epidermal growth factor receptor

(redirected from Egr-1)
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epidermal growth factor receptor (EGFR),

[MIM*131550]
receptor often upregulated in epithelial tumors.

EGFR

A gene on chromosome 7p12 that encodes epidermal growth factor, a transmembrane glycoprotein of the protein kinase superfamily, which is a receptor for members of the epidermal growth factor family. Binding of the protein to a ligand induces receptor dimerisation and tyrosine autophosphorylation and leads to cell proliferation.

Molecular pathology
EGFR mutations are associated with lung cancer.

ep·i·der·mal growth fac·tor re·cep·tor

(EGFR) (ep'i-dĕr'măl grōth fak'tŏr rĕ-sep'tŏr)
Receptor often upregulated in epithelial tumors.
References in periodicals archive ?
To investigate whether EGR-1 could regulate ICAM-1expression in VGF, we established a mouse vein graft model in WT and Egr-1 KO mice.
To confirm the regulatory effect of Egr-1 on Icam-1 at the molecular level, we isolated endothelial cells from the veins of WT and Egr-1 KO mice and subjected them to mechanical stretch stimulation.
In this study, miR-551b-5p was found to have a potential to regulate EGR1 expression, which is a critical factor in VGF,[sup][10],[15],[16] indicating that miR-551b-5p might be involved in the process of VGF via regulating of EGR-1 expression.
Endothelial dysfunction plays key roles in the processes of hypertension, diabetes, atherosclerosis, and many other diseases.[sup][21] After CABG surgery, vein grafts are stimulated by high arterial blood pressure, and endothelial cells are injured by mechanical stretch.[sup][22] ICAM-1 has been widely known for its effect in endothelial dysfunction.[sup][23] In this study, we also investigated the effect of Egr-1 in regulation of Icam-1 expression in VGF model in mice.
In conclusion, mechanical stretch increased miR-551b-5p expression, which promoted HUVECs proliferation and upregulated EGR-1 expression, thereby inducing endothelial dysfunction via upregulating of ICAM-1.
Disease progression mediated by egr-1 associated signaling in response to oxidative stress.
Moreover, we demonstrated that EA at PC6 acupoints significantly attenuated I/R-induced upregulation of Egr-1 as well as ERK1/2 activation in the myocardium.
Egr-1 is initially linked to the control of cell growth, survival, and transformation [24].
Consistently, in the current study, we found the I/R-induced myocardial expression of both p-ERK1/2 and Egr-1 was downregulated by EA at PC6 acupoints.
Zheng et al., "The protective effect of Egr-1 antisense oligodeoxyribonucleotide on myocardial injury induced by ischemia-reperfusion and hypoxia-reoxygenation," Cellular Physiology and Biochemistry, vol.
Lu et al., "Egr-1, a master switch coordinating upregulation of divergent gene families underlying ischemic stress," Nature Medicine, vol.
Lowe, "Intracoronary delivery of DNAzymes targeting human EGR-1 reduces infarct size following myocardial ischaemia reperfusion," The Journal of Pathology, vol.