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we showed that epidermal growth factor (show EGF Proteins) receptors (EGFR (show EGFR Proteins)) were constitutively activated in metastatic lung subtypes of salivary adenoid cystic carcinoma cells, and that this activation was induced by autocrine expression of epiregulin
Study shows how the EGFR (show EGFR Proteins) ligands epiregulin (EREG) and epigen (EPGN (show EPGN Proteins)) stabilize different dimeric conformations of the EGFR (show EGFR Proteins) extracellular region. Results reveal how responses to different EGFR (show EGFR Proteins) ligands are defined by receptor dimerization strength and signaling dynamics. These findings have broad implications for understanding receptor tyrosine kinase (show RET Proteins) (RTK) signaling specificity.
EREG and MMP-1 (show MMP1 Proteins) were found to be elevated in nasal polyp and uncinate tissues in patients with Chronic rhinosinusitis with nasal polyps.
upregulation of EREG expression through promoter demethylation might be an important means of activating the EGFR (show EGFR Proteins) pathway during the genesis of colorectal adenocarcinoma (CRC (show CALR Proteins)) and potentially other cancers.
EREG and AREG (show AREG Proteins) are strongly regulated by methylation, and their expression is associated with CIMP status and primary tumour site.
three-dimensional structure of the EPR antibody (the 9E5(Fab (show FANCB Proteins)) fragment) in the presence and absence of EPR
Together, these studies lead to identification of a novel pathway involving EREG and MMP-1 (show MMP1 Proteins) that contributes to the formation of early stage breast cancer
These results suggested that EREG is one of the molecules involved in glioma malignancy
Data indicate that the effects of epiregulin (EREG) and V-ATPase (show ATP6V1H Proteins) (TCIRG1 (show TCIRG1 Proteins)) single nucleotide polymorphism (SNP) on pulmonary tuberculosis susceptibility, to the extent that they exist, are dependent on gene-gene interactions in West African populations.
Patients homozygous for the minor allele A of EREG rs12641042 had a significantly higher 3-year survival rate than patients with allele C (HR 0.48; P=0.034), but significance was lost in multivariable analysis
Epiregulin and EGFR (show EGFR Proteins) interactions have roles in pain processing
High expression of EREG is associated with lung carcinogenesis.
The lack of the growth factor Ereg results in significantly reduced lung tumor development in a primary chemically induced tumor promotion model compared to wildtype controls (Ereg+/+ mice).
Pre-maturation with cAMP modulators in conjunction with EGF (show EGF Proteins)-like peptides during in vitro maturation enhances mouse oocyte developmental competence.
Epiregulin promotes the proliferation of liver progenitor cells and DNA synthesis by hepatocytes and is upregulated in the serum of patients with liver injury.
EREG and tumor-associated fibroblasts play a crucial role in controlling tumor growth in colitis-associated neoplasms.
Epiregulin can effectively mature isolated cumulus-oocyte complexes, but fails as a substitute for the hCG (show CGA Proteins)/epidermal growth factor (show EGF Proteins) stimulus on cultured follicles.
This study implicates that EREG mediates signals downstream of Areg (show AREG Proteins) mRNA expression and that EGFR (show EGFR Proteins)-ERBB2 (show ERBB2 Proteins) signals contributes to regulation of ovulation process.
A TLR-->MyD88 (show MYD88 Proteins)-->AREG (show AREG Proteins)/EREG-->EGFR (show EGFR Proteins) signaling pathway is represented in nonhematopoietic cells of the intestinal tract, responds to microbial stimuli once barriers are breached, and mediates protection against dextran sulfate sodium-induced colitis.
Epiregulin is a member of the epidermal growth factor family. Epiregulin can function as a ligand of EGFR (epidermal growth factor receptor), as well as a ligand of most members of the ERBB (v-erb-b2 oncogene homolog) family of tyrosine-kinase receptors.