Extracts of A431 cells unstimulated (1) or stimulated with 200 ng/mL EGF for 15 minutes (2-5), were resolved by SDS-PAGE on a 10% Tris-glycine gel and transferred to PVDF. The membrane was blocked with a 5% BSA-TBST buffer for one hour at room temperature, then incubated with the EGFR [pY1068] antibody for two hours at room temperature in a 1% BSA-TBST buffer, following prior incubation with: no peptide (1 and 2), the nonphosphopeptide corresponding to the phosphopeptide immunogen (3), a generic phosphotyrosine-containing peptide (4) or the phosphopeptide immunogen (5). After washing, the membrane was incubated with goat F(ab’)2 anti-rabbit IgG HRP conjugate and signals were detected using the Pierce SuperSignal™ method. The data show that only the phosphopeptide corresponding to EGFR [pY1068] blocks the antibody signal, demonstrating the specificity of the antibody. The data also show the induction of EGFR [pY1068] phosphorylation by the addition of EGF to this cell system.
|Tested species reactivity||Human, Rat|
|Published species reactivity||Non-human primate, Human, Mouse, Not Applicable|
|Host / Isotype||Rabbit / IgG|
|Immunogen||The antiserum was produced against a chemically synthesized phosphopeptide derived from the region of human EGFR that contains tyrosine 1068. The sequence is conserved in rat.|
|Purification||Antigen affinity chromatography|
|Storage buffer||Dulbecco's PBS, pH 7.3, with 50% glycerol, 1mg/ml BSA|
|Contains||0.05% sodium azide|
|Tested Applications||Dilution *|
|Western Blot (WB)||Assay Dependent|
* Suggested working dilutions are given as a guide only. It is recommended that the user titrate the product for use in their own experiment using appropriate negative and positive controls.
Epidermal Growth Factor Receptor (EGFR) is a 175 kDa transmembrane glycoprotein belonging to tyrosine kinase superfamily. It acts as a receptor for epidermal growth factor (EGF) family proteins. Binding of EGFR to its ligands causes autophosphorylation of tyrosine kinase followed by activation of signal transduction pathways connected to cell proliferation and differentiation. Tyrosine 1068 present within the cytoplasmic domain of the receptor is a major autophosphorylation site that allows binding of Grb2 and activation of the Ras-Raf-ERK1 and ERK2 signaling pathway.
For Research Use Only. Not for use in diagnostic procedures. Not for resale without express authorization.
ZEB1 Mediates Acquired Resistance to the Epidermal Growth Factor Receptor-Tyrosine Kinase Inhibitors in Non-Small Cell Lung Cancer.
44-788G was used in western blot to study how ZEB1 drives the epithelial-mesenchymal transition-related resistance to EGFR-tyrosine kinases inhibitors in non-small cell lung cancer
|Yoshida T,Song L,Bai Y,Kinose F,Li J,Ohaegbulam KC,Muñoz-Antonia T,Qu X,Eschrich S,Uramoto H,Tanaka F,Nasarre P,Gemmill RM,Roche J,Drabkin HA,Haura EB||PloS one (11:null)||2016|
Activated EGFR stimulates MUC1 expression in human uterine and pancreatic cancer cell lines.
44-788G was used in western blot to examine the role that EGFR activation plays in modulating MUC1 levels.
|Engel BJ,Carson DD||Journal of cellular biochemistry (114:2314)||2013|
MAPK and PI3K signalling differentially regulate angiogenic and lymphangiogenic cytokine secretion in squamous cell carcinoma of the head and neck.
44-788G was used in western blot to investigate signaling pathways that regulate the induction of VEGF-C and VEGF-A
|Luangdilok S,Box C,Harrington K,Rh¿s-Evans P,Eccles S||European journal of cancer (Oxford, England : 1990) (47:520)||2011|
|Not Applicable||Not Cited||
In vitro modeling to determine mutation specificity of EGFR tyrosine kinase inhibitors against clinically relevant EGFR mutants in non-small-cell lung cancer.
44-788G was used in western blot to study a non-small-cell lung cancer and relevant EGFR mutants in an in vitro model to determine mutation specificity of EGFR tyrosine kinase inhibitors
|Hirano T,Yasuda H,Tani T,Hamamoto J,Oashi A,Ishioka K,Arai D,Nukaga S,Miyawaki M,Kawada I,Naoki K,Costa DB,Kobayashi SS,Betsuyaku T,Soejima K||Oncotarget (6:38789)||2015|
Effects of AKT inhibition on HGF-mediated erlotinib resistance in non-small cell lung cancer cell lines.
44-788G was used in western blot to determine if inhibition of AKT signaling augments erlotinib activity and abrogates HGF-mediated resistance.
|Holland WS,Chinn DC,Lara PN,Gandara DR,Mack PC||Journal of cancer research and clinical oncology (141:615)||2015|
Short-course treatment with gefitinib enhances curative potential of radiation therapy in a mouse model of human non-small cell lung cancer.
44-788G was used in western blot to assess the combination of radiation and an epidermal growth factor receptor tyrosine kinase inhibitor in preclinical models of human non-small cell lung cancer.
|Bokobza SM,Jiang Y,Weber AM,Devery AM,Ryan AJ||International journal of radiation oncology, biology, physics (88:947)||2014|
A functional siRNA screen identifies genes modulating angiotensin II-mediated EGFR transactivation.
44-788G was used in western blot to identify factors that mediate ATR-EGFR transactivation.
|George AJ,Purdue BW,Gould CM,Thomas DW,Handoko Y,Qian H,Quaife-Ryan GA,Morgan KA,Simpson KJ,Thomas WG,Hannan RD||Journal of cell science (126:5377)||2013|
ADAM17 silencing by adenovirus encoding miRNA-embedded siRNA revealed essential signal transduction by angiotensin II in vascular smooth muscle cells.
44-788G was used in western blot to examine the roles of disintegrin and metalloprotease 7 in angiotensin II signal transduction.
|Elliott KJ,Bourne AM,Takayanagi T,Takaguri A,Kobayashi T,Eguchi K,Eguchi S||Journal of molecular and cellular cardiology (62:1)||2013|
Activation of the FGF2-FGFR1 autocrine pathway: a novel mechanism of acquired resistance to gefitinib in NSCLC.
44-788G was used in western blot to identify mechanism of acquired resistance to EGFR-tyrosine kinase inhibitors.
|Terai H,Soejima K,Yasuda H,Nakayama S,Hamamoto J,Arai D,Ishioka K,Ohgino K,Ikemura S,Sato T,Yoda S,Satomi R,Naoki K,Betsuyaku T||Molecular cancer research : MCR (11:759)||2013|
EGFR/Src/Akt signaling modulates Sox2 expression and self-renewal of stem-like side-population cells in non-small cell lung cancer.
44-788G was used in western blot to test if the self-renewal of side population cells is dependent on EGFR mediated signaling and assess their contribution to generate tumors.
|Singh S,Trevino J,Bora-Singhal N,Coppola D,Haura E,Altiok S,Chellappan SP||Molecular cancer (11:null)||2012|
Wounding-induced synthesis of hyaluronic acid in organotypic epidermal cultures requires the release of heparin-binding egf and activation of the EGFR.
44-788G was used in western blot to elucidate how hyaluronic acid accumulates following skin wounding in rats
|Monslow J,Sato N,Mack JA,Maytin EV||The Journal of investigative dermatology (129:2046)||2009|
Determinants of response to epidermal growth factor receptor tyrosine kinase inhibition in squamous cell carcinoma of the head and neck.
44-788G was used in western blot to assess the sensitivity of 8 squamous cell carcinoma of the head and neck cell lines to gefitinib.
|Rogers SJ,Box C,Chambers P,Barbachano Y,Nutting CM,Rh¿s-Evans P,Workman P,Harrington KJ,Eccles SA||The Journal of pathology (218:122)||2009|
|Not Applicable||Not Cited||
Quantitative measurement of epidermal growth factor receptor-mitogen-activated protein kinase signal transduction using a nine-plex, peptide-based immunoassay.
44-788G was used in western blot to develop an assay to measure temporal, site-specific phosphorylation of key members of the EGFR pathway in A431 cells stimulated with epidermal growth factor
|Rauh-Adelmann C,Moskow JM,Graham JR,Yen LG,Boucher JI,Murphy CE,Nadler TK,Gordon NF,Radding JA||Analytical biochemistry (375:255)||2008|
|Human||Not Cited||Tumor growth inhibition with cetuximab and chemotherapy in non-small cell lung cancer xenografts expressing wild-type and mutated epidermal growth factor receptor.||Steiner P,Joynes C,Bassi R,Wang S,Tonra JR,Hadari YR,Hicklin DJ||Clinical cancer research : an official journal of the American Association for Cancer Research (13:1540)||2007|
|Non-human primate||Not Cited||G protein coupling and second messenger generation are indispensable for metalloprotease-dependent, heparin-binding epidermal growth factor shedding through angiotensin II type-1 receptor.||Mifune M,Ohtsu H,Suzuki H,Nakashima H,Brailoiu E,Dun NJ,Frank GD,Inagami T,Higashiyama S,Thomas WG,Eckhart AD,Dempsey PJ,Eguchi S||The Journal of biological chemistry (280:26592)||2005|
|Mouse||Not Cited||Aplidin induces apoptosis in human cancer cells via glutathione depletion and sustained activation of the epidermal growth factor receptor, Src, JNK, and p38 MAPK.||Cuadrado A,Garcia-Fernandez LF,Gonzalez L,Suarez Y,Losada A,Alcaide V,Martinez T,Fernandez-Sousa JM,Sanchez-Puelles JM,Munoz A||The Journal of biological chemistry (278:241)||2003|
|Not Applicable||Not Cited||
Hydrocortisone and indomethacin negatively modulate EGF-R signaling in human fetal intestine.
44-788G was used in immunocytochemistry to examine if EGF-R contributes to the hydrocortisone and indomethacin-induced intestinal perforations of preterm infants
|Kajanne R,Leppä S,Luukkainen P,Ustinov J,Thiel A,Ristimäki A,Miettinen PJ||Pediatric research (62:570)||2007|