anti-Early Growth Response 3 (EGR3) Anticorps

Human Early Growth Response 3 (EGR3) interaction partners

1. Study demonstrated that EGR3 expression was enhanced in prostate cancer (PC) tissues. EGR3 was proposed as a possible target of miR335, and was negatively regulated by miR335. Silencing EGR3 suppressed the viability and angiogenesis of PC cell line.

2. KSRP decreased EGR3 mRNA stability in an ARE-independent manner.

3. miR-718 acts as a tumor suppressive microRNA in hepatocellular carcinoma via regulating the expression of EGR3, which may provide a new diagnostic marker and treatment target for HCC

4. 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.

5. EGR3 contributes to cell growth inhibition via upregulation of FasL in Hepatocellular carcinoma.

6. 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.

7. These findings support previously reported associations between EGR3 and schizophrenia.

8. EGR3 promotes excessive production of IL6 and IL8 observed during the progression of prostate cancer.

9. Data shows association of Egr3 genetic polymorphisms and coronary artery disease in the Uygur and Han of China

10. Genetic variation in EGR3 may affect prefrontal function through neurodevelopment

11. These results provide the first evidence that Egr-3, is up-regulated in scleroderma and is necessary and sufficient for profibrotic responses.

12. Decreased EGR3 expression might play a critical role in the differentiation, proliferation, metastasis and progression of gastric cancer cells.

13. These data suggest that type I IFN stimulation induces a rapid recruitment of a repressive Egr3/Nab1 complex that silences transcription from the ifngr1 promoter.

14. Our results suggest that Egr-3 is a transcription factor associated with TGF-beta1 expression and in vivo regulatory activity

15. Egr3 mRNA expression reveals that Egr3 mRNA expression is increased in tumor cells of non-relapsed samples compared to normal prostate cells, but is significantly lower in relapsed samples compared to non-relapse.

16. 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

17. EGR3, a gene that translates environmental stimuli into long-term changes in the brain, may be associated with risk for child bipolar disorder 1.

18. Study supports the association of EGR3 with schizophrenia in Han Chinese sample.

19. EGR3 gene may play an important role in schizophrenia susceptibility

20. EGR3 bound to the TREM-1 promoter.

Mouse (Murine) Early Growth Response 3 (EGR3) interaction partners

1. Our results suggest that Egr3-/- mice retain control over the circadian timekeeping of sleep and wake, while showing impaired sleep.

2. 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.

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

4. Study demonstrates in mice that explored novel spatial environments, the involvement of Egr3 in regulating the late protein-dependent phase of Arc expression in the dentate gyrus.

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

6. 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.

7. Egr3 knockout mice, lacking muscle spindles, but not Golgi tendon organs, displayed a less severe prepubertal scoliosis.

8. Egr3 is involved in myoblast proliferation by interaction with survival signaling.

9. Study showed that acute stress activates 5-HT2AR expression in the mouse cortex and this activation requires the immediate early gene Egr3

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

11. Gene expression profiling and further functional validation revealed that Egr3 was a strong limiting factor for the proliferative potential of hematopoietic stem cells in leukemia.

12. Egr3 overexpression in medium spiny neurons subtypes oppositely mediates behavioral responses to cocaine. Egr3 regulates cocaine-associated genes transcriptionally

13. Thios study demonstrated that Egr3 has an essential role in regulating gene expression that promotes normal intrafusal muscle fiber differentiation and fusimotor innervation homeostasis

14. our result shows for the first time that the Egr3 a transcription factor may play a novel non-transcriptional function during microtubule organization in mouse oocytes.

15. Egr3 induces a Th17 response by promoting the development of gamma-delta T cells.

16. These results suggest that Erk1/2 acts in intrafusal fibers of muscle spindles to induce transcription of Egr3

17. These results provide the first evidence that Egr-3, is up-regulated in scleroderma and is necessary and sufficient for profibrotic responses

18. These data suggest that type I IFN stimulation induces a rapid recruitment of a repressive Egr3/Nab1 complex that silences transcription from the ifngr1 promoter.

19. Our results suggest that Egr-3 is a transcription factor associated with TGF-beta1 expression and in vivo regulatory activity

20. Te results of this study reveled that Egr3 has an essential role in regulating sympathetic neuron dendrite morphology and terminal axon branching, but not in regulating sympathetic axon guidance to their targets.

Medaka Early Growth Response 3 (EGR3) interaction partners

1. Expression of both the egr1 and egr3 mRNAs were observed in the telencephalon, hypothalamus, and optic tectum, however, the positions at which the genes were expressed were different.