Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04626 (erbB-2)
 5,251 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Breast cancer is a leading cause of cancer death among women. Factors useful for determining the prognosis of breast cancer include axillary lymph node involvement, tumor size, hormonal receptor status, nuclear grade, and relative DNA content. The c-erbB-2 protooncogene is amplified in 10-40% of primary breast tumors, as well as in breast cancer cell lines; where it is amplified there is increased expression of its product. We have investigated the DNA content and c-erbB-1 protein expression in tumor cell lines and in breast cancer patient specimens by multiparameter flow cytometry. The study was enabled by the discovery that both cellular integrity and c-erbB-2 antigen reactivity were preserved in cells and tissues following fixation in 70% ethanol. We demonstrate that flow cytometric analysis of c-erbB-2 expression in populations of ethanol-fixed tumor cells is a reliable and sensitive quantitative method that correlates well with previously documented semiquantitative techniques. This is a feasible method for analyzing archived clinical samples, and further allows correlations between c-erbB-2 levels and other cellular parameters. Additionally, this method detects abnormal populations not identified by DNA content analysis alone. Further studies utilizing this approach are necessary to evaluate the prognostic value of this oncoprotein in human breast cancer.
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PMID:Analysis of c-erbB-2 protein expression in conjunction with DNA content using multiparameter flow cytometry. 218 18

The present study investigated the effect of acute ethanol (ETOH) treatment on the epidermal growth factor (EGF) receptor in rat gastric mucosa using two different experimental models. In the in vitro experiments, gastric mucosal cells were incubated with 0, 0.05, 0.1, 0.25, and 0.5% ethanol in Dulbecco's modified Eagle's medium (DMEM) for 30 min and then used for the membrane preparation. The EGF receptor binding assay indicated that cells incubated in the presence of ethanol displayed a concentration-dependent increase (r = 0.85) in the 125I-EGF binding. The Western blot analysis using anti-EGF-receptor antibody revealed that ethanol in vitro caused reduction in the immunoreactivity of the major 170-kDa protein. There were also alterations in the minor protein bands (140, 120, and 50 kDa). In the in vivo experiments, rats that fasted overnight were given 1.0 ml of saline or ethanol (5, 10, or 15%) by gastric intubation 30 min before sacrifice. In comparison with the saline controls, ethanol treatment caused a decrease of the EGF receptor binding to the gastric mucosal membrane (saline: 5%: 10%; 15% ETOH, 1.46 +/- 0.18: 1.13 +/- 0.17: 1.27 +/- 0.19: 0.84 +/- 0.14, p < 0.02; mean +/- SEM, n = 9). Furthermore, the immunoblot analysis revealed concentration-dependent decrease in the intensity of the major 170-kDa protein with ethanol. The reduction in the EGF receptor binding and the impairment of the receptor protein might be due to the nonspecific damage of the gastric mucosal membrane by ethanol.
Alcohol
PMID:Effect of acute ethanol treatment on epidermal growth factor receptor in the rat stomach. 814 61

The aim of this study was to determine the pathway(s) by which ethanol activates mitogen-activated protein kinase (MAPK) signaling and to determine the role of Ca2+ in the signaling process. MAPK signaling was determined by assessing MAPK activity, measuring phosphorylated extracellular signaling-regulated kinase (pp 44 ERK-1 and pp 42 ERK-2) expression and ERK activity by measuring ERK-2-dependent phosphorylation of a synthetic peptide as a MAPK substrate in rat vascular smooth muscle cells. Ethanol activated extracellular signal-regulated kinase expression (ERK 1 and 2) could be observed when vascular smooth muscle cells (VSMCs) were stimulated for 5 min or less, but was inhibited when cells are treated for 10 min or more with 1-16 mM of ethanol. Maximum ethanol-induced MAPK activity was observed within 5 min with 4 or 8 mM. Ethanol stimulated MAPK activity was blocked by the protein kinase C (PKC) inhibitor (GF109203X) and epidermal growth factor (EGF) receptor antagonist (PD153035) by 41 +/- 24 and 34 +/- 12.3%, respectively. The calcium channel blocker, diltiazem and the chelating agent, BAPTA, reduced the activation of MAPK activity by ethanol, significantly. The data demonstrate that ethanol-stimulated MAPK expression is mediated partially through both the EGF-receptor and PKC intermediates and that activation through the PKC intermediate is calcium-dependent.
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PMID:Ethanol-induced mitogen activated protein kinase activity mediated through protein kinase C. 1498 9