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P egfr tyr1173

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P-EGFR (Tyr1173) is a primary antibody that detects the epidermal growth factor receptor (EGFR) phosphorylated at tyrosine 1173. It is used to analyze the activation status of EGFR in cells and tissues.

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Lab products found in correlation

P akt ser473, by Cell Signaling Technology (4 mentions) Erk1 2, by Cell Signaling Technology (2 mentions) P erk1 2 thr202 tyr204, by Cell Signaling Technology (2 mentions) Stat3, by Cell Signaling Technology (2 mentions) P her2 tyr1248, by Cell Signaling Technology (1 mentions) Gefitinib zd1839, by Selleck Chemicals (1 mentions) Recombinant human egf, by Thermo Fisher Scientific (1 mentions) Cell culture medium, by Thermo Fisher Scientific (1 mentions) Hsp70, by Cell Signaling Technology (1 mentions) Pstat1 ser727, by Cell Signaling Technology (1 mentions) Fetal bovine serum (fbs), by Atlas Biologicals (1 mentions) P fak tyr397, by Cell Signaling Technology (1 mentions) Ikkα β, by Cell Signaling Technology (1 mentions) Perk1 2thr202 204, by Cell Signaling Technology (1 mentions) Pfak tyr 925, by Cell Signaling Technology (1 mentions) Stat1, by Cell Signaling Technology (1 mentions) Cleaved parp, by Cell Signaling Technology (1 mentions) P akt thr308, by Cell Signaling Technology (1 mentions) Pmet tyr1234 1235, by Cell Signaling Technology (1 mentions) Pher2 tyr1221 1222, by Cell Signaling Technology (1 mentions)

Spelling variants of this product

P-EGFR (216 citations) Tyr1173 (2 citations) P-HER2 (T1248)/p-EGFR (Tyr1173), (2 citations)

7 protocols using p egfr tyr1173

1

CMTM5 Antibody Profiling in Prostate Tissue

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A polyclonal antibody against CMTM5 (epitope mapping at the C-terminus, capable of detecting CMTM5 isoforms 1-5 of human origin) was given as a gift from Prof. Wenling Han (Peking University Center for Human Disease Genomics, Beijing, China). Monoclonal antibodies against EGFR, p-EGFR (Tyr1173), protein kinase B (Akt), p-Akt (Ser473), human epidermal growth factor receptor-2 (HER2) and p-HER2 (Tyr1248) were purchased from Cell Signaling Technology (Beverly, MA, USA). Horseradish peroxidase (HRP)-conjugated monoclonal antibody against glyceraldehyde 3-phosphate dehydrogenase (GAPDH) was obtained from Kang Chen Biotech (Shanghai, China). Recombinant human EGF was purchased from Peprotech (Rocky Hill, NJ, USA). Gefitinib (ZD1839) was purchased from Selleck Chemicals (Houston, TX, USA). Human benign prostatic hyperplasia (BPH) tissues were obtained from patients undergoing transurethral resection of the prostate at the Peking University People's Hospital with the patients' consent and institutional ethics approval.
Yuan Y., Sheng Z., Liu Z., Zhang X., Xiao Y., Xie J., Zhang Y, & Xu T. (2020). CMTM5-v1 inhibits cell proliferation and migration by downregulating oncogenic EGFR signaling in prostate cancer cells. Journal of Cancer, 11(13), 3762-3770.
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2

Signaling Pathway Analysis in Cancer Cells

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Cell culture medium was purchased from Invitrogen (Grand Island, NY). Fetal bovine serum (FBS) was purchased from Atlas Biologicals (Fort Collins, CO). Primary antibodies targeting the following were as detailed: Actin, EGFR, pEGFRTyr1069, pEGFRTyr1173, pEGFRTyr1110, ERK1/2, pERK1/2Thr202/204, mTOR, pmTORSer2441, pFAKTyr397, pFAKTyr527, pFAKTyr925, FAK, pMEKSer221, MEK, IKKα/β, pIKK α/βSer180/181, pSRCTyr418, SRC, pAKTSer473, AKT, pSTAT1Ser727, STAT1, Hsp70 and PLCγ were from Cell Signalling (Danvers, MA). Antibodies specific for BAG3 were from Abcam (Cambridge, UK). Secondary HRP-conjugated antibodies, including anti-rabbit Gig and anti-mouse IgG were from Cell Signalling (Danvers, MA). YM-1 was obtained from Sigma Aldrich and the compounds 5-carbamimidamido-2-[2-(phenylformamido) acetamido pentanoic acid (ZINC02516109) and 2-(quinoline-3-carbonyl)-2,8-diazaspiro[4.5]decane-3-carboxylic acid (ZINC72169376) sourced from MolPort (Europe).
Shields S., Conroy E., O’Grady T., McGoldrick A., Connor K., Ward M.P., Useckaite Z., Dempsey E., Reilly R., Fan Y., Chubb A., Matallanas D.G., Kay E.W., O’Connor D., McCann A., Gallagher W.M, & Coppinger J.A. (2018). BAG3 promotes tumour cell proliferation by regulating EGFR signal transduction pathways in triple negative breast cancer. Oncotarget, 9(21), 15673-15690.
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3

Immunoblot Analysis of Signaling Proteins

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Total protein was extracted from the cell lines following the standard protocol, and 20–40 μg of protein was used for immunoblotting27 (link). The blots were cut prior to hybridization with antibodies during blotting. The primary antibodies purchased from Cell Signaling Technology, Inc. (Danvers, MA, USA) were as follows: pHER2-Tyr1221/1222 (#2249), pEGFR-Tyr1173 (#4407), EGFR (#2232), pHER3-Tyr1289 (#4791), pMET-Tyr1234/1235 (#3077), pIGF1R-Tyr1135/1136 (#3024), IGF1R (#9750), ERK (#4695), pAKT-Ser473 (#4060), pAKT-Thr308 (#4056), AKT (#9272), pH2A.X-Ser139 (#9718), cleaved PARP (#9541), and PCNA (#2586). Other primary antibodies [HER3 (sc-285), MET (sc-514148), pERK-Tyr204 (sc-7383), and PTEN (sc-6818)] were purchased from Santa Cruz Biotechnology, Inc. Anti-HER2 (ab16901) and anti-α-tubulin (T6199) antibodies were purchased from Abcam Inc. and Sigma-Aldrich, Inc., respectively. After incubation with peroxidase-conjugated secondary antibodies for 1 h at 20 °C, the protein blots were developed using an enhanced chemiluminescent reagent (Amersham Inc., Amersham, UK). Total protein visualized on the ChemiDoc™ XRS + System (Bio-Rad) and analysed on Image Lab software (Image Lab 6.0, Bio-Rad).
Park J., Kang S.K., Kwon W.S., Jeong I., Kim T.S., Yu S.Y., Cho S.W., Chung H.C, & Rha S.Y. (2023). Novel HER2-targeted therapy to overcome trastuzumab resistance in HER2-amplified gastric cancer. Scientific Reports, 13, 22648.
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4

Synthesis and Characterization of COX-2/sEH Dual Inhibitor PTUPB

Cited 1 time
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The cyclooxygenase (COX)-2/soluble epoxide hydrolase (sEH) dual inhibitor, PTUPB, was synthesized by Dr. Sung Hee Hwang as described [18 (link), 47 (link)]. The recombinant human EGF (hEGF) (#8916) and primary antibodies against β-actin (#3700), CDK2 (#2546), p27Kip1 (#3686), Cyclin D3 (#2936), c-Myc (#13987), Cyclin D1 (#2978), p21Waf1/Cip1 (#2947), CDK4 (#12790), CDK6 (#3136), EGFR (#4267), p-EGFRTyr1068 (#3777), p-EGFRTyr1173 (#4407), AKT (#2920), p-AKTSer473 (#4060), ERK1/2 (#4695), p-ERK1/2Thr202/Tyr204 (#4377), GRB2 (#3972), BMI1 (#6964), ZEB1 (#3396) and SOX2 (#3579) were all purchased from Cell Signaling Technology (Beverly, MA, USA). Antibody against HMMR (#GTX121502) was purchased from GeneTex (Irvine, CA, USA).
Li J., Zhou Y., Wang H., Gao Y., Li L., Hwang S.H., Ji X, & Hammock B.D. (2017). COX-2/sEH dual inhibitor PTUPB suppresses glioblastoma growth by targeting epidermal growth factor receptor and hyaluronan mediated motility receptor. Oncotarget, 8(50), 87353-87363.
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5

Western Blotting Protein Expression Analysis

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Western blotting (WB) was performed as described [25 (link)]. Antibodies were used as per the manufacturer’s instructions and were as follows: CEBPD (Abcam, ab245214; or Invitrogen, PA5-30262); HIF1α (Abcam, #ab179483): EGFR (Cell Signaling Technology, #4267); p-EGFR (Tyr1173) (Cell Signaling Technology, #4407), ERK1/2 (Cell Signaling Technology, #4695), p-ERK1/2 (thr202/tyr204) (Cell Signaling Technology, #4370), AKT (Cell Signaling Technology, #4685), p-AKT (Ser473) (Cell Signaling Technology, #4060), mTOR (Wanleibio, Shenyang, China, WL02477), p-mTOR (Ser2448) (Wanleibio, WL03694), STAT3 (Cell Signaling Technology, #9139), p-STAT3 (Ser 727) (Cell Signaling Technology, #9134), FN1 (Proteintech, 15613-1-AP), COL1A1 (Wanleibio, WL0088), TNC (Proteintech, 67710-1-Ig), β-actin (Wanleibio, WL01372). All WBs were performed in triplicate, and quantification of protein expression levels were performed by using the ImageJ software (National Institutes of Health, Bethesda, MD).
Mao X.G., Xue X.Y., Lv R., Ji A., Shi T.Y., Chen X.Y., Jiang X.F, & Zhang X. (2023). CEBPD is a master transcriptional factor for hypoxia regulated proteins in glioblastoma and augments hypoxia induced invasion through extracellular matrix-integrin mediated EGFR/PI3K pathway. Cell Death & Disease, 14(4), 269.
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6

Resveratrol Sensitizes Cancer Cells

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DMU-212 was obtained from Sigma (St Louis, MO, USA), and resveratrol was purchased from Herbest (ShanXi, China). Fetal bovine serum (FBS), antibiotics, RPMI-1640 medium and DMEM medium were purchased from Gibco (Carlsbad, CA, USA). Sulforhodamine B (SRB) was obtained from Meryer Chemical Technology (ShangHai, China) and Trichloroacetic acid (TCA) was purchased from aladdin (ShangHai, China). Tris-base was obtained from Sangon Biotech (Shanghai, China). The primary antibodies Cyclin B1, P21, P-PI3K, PI3K, P-AKT, AKT, P-EGFR (Tyr 1173), EGFR, P-Erk, P-STAT3 (Tyr705), STAT3, P-mTOR, mTOR, P-S6 and Erk were purchased from Cell Signaling Technology (Danvers, MA, USA), and other primary antibodies GAPDH, β-actin, S6, P-AMPK and AMPK were obtained from Santa Cruz (Dallas, TX, USA). The AffiniPure Goat Anti-Mouse secondary antibodies and the AffiniPure Goat Anti-Rabbit secondary antibodies were purchased from Jackson ImmunoResearch Labs (PA, USA). Annexin V/Propidium iodide (PI) staining kit was obtained from BD Biosciences (San Jose, CA, USA).
Zhao X.P., Zheng X.L., Huang M., Xie Y.J., Nie X.W., Nasim A.A., Yao X.J, & Fan X.X. (2023). DMU-212 against EGFR-mutant non-small cell lung cancer via AMPK/PI3K/Erk signaling pathway. Heliyon, 9(5), e15812.
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7

Western Blotting of Signaling Proteins

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Cells were lysed on ice with radioimmunoprecipitation assay (RIPA) buffer containing a proteinase inhibitor (Roche) and a phosphatase inhibitor cocktail (Sigma‐Aldrich). Immunoblotting was performed using antibodies against MIG‐6 (Cell Signaling Technology, Cat. #2440), GLUT1 (Abcam, clone SPM498), p‐EGFR (Tyr1173) (Cell Signaling Technology, clone 53A5), EGFR (Santa Cruz Biotechnology, clone 1005), pAKT(S473) (Cell Signaling Technology, Cat.9271), AKT (Cell Signaling Technology, clone C67E7), HIF1α (BD Biosciences, Clone 54), cMyc (Roche, clone 9E10), β‐actin (Sigma‐Aldrich, clone AC‐15), and α‐Tubulin (Sigma‐Aldrich, clone B‐5‐1‐2). Detailed antibody information is listed in Table EV4.
He J., Li C., Lee H., Shin D., Chern Y., Pereira De Carvalho B, & Chan C. (2021). MIG‐6 is essential for promoting glucose metabolic reprogramming and tumor growth in triple‐negative breast cancer. EMBO Reports, 22(5), e50781.
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