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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
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LAG3(+) Tregs suppress humoral immune responses via transforming growth factor beta3 production in an Egr2- and Egr3-dependent manner.
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Low EGR2 expression is associated with hepatocellular carcinoma.
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The study suggests that acetylation of EGR2 is regulated independently of nucleosome remodeling and deacetylase.
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Egr2-driven cell surface proteins LAG-3 and 4-1BB can identify dysfunctional tumor antigen-specific CD8(+) TIL.
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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.
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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.
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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.
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EGR2 mutation presents as an axonal Charcot-Marie-Tooth phenotype with variable severity.
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MicroRNA20a promotes the proliferation and cell cycle of human osteosarcoma cells by suppressing EGR2 expression.
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These results suggested that EGR2 overexpression has a pivotal role in the downregulation of cytokines implicated in the pathophysiology of Guillain-Barre syndrome
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A recurrent mutation was identified in EGR2 which appears to be associated with the pathogenesis of schizophrenia.
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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
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Dysregulated Egr-2 is observed in some human autoimmune disorders.
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EGR2 knockdown inhibited proliferation, clonogenicity and spheroidal growth in vitro and induced regression of Ewing sarcoma xenografts.
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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.
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transcription factor early growth response gene-2 is a novel molecular switch regulating known immunomodulatory molecules in human mesenchymal stem cells.
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Overexpression of EGR2 significantly attenuated the oncogenic effect of miR-20a.
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Lack of association of EGR2 variants with bipolar disorder in Japanese population.
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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