The members of epidermal growth factor receptor (EGF R) or the ErbB receptor family have been identified as useful biomarkers and targets for cancer therapy. The EGFR family includes four receptor tyrosine kinases, EGF R (ErbB1), ErbB2 (neu), ErbB3, and ErbB4. EGF R binds EGF and induces tyrosine phosphorylation leading to proliferation of cells. EGF R is present on many cell types of epithelial and mesenchymal lineages. EGF R is capable of binding transforming growth factor-α and heparin-binding EGF in addition to EGF. There are numerous effector molecule activated by EGF R that result in a variety of biological processes such as morphogenesis, cell motility, apoptosis, differentiation and organ repair and maintenance. Deregulation of EGF R signaling is implicated in progression of a wide variety of tumors, invasion and metastasis Monoclonal anti-EGF Receptor detects human EGF receptor. This antibody shows no cross-reactivity with recombinant mouse EGF R, recombinant human ErbB2, recombinant mouse ErbB2, recombinant human ErbB3, or recombinant human ErbB4.
Anti-EGF R antibody may be used at a working concentration of 1-2 μg/ml for detection of human EGF R by immunoblotting.
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Lyophilized from a 0.2 μm filtered solution in phosphate buffered saline with 5% trehalose.
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Expert opinion on therapeutic targets, 16(1), 15-31 (2012-01-14)
Cancer is a devastating disease; however, several therapeutic advances have recently been made, wherein EGFR and its family members have emerged as useful biomarkers and therapeutic targets. EGFR, a transmembrane glycoprotein is a member of the ERBB receptor tyrosine kinase
The international journal of biochemistry & cell biology, 31(6), 637-643 (1999-07-15)
The receptor for the epidermal growth factor (EGF) and related ligands (EGFR), the prototypal member of the superfamily of receptors with intrinsic tyrosine kinase activity, is widely expressed on many cell types, including epithelial and mesenchymal lineages. Upon activation by
The epidermal growth factor receptor (EGFR) pathway is one of the most dysregulated molecular pathways in human cancers. Despite its well-established importance in tumor growth, progression and drug-resistant phenotype over the past several decades, targeted therapy designed to circumvent EGFR
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