Anti-phospho-EGFR (Tyr1110)(E10-65ER)

Anti-phospho-EGFR (Tyr1110)(E10-65ER)

  • $270.00


Description :Rabbit Polyclonal Antibody

Species :

Tag :

Expression System:

Sequence :

Specificity :Recognizes the EGFR protein phosphorylated at tyrosine 1110

Cited Applications :WB

Cross Reactivity :Human, Mouse and Rat

Host / Isotype / Clone# :Rabbit, IgG

Immunogen :Synthetic phospho-peptide corresponding to amino acid residues surrounding Tyr1110

Purification :Affinity chromatography

Stability :Store at 4oC (add 0.1% NaN3) for several months, and at -20oC for longer periods. For optimal storage, aliquot target into smaller quantities after centrifugation and store at recommended temperature. For most favorable performance, avoid repeated handling and multiple freeze/thaw cycles.

Sample Data :Western blot analysis of extracts from A431 cells untreated or treated with EGF (200ng/ml, 5min), using EGFR antibody (lanes 1 and 2) and anti-phospho-EGFR (Tyr1110) antibody (lanes 3 and 4).

Scientific Background :The epidermal growth factor receptor (EGFR) is a transmembrane tyrosine kinase. Known ligands of EGFR include EGF, TGFA/TGF-alpha, amphiregulin, epigen/EPGN, BTC/betacellulin, epiregulin/EREG and HBEGF/heparin-binding EGF. Ligand binding induces receptor homo- and hetero-dimerization and tyrosine autophosphorylation, which triggers downstream signaling events. The consequences of EFGR signaling include cell proliferation, differentiation, motility, and cell survival (1). Activation of EGFR triggers mitogenic signaling in gastrointestinal mucosa and EGFR upregulated in colon cancers and most neoplasms (2). EGFR stimulation also activates the ERK-signaling pathway in normal gastric epithelial and colon cancer cell lines. In contrast, selective inhibition of EGFR significantly reduces ERK2 activation, c-fos mRNA expression and cell proliferation. Mutations in EGFR are also implicated in specific forms of lung cancer.

References :
1. Wang K, et al: Epidermal growth factor receptor-deficient mice have delayed primary endochondral ossification because of defective osteoclast recruitment. J. Biol. Chem. 279: 53848-53856, 2004.

2. Kobayashi S, et al: EGFR mutation and resistance of non-small-cell lung cancer to gefitinib. New Eng. J. Med. 352: 786-792, 2005.

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Research Areas :AKT/PKB Pathway, Angiogenesis, Apoptosis/Autophagy, Cancer, Cardiovascular Disease, Cell Cycle, ERK/MAPK Pathway, Inflammation, Invasion/Metastasis, Metabolic Disorder, PKA/PKC Pathway, Receptor Tyrosine Kinases, Cancer, Inflammation, Metabolic Disorder, Cardiovascular Disease, AKT/PKB Pathway, ERK/MAPK Pathway, PKA/PKC Pathway, Apoptosis/Autophagy, Cell Cycle, Angiogenesis, Invasion/Metastasis, Receptor Tyrosine Kinases