EGFR (Phospho-Tyr¹¹⁷³) Rabbit Monoclonal Antibody (Clone RM269)

Epidermal growth factor receptor (EGFR), also known as HER1 and ERBB1, is a cell surface receptor and member of the EGF family of receptor tyrosine kinases with roles in cell proliferation, differentiation, and survival.^1,2 It is a transmembrane receptor composed of an intracellular tyrosine kinase domain, a transmembrane lipophilic segment, and an extracellular domain that is expressed in epithelial, mesenchymal, and neuronal tissues.^1,2,3 Under unstimulated conditions, EGFR is an auto-inhibited monomer in the plasma membrane.¹ Upon canonical ligand binding, EGFR undergoes homodimerization or heterodimerization with HER2, HER3, or HER4, which induces a conformational change in the cytoplasmic domain that facilitates autophosphorylation and intracellular signaling. EGFR contains five C-terminal autophosphorylation sites, tyrosine 1068 (Tyr¹⁰⁶⁸), Tyr¹¹⁴⁸, Tyr¹¹⁷³, Tyr¹⁰⁸⁶, and Tyr⁹⁹².⁴ EGFR autophosphorylation at Tyr¹¹⁷³ (phospho-Tyr¹¹⁷³) leads to interaction with phospholipase Cγ (PLCγ) and Shc, which have roles in activating the MAPK signaling pathway. Increased levels of EGFR (phospho-Tyr¹¹⁷³) are associated with poor progression-free survival in patients with non-small cell lung cancer (NSCLC). Levels of EGFR (phospho-Tyr¹¹⁷³) are increased in, and positively correlate with activation of MAPK signaling and cytokine production in, bronchial epithelial biopsies from healthy individuals exposed to diesel exhaust.⁵ Cayman’s EGFR (Phospho-Tyr¹¹⁷³) Rabbit Monoclonal Antibody (Clone RM269) can be used for immunohistochemistry (IHC) and Western blot (WB) applications.

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1. Sigismund, S., Avanzato, D., and Lanzetti, L. Emerging functions of the EGFR in cancer. Mol. Oncol. 12(1), 3-20 (2018).

2. Herbst, R.S. Review of epidermal growth factor receptor biology. Int. J. Radiat. Oncol. Biol. Phys. 59(2 Suppl), 21-26 (2004).

3. Yano, S., Kondo, K., Yamaguchi, M., et al. Distribution and function of EGFR in human tissue and the effect of EGFR tyrosine kinase inhibition. Anticancer Res. 23(5A), 3639-3650 (2003).

4. Wang, F., Wang, S., Wang, Z., et al. Phosphorylated EGFR expression may predict outcome of EGFR-TKIs therapy for the advanced NSCLC patients with wild-type EGFR. J. Exp. Clin. Cancer Res. 31(1), 65 (2012).

5. Pourazar, J., Blomberg, A., Kelly, F.J., et al. Diesel exhaust increases EGFR and phosphorylated C-terminal Tyr 1173 in the bronchial epithelium. Part. Fibre Toxicol. 5, 8 (2008).