anti-Early Growth Response 2 (EGR2) Antibodies

Human Early Growth Response 2 (EGR2) interaction partners

1. In Greek Charcot-Marie-Tooth type 1 patients, 3 pathogenic mutations were found (3.5%); two recently reported micromutations in PMP22 3, and one known point mutation in EGR2

2. LAG3(+) Tregs suppress humoral immune responses via transforming growth factor beta3 production in an Egr2- and Egr3-dependent manner.

3. Low EGR2 expression is associated with hepatocellular carcinoma.

4. The study suggests that acetylation of EGR2 is regulated independently of nucleosome remodeling and deacetylase.

5. Egr2-driven cell surface proteins LAG-3 and 4-1BB can identify dysfunctional tumor antigen-specific CD8(+) TIL.

6. Egr2 and Egr3 have emerged as regulatory molecules that suppress excessive immune responses. Mice deficient for Egr2 and Egr3 develop a lupus-like disease with dysregulated activation of effector T cells. Egr2 and Egr3 confer suppressive activity to CD4(+) T cells and regulate the production of inhibitory cytokines such as IL-10 and TGF-beta1.

7. Analysis of consensus EGR-binding elements (EBEs) showed that the immediate early response 3 gene (IER3) is a novel transcriptional target gene of EGR2 as confirmed by the luciferase assay, electrophoretic mobility-shift assay (EMSA), chromatin immunoprecipitation (ChIP), and western blot analysis.

8. In the PPI network, genes may be involved in Down syndrome (DS) by interacting with others, including nuclear receptor subfamily 4 group A member 2 (NR4A2)early growth response (EGR)2 and NR4A2EGR3. Therefore, RUNX1, NR4A2, EGR2, EGR3 and ID4 may be key genes associated with the pathogenesis of DS.

9. EGR2 mutation presents as an axonal Charcot-Marie-Tooth phenotype with variable severity.

10. MicroRNA20a promotes the proliferation and cell cycle of human osteosarcoma cells by suppressing EGR2 expression.

11. These results suggested that EGR2 overexpression has a pivotal role in the downregulation of cytokines implicated in the pathophysiology of Guillain-Barre syndrome

12. A recurrent mutation was identified in EGR2 which appears to be associated with the pathogenesis of schizophrenia.

13. Knock-down of EGR2 with siRNA was demonstrated to have a similar effect as the over-expression of miR-330-3p in NSCLC cell lines

14. Dysregulated Egr-2 is observed in some human autoimmune disorders.

15. EGR2 knockdown inhibited proliferation, clonogenicity and spheroidal growth in vitro and induced regression of Ewing sarcoma xenografts.

16. our data suggest that robust CD26 costimulatory signaling induces preferential expression of EGR2 and IL-10 as a potential mechanism for regulating CD26-mediated activation.

17. transcription factor early growth response gene-2 is a novel molecular switch regulating known immunomodulatory molecules in human mesenchymal stem cells.

18. Overexpression of EGR2 significantly attenuated the oncogenic effect of miR-20a.

19. Lack of association of EGR2 variants with bipolar disorder in Japanese population.

20. EGR2 and EGR3 are regulated by NFkappaB and MAPK signalling pathways downstream of TNFalpha stimulation in breast adipose fibroblasts, and this in turn is upstream of CYP19A1 transcription via PI.4

Mouse (Murine) Early Growth Response 2 (EGR2) interaction partners

1. Egr2 was critical for the expression of transcription factors CEBPbeta and PPARgamma in M2 macrophages, and CEBPbeta was highly expressed in M1-polarized macrophages.

2. miR-138 is an Egr2-dependent microRNA but is dispensable for Schwann cell myelination

3. data reveal a regulatory circuit involving Egr2-Id3-E2A, which normally restricts the population size of gammadelta NKT cells by adjusting Egr2 dosage and c-Myc expression.

4. Study findings demonstrated that despite impaired proliferation and IL2 production, tolerant T cells can display inflammatory responses in response to antigen stimulation and this is controlled at least partly by Egr2 and Egr3.

5. Egr2 may play an important role during embryo implantation and decidualization in the mouse.

6. Study shows the conversion of mouse skin fibroblasts into induced Schwann cells by driving the expression of two transcription factors, Sox10 and Egr2.

7. Egr2 and Egr3 expressed in T cells cooperatively prevent humoral immune responses by supporting TGF-beta3 secretion.

8. study revealed GCN5-mediated EGR2 acetylation as a molecular mechanism that regulates iNKT development.

9. findings demonstrate a crucial role for Krox20 in arterial valve development and reveal that an excess of neural crest cells may be associated with bicuspid aortic valve.

10. these results suggested that the basal promoter activity of the mIRF-3 gene is regulated by transcription factors Egr2 and YY1 in NIH3T3 cells

11. Prss56 expression was regulated by Egr2 during mouse decidualization.

12. Egr2 and 3 are upstream regulators of effector CD4 and CD8 T cells that are essential for optimal responses with limited immunopathology.

13. Egr2 and 3 are antagonists of T-bet function in effector T cells and are important for the control of inflammatory responses of T cells.

14. We discovered that Tead1 and co-activators Yap and Taz are required for Pmp22 expression, as well as for the expression of Egr2 Tead1 directly binds Pmp22 and Egr2 enhancers early in development and Tead1 binding is induced during myelination, correlating with Pmp22 expression. The data identify Tead1 as a novel regulator of Pmp22 expression during development in concert with Sox10 and Egr2

15. endogenous KLF4 and Krox20 are dispensable for adipogenesis in culture and for brown adipose tissue development in mice. In contrast, the master adipogenic transcription factor peroxisome proliferator-activated receptor gamma (PPARgamma) is essential.

16. Decreased expression of Krox20 in mice causes degeneration of the aortic leaflets and disorganization of the extracellular matrix, causing valvular dysfunction.

17. Mir106b regulates pro-allergic properties of dendritic cells and Th2 polarisation by targeting Egr-2 in vitro

18. let-7 miRNAs promote expression of the myelination-driving master transcription factor Krox20

19. The data suggest that Pak2 controls thymic Natural Killer T-cell development by providing a signal that links Egr2 to induce PLZF, in part by regulating signaling lymphocyte activation molecule 6 expression.

20. demonstrate a novel function of EGR2/3 that is important for Tfh cell development and Tfh cell-mediated B cell immune responses

Zebrafish Early Growth Response 2 (EGR2) interaction partners

1. We performed a global analysis of the cis-acting elements involved in the control of the zebrafish developmental gene krox20. krox20 encodes a transcription factor required for hindbrain segmentation and patterning, a morphogenetic process highly conserved during vertebrate evolution.

2. A direct, positive autoregulatory loop amplifies and maintains the expression of Krox20, a transcription factor governing vertebrate hindbrain segmentation.

3. Hindbrain patterning requires fine-tuning of early krox20 transcription by Sprouty 4.

4. Data show that Irx7 and Irx1b are required for the proper formation and specification of rhombomeres 1 to 4, and that Irx7 functionally interacts with Meis1.1 to activate the expression of anterior hindbrain markers, such as krox20.