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EGR1Early Growth Response 1
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EGR1 binds to the promoter regions of many genes associated with nociceptive sensitization and increased pain.
The presented data indicate that, among others, the activation takes place due to the opposed expression profile of genes and their regulating microRNAs at the site of inflammation (Figure 6); while the expression of all tested mesenchymal markers (Egr1, Fgf2, Fgf7, Jak2, Notch2, Hif1a, Zeb2, Mmp9, Lox, and Vim) was significantly induced, microRNAs regulating their expression decreased (miR-192, miR-143, miR-375, miR-30a, miR-107, miR200b, and miR-125a).
Of these, the upregulated genes were found to be HSPs, BAG3, SOCS3, GADD45G, GCLM, VLDLR, CYR61, DUSP1, DUSP5, FOS, EGR1, MAFB, NR4A1, PROP1, TGFB1, DNAJB1, ADM, and DDIT3.
Differential peak calling on NMDA-treated samples showed that yH2AX enrichment was confined to only 21 loci including the nIEGs Fos, FosB, Npas4, Egr1, Nr4a1, and Nr4a3 among other transcription factors and noncoding RNAs, pointing to the specific localisation of DSB induction following neuronal stimulation [12].
Gerdin et al., "A cAMP-dependent, protein kinase A-independent signaling pathway mediating neuritogenesis through Egr1 in PC12 cells," Molecular Pharmacology, vol.
miR-499 plays a crucial role in the development of myocardial hypertrophy and fibrosis by targeting many intracellular signaling molecules and transcription factors including Akt, MAPKs, Egr1, Egr2, and Fos or promoting Myh7 and Acta1 expressions [68].
Cigarette smoke-induced pulmonary inflammatory responses are mediated by EGR1 /GGPPS/MAPK signaling.
identified EGR1 and FOS as novel candidate targets of Notch signaling in human, but not found in mouse, radial glia.
The Egr1 gene was found to be significant and between-group differences were obtained: P = .011, [[eta].sup.2] = .218.
Hofer, "Vascular endothelial cell growth factor-induced tissue factor expression in endothelial cells is mediated by EGR1," Blood, vol.
It is interesting to note that zinc finger-containing transcription factors such as egr1, egr2, and egr3 and immediate early genes such as fos and jun, were found to be remarkably upregulated in the present study; egr1, egr 2, and egr 3 have been implicated in the proliferation and differentiation of many cell types [7, 8], and fos and jun have been linked to the regulation of angiogenesis [9].
In addition, 4Ebp1 gene transcription was negatively regulated by induction of Egr1 expression in various cells in response to activation of ERK/mitogen-activated protein kinase or PI3K signaling pathways [24,25].