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Whole genome bisulfite sequencing revealed that integrin alpha6beta4 signaling promotes an overall hypomethylated state and site specific DNA demethylation of enhancer elements within the proximal promoters of AREG and EREG in pancreatic neoplasm cells as well as their expression. Additionally, base excision repair (BER) pathway is required to maintain the expression of AREG and EREG.
in Caco-2 CFTR-shRNA cells, the EGFR ligand EREG is overexpressed due to an active IL-1beta autocrine loop that indirectly activates EGFR, constituting new signaling effectors for the CFTR signaling pathway, downstream of CFTR, Cl(-) , and IL-1beta.
we showed that epidermal growth factor receptors (EGFR) 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 ligands epiregulin (EREG) and epigen (EPGN) stabilize different dimeric conformations of the EGFR extracellular region. Results reveal how responses to different EGFR ligands are defined by receptor dimerization strength and signaling dynamics. These findings have broad implications for understanding receptor tyrosine kinase (RTK) signaling specificity.
EREG and MMP-1 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 pathway during the genesis of colorectal adenocarcinoma (CRC) and potentially other cancers.
EREG and AREG 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) fragment) in the presence and absence of EPR
Together, these studies lead to identification of a novel pathway involving EREG and MMP-1 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 (TCIRG1) 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 is a transcriptional target of TSC2 (tuberin).
Epiregulin promotes the proliferation of liver progenitor cells and DNA synthesis by hepatocytes and is upregulated in the serum of patients with liver injury.
Plasma HGF and EREG levels are associated with resistance to treatment with anti-EGFR antibodies in KRAS wild-type patients with metastatic colorectal cancer.
Data suggest that EREG (epiregulin), AREG (amphiregulin), and BTC (betacellulin) induced prostaglandin E2 production by induction of COX-2 (prostaglandin-endoperoxide synthase 2) through MAP kinase signaling in granulosa cells.
In pre-treated K-ras wild-type status colorectal cancer, patients with high EREG gene expression appear to benefit more from cetuximab therapy compared with low expression.
EREG may contribute to glioma progression under the control of IRE1a.
keratinocyte hyperproliferation in cholesteatoma is promoted through overexpression of epiregulin by subepithelial fibroblasts via epithelial-mesenchymal interactions, which may play a crucial role in the pathogenesis of middle ear cholesteatoma
Depletion of Epiregulin with shRNA inhibited SCAP proliferation.
RHOA loss reduces YAP signaling of the Hippo pathway and affects YAP effector epiregulin (EREG) expression in the crypts. Expression of an active YAP (S112A) mutant rescues ntestinal stem cells (ISCs) marker expression, ISC regeneration, and ISC-associated Wnt signaling, but not defective epithelial polarity, in RhoA knockout mice, implicating YAP in RHOA-regulated ISC function.
Collectively, these data indicate that Yap-induced Epiregulin signaling promotes the identity of submandibular gland ductal progenitors and that removal of nuclear Yap by Lats1/2-mediated signaling is critical for proper ductal maturation.
Epiregulin and EGFR 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-like peptides during in vitro maturation enhances mouse oocyte developmental competence.
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/epidermal growth factor stimulus on cultured follicles.
This study implicates that EREG mediates signals downstream of Areg mRNA expression and that EGFR-ERBB2 signals contributes to regulation of ovulation process.
A TLR-->MyD88-->AREG/EREG-->EGFR 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.
epidermal growth factor (EGF) family members amphiregulin, epiregulin, and beta-cellulin are paracrine mediators that propagate the LH signal throughout the ovulatory follicle
Epiregulin plays a critical role in immune/inflammatory-related responses of keratinocytes and macrophages.
Data suggest that epiregulin (Ereg) deficiency does not alter intestinal cancer susceptibility, but that Ereg-null mice are highly susceptible to cancer-predisposing intestinal damage caused by oral dextran sulfate sodium.
Castration leads to adaptive increase in the concentrations of a subset of growth factors from the EGF network in the androgen sensitive CWR22 prostate cancer xenograft
Epiregulin may have a critical role in the regulation of peptidoglycan-mediated interleukin-6 production in antigen presenting cells and innate immunity.
Epiregulin appears as a new growth and insulinotropic factor in pancreatic beta cell lines.
Data observed that the expression of amphiregulin, betacellulin and epiregulin was significantly increased in young erythropoietic protoporphyria mice when compared to aged-matched controls in all genetic backgrounds.
Mycobacterium tuberculosis-infected macrophages play a pivotal role in TB-induced carcinogenesis by inducing DNA damage and by the production of a potent epidermal growth factor epiregulin responsible for squamous metaplasia and tumorigenesis.
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.