Disease relevance of Areg

• Up-regulation of transmembrane tyrosine kinase receptors c-met, IGFR1, IGFR2 and EGFR family-related ligands such as HB-EGF, TGFa, amphiregulin and neuregulin as well as c-met ligand HGF point to a possible role of this system in metastasis [1].

High impact information on Areg

• Here we report the purification and characterization of a mitogenic molecule, designated schwannoma-derived growth factor (SDGF), from the growth-conditioned medium of the JS1 Schwann cell line [2].
• RESULTS: Oxidative stress and osmotic stress induced tyrosine phosphorylation of EGFR within 2 minutes, followed by a marked increase in HB-EGF and amphiregulin transcripts in RGM1 cells [3].
• ERK phosphorylation was attenuated by 1) neutralizing EGFR antibodies and the EGFR kinase inhibitor, AG1478, 2) neutralizing HB-EGF, but not amphiregulin, antibodies, heparin, or CM197, and 3) pharmacological inhibitors of matrix-degrading metalloproteinases or TACE small interfering RNA [4].
• Furthermore, the addition of ER, AR, and BTC to the culture medium could mimic some of LH actions [5].
• In adult cycling rats, epiregulin and amphiregulin were strongly induced at 1800 and 2000 h on proestrus coinciding with the preovulatory LH surge [6].

Biological context of Areg

• These observations suggested that the EGF family members, epiregulin and amphiregulin, may play a role in the ovulatory process of cycling rats as well as in the induction of ovulation in immature rats [6].
• In response to stimulation with hydrogen peroxide (100-400 microM), gene expression of HB-EGF and AR increased in a dose-dependent manner, peaked at 3 h, and returned to the base line at 7 h [7].
• Oxidative stress increases gene expression of heparin-binding EGF-like growth factor and amphiregulin in cultured rat gastric epithelial cells [7].
• We observed no effect of amphiregulin on cell differentiation as assessed by alkaline phosphatase expression [8].
• Amphiregulin inhibited cell proliferation in KM12 cells and stimulated the strongly metastatic cell line KM12SM to a slight extent [8].

Anatomical context of Areg

• In situ hybridization revealed that epiregulin and amphiregulin mRNAs were localized in the granulosa cells of large antral follicles [6].
• It suppresses hepatocyte growth by suppressing many molecules associated with growth in liver and other tissues, including IL-6, CXC-chemokine receptor, amphiregulin, COX-2, HIF, etc [9].
• The regulation of amphiregulin, an epidermal growth factor (EGF) family member, and its effect on vascular smooth muscle cells (VSMC) were examined [10].

Associations of Areg with chemical compounds

• Hydrogen peroxide-induced HB-EGF and AR gene expression was blocked by pretreatment with an antioxidant N-acetyl-cysteine [7].
• Calphostin C induces expression of amphiregulin mRNA via reactive oxygen species in IEC-6 cells [11].

Other interactions of Areg

• Elfin, amphiregulin, and clusterin mRNAs were selected for further confirmation by real-time PCR [12].

Analytical, diagnostic and therapeutic context of Areg

• Northern blot analysis revealed that PMSG treatment induced the expression of both epiregulin and amphiregulin mRNA after 24 h, but the expression then decreased 48 h after treatment [6].

References