenetic changes, in the brain. How life experience is translated into storable epigenetic information remains largely unknown. With unbiased data-driven approaches, we predicted that Egr1, a transcription factor important for memory formation, plays an essential role in brain epigenetic programming. We performed EGR1 ChIP-seq and validated thousands of EGR1 binding sites with methylation patterns established during postnatal brain development. More specifically, these EGR1 binding sites become hypomethylated in mature neurons but remain heavily methylated in glia. We further demonstrated that EGR1 recruits a DNA demethylase TET1 to remove the methylation marks and activate downstream genes. The frontal cortices from the knockout mice lacking Egr1 or Tet1 share strikingly similar profiles in both gene expression and DNA methylation. In summary, our study reveals EGR1 programs the brain methylome together with TET1 providing new insight into how life experience may shape the brain methylome.