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Journal articles on the topic 'EGFR tyrosine kinase'

Author: Grafiati

Published: 5 June 2025

Last updated: 1 August 2025

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1

Noguchi, Rei, Akihiro Yoshimura, Junji Uchino, et al. "Comprehensive Kinase Activity Profiling Revealed the Kinase Activity Patterns Associated with the Effects of EGFR Tyrosine Kinase Inhibitor Therapy in Advanced Non-Small-Cell Lung Cancer Patients with Sensitizing EGFR Mutations." Proteomes 11, no. 1 (2023): 6. http://dx.doi.org/10.3390/proteomes11010006.

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EGFR mutations are strong predictive markers for EGFR tyrosine kinase inhibitor (EGFR-TKI) therapy in patients with non-small-cell lung cancer (NSCLC). Although NSCLC patients with sensitizing EGFR mutations have better prognoses, some patients exhibit worse prognoses. We hypothesized that various activities of kinases could be potential predictive biomarkers for EGFR-TKI treatment among NSCLC patients with sensitizing EGFR mutations. In 18 patients with stage IV NSCLC, EGFR mutations were detected and comprehensive kinase activity profiling was performed using the peptide array PamStation12 f

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2

Segatto, O., F. Lonardo, D. Wexler, et al. "The juxtamembrane regions of the epidermal growth factor receptor and gp185erbB-2 determine the specificity of signal transduction." Molecular and Cellular Biology 11, no. 6 (1991): 3191–202. http://dx.doi.org/10.1128/mcb.11.6.3191-3202.1991.

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The epidermal growth factor receptor (EGFR) and gp185erbB-2 are closely related tyrosine kinases. Despite extensive sequence and structural homology, these two receptors display quantitative and qualitative differences in their ability to couple with mitogenic signalling pathways. By using chimeric molecules between EGFR and erbB-2, we found that the determinants responsible for the specificity of mitogenic signal transduction are located in the amino-terminal half of the tyrosine kinase domain of either receptor. In the EGFR, mutational analysis within this subdomain revealed that deletion of

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3

Segatto, O., F. Lonardo, D. Wexler, et al. "The juxtamembrane regions of the epidermal growth factor receptor and gp185erbB-2 determine the specificity of signal transduction." Molecular and Cellular Biology 11, no. 6 (1991): 3191–202. http://dx.doi.org/10.1128/mcb.11.6.3191.

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The epidermal growth factor receptor (EGFR) and gp185erbB-2 are closely related tyrosine kinases. Despite extensive sequence and structural homology, these two receptors display quantitative and qualitative differences in their ability to couple with mitogenic signalling pathways. By using chimeric molecules between EGFR and erbB-2, we found that the determinants responsible for the specificity of mitogenic signal transduction are located in the amino-terminal half of the tyrosine kinase domain of either receptor. In the EGFR, mutational analysis within this subdomain revealed that deletion of

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4

Perez-Soler, R., N. J. Donato, D. M. Shin, et al. "Tumor epidermal growth factor receptor studies in patients with non-small-cell lung cancer or head and neck cancer treated with monoclonal antibody RG 83852." Journal of Clinical Oncology 12, no. 4 (1994): 730–39. http://dx.doi.org/10.1200/jco.1994.12.4.730.

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PURPOSE Tumor tyrosine kinase activity associated with the epidermal growth factor receptor (EGFR) and localization of anti-EGFR monoclonal antibody RG 83852 were studied in patients with non-small-cell lung cancer (NSCLC) and head and neck cancer. PATIENTS AND METHODS Fifteen patients were treated with escalating doses of RG 83852 by continuous intravenous infusion for 5 days. Fresh tumor specimens were obtained 24 hours after therapy in 10 patients (of whom five had a pretherapy sample taken). Tumor EGFR tyrosine kinase activity was determined in fresh tumor samples by autophosphorylation of

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5

Krieg, Thomas, Qining Qin, Elizabeth C. McIntosh, Michael V. Cohen, and James M. Downey. "ACh and adenosine activate PI3-kinase in rabbit hearts through transactivation of receptor tyrosine kinases." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 6 (2002): H2322—H2330. http://dx.doi.org/10.1152/ajpheart.00474.2002.

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Adenosine and acetylcholine (ACh) trigger preconditioning through different signaling pathways. We tested whether either could activate myocardial phosphatidylinositol 3-kinase (PI3-kinase), a putative signaling protein in ischemic preconditioning. We used phosphorylation of Akt, a downstream target of PI3-kinase, as a reporter. Exposure of isolated rabbit hearts to ACh increased Akt phosphorylation 2.62 ± 0.33 fold ( P = 0.001), whereas adenosine caused a significantly smaller increase (1.52 ± 0.08 fold). ACh-induced activation of Akt was abolished by the tyrosine kinase blocker genistein ind

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6

Torri, Valter, Massimo Broggini, and Marina Chiara Garassino. "EGFR mutations and EGFR tyrosine kinase inhibitors." Lancet Oncology 16, no. 7 (2015): 746–48. http://dx.doi.org/10.1016/s1470-2045(15)00028-5.

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7

Ommurugan, Balaji, Amita Priya D, and Navin Patil. "SORAFENIB INDUCED ACNEIFORM ERUPTIONS: A CASE REPORT." Asian Journal of Pharmaceutical and Clinical Research 10, no. 4 (2017): 6. http://dx.doi.org/10.22159/ajpcr.2017.v10i4.16805.

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ABSTRACTSorafenib an oral tyrosine kinase inhibitor is used in the treatment of hepatocellular carcinoma, renal cell carcinoma and thyroid cancer. Sorafenib acts by inhibiting various kinases like tyrosine kinase, RET tyrosine kinase, endothelial growth factor receptor, vascular endothelial growth factor 2 and 3 inhibits angiogenesis and cell proliferation. Acneiform eruptions are known side effect of EGFR inhibitors with incidence ranging between 20 to 90 percent [3], but acneiform eruptions with Sorafenib is seldom seen. Hence, we report a case of Sorafenib induced acneiform eruptions.Keywor

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8

Jiwacharoenchai, Nattanan, Duangnapa Kiriwan, Lueacha Tabtimmai, et al. "Exploring Quinoxalinone Derivatives as Promising Epidermal Growth Factor Receptor (EGFR) Kinase Inhibitors for Cancer Therapy." Chiang Mai Journal of Science 51, no. 3 (2024): 1–14. http://dx.doi.org/10.12982/cmjs.2024.049.

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E GFR plays an extensive role in the signaling pathway such as proliferation, migration, invasion. However, the malfunctioning of the epidermal growth factor receptor (EGFR) is a crucial factor in cancer progression. The search for new kinase inhibitors is necessary due to the evolving nature of diseases and the emergence of resistant strains, prompting the need for novel compounds that can effectively target and inhibit specific kinases for therapeutic purposes. This study explores quinoxalinone derivatives, comprised of benzene and pyrazine aromatic rings, as novel potential EGFR kinase inhi

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9

Harvey, R. Donald, Val R. Adams, Tyler Beardslee, and Patrick Medina. "Afatinib for the treatment of EGFR mutation-positive NSCLC: A review of clinical findings." Journal of Oncology Pharmacy Practice 26, no. 6 (2020): 1461–74. http://dx.doi.org/10.1177/1078155220931926.

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Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors represent the standard of care in patients with EGFR mutation-positive ( EGFRm+) non-small cell lung cancer (NSCLC). The availability of several EGFR tyrosine kinase inhibitors approved for use in the first-line or later settings in NSCLC warrants an in-depth understanding of the pharmacological properties of, and clinical data supporting, these agents. The second-generation, irreversible ErbB-family blocker, afatinib, has been extensively studied in the context of EGFRm+ NSCLC. Results from the LUX-Lung 3 and 6 studies showed

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10

Chen, Yuejun, Hui Long, Ziyan Wu, Xi Jiang, and Lan Ma. "EGF Transregulates Opioid Receptors through EGFR-mediated GRK2 Phosphorylation and Activation." Molecular Biology of the Cell 19, no. 7 (2008): 2973–83. http://dx.doi.org/10.1091/mbc.e07-10-1058.

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G protein–coupled receptor (GPCR) kinases (GRKs) are key regulators of GPCR function. Here we demonstrate that activation of epidermal growth factor receptor (EGFR), a member of receptor tyrosine kinase family, stimulates GRK2 activity and transregulates the function of G protein–coupled opioid receptors. Our data showed that EGF treatment promoted DOR internalization induced by DOR agonist and this required the intactness of GRK2-phosphorylation sites in DOR. EGF stimulation induced the association of GRK2 with the activated EGFR and the translocation of GRK2 to the plasma membrane. After EGF

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11

Chemmalar, S., A. R. Intan Shameha, Che Azurahanim Che Abdullah, et al. "Busting the Breast Cancer with AstraZeneca’s Gefitinib." Advances in Pharmacological and Pharmaceutical Sciences 2023 (December 4, 2023): 1–26. http://dx.doi.org/10.1155/2023/8127695.

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Breast cancer is the most common cancer diagnosed in women, and in 2020, there were 684, 996 deaths due to this disease. Epidermal growth factor receptors (EGFRs) and their respective ligands have been blamed for the pathogenesis and resistance to treatment in specific breast cancer cases. With EGFR having four homologues: EGFR1, EGFR2, EGFR3, and EGFR4, in-depth understanding of EGFR biology led to the discovery of small-molecule inhibitors and antibodies against this receptor. Gefitinib (GEF), a tyrosine kinase inhibitor of EGFR1, possesses a vast potential for treatment against breast cance

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Al-Salem, Huda S., Md Arifuzzaman, Iman S. Issa, and A. F. M. Motiur Rahman. "Isatin-Hydrazones with Multiple Receptor Tyrosine Kinases (RTKs) Inhibitory Activity and In-Silico Binding Mechanism." Applied Sciences 11, no. 9 (2021): 3746. http://dx.doi.org/10.3390/app11093746.

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Recently, we have reported a series of isatin hydrazone, two of them, namely, 3-((2,6-dichlorobenzylidene)hydrazono)indolin-2-one (1) and 3-((2-chloro-6-fluorobenzylidene)hydrazono)indolin-2-one (2) having potent cytotoxicity, showing cyclin-dependent kinases (CDK2) inhibitory activity and bearing recommended drug likeness properties. Since both compounds (1 and 2) showed inhibitory activity against CDK2, we assumed it would also have multiple receptor tyrosine kinases (RTKs) inhibitory activity. Considering those points, here, above-mentioned two isatin hydrazone 1 and 2 were synthesized usin

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13

Bowlby, Mark R., Debra A. Fadool, Todd C. Holmes, and Irwin B. Levitan. "Modulation of the Kv1.3 Potassium Channel by Receptor Tyrosine Kinases." Journal of General Physiology 110, no. 5 (1997): 601–10. http://dx.doi.org/10.1085/jgp.110.5.601.

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The voltage-dependent potassium channel, Kv1.3, is modulated by the epidermal growth factor receptor (EGFr) and the insulin receptor tyrosine kinases. When the EGFr and Kv1.3 are coexpressed in HEK 293 cells, acute treatment of the cells with EGF during a patch recording can suppress the Kv1.3 current within tens of minutes. This effect appears to be due to tyrosine phosphorylation of the channel, as it is blocked by treatment with the tyrosine kinase inhibitor erbstatin, or by mutation of the tyrosine at channel amino acid position 479 to phenylalanine. Previous work has shown that there is a

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Inamura, Kentaro, Hironori Ninomiya, Yuichi Ishikawa, and Osamu Matsubara. "Is the Epidermal Growth Factor Receptor Status in Lung Cancers Reflected in Clinicopathologic Features?" Archives of Pathology & Laboratory Medicine 134, no. 1 (2010): 66–72. http://dx.doi.org/10.5858/2008-0586-rar1.1.

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Abstract Context.—Epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors are molecular-targeted drugs that are innovatively effective for non–small cell lung carcinomas with EGFR mutations. Epidermal growth factor receptor is a transmembrane receptor forming dimers on ligand binding. These then stimulate signals by activating receptor autophosphorylation through tyrosine kinase activity. Autophosphorylation triggers intracellular pathways facilitating malignant conversion. The most clinically advanced EGFR inhibition strategies include small-molecule inhibition of the intracellular

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Bae, Seyeon, Eunsil Hahm, Kyung Eun Lee, et al. "Vitamin C potentiates gefitinib-mediated tumor cell growth inhibition in human lung cancer cells (49.26)." Journal of Immunology 178, no. 1_Supplement (2007): S88. http://dx.doi.org/10.4049/jimmunol.178.supp.49.26.

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Abstract Malignancies of lung are the leading causes of cancer mortality in world wide and there are so many limitations in early detection of lung cancer, which eventually made the cancer detected at advanced stage. Conventional cytotoxic drugs have showed more increased response rate with grave toxicities. Recently, successful therapy with epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor in lung cancer patients have been reported, although a mono-therapy still showed low response rate. Here, we investigated to elucidate whether the vitamin C has the adjuvant role as an antio

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16

Wiiger, Merete, and Hans Prydz. "The epidermal growth factor receptor (EGFR) and proline rich tyrosine kinase 2 (PYK2) are involved in tissue factor dependent factor VIIa signalling in HaCaT cells." Thrombosis and Haemostasis 92, no. 07 (2004): 13–22. http://dx.doi.org/10.1160/th03-08-0549.

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SummaryBinding of the coagulation protease factor VIIa to its receptor Tissue Factor (TF) induces intracellular signals in several cell types including HaCaT keratinocytes. TF belongs to the cytokine receptor family, but is most likely not alone in transferring the complete TF/FVIIa signal over the plasma membrane. The protease activated receptor PAR2 is involved in factor VIIa and factor Xa signal transduction. Our results indicate that the epidermal growth factor receptor (EGFR) and the proline rich tyrosine kinase 2 (PYK2) participate in TF/FVIIa signalling as formation of the TF/FVIIa comp

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Zubair, Tanzida, and Debasish Bandyopadhyay. "Small Molecule EGFR Inhibitors as Anti-Cancer Agents: Discovery, Mechanisms of Action, and Opportunities." International Journal of Molecular Sciences 24, no. 3 (2023): 2651. http://dx.doi.org/10.3390/ijms24032651.

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Epidermal growth factor receptors (EGFRs) are a class of receptor tyrosine kinase that are also called ErbB1 and HER1. EGFR tyrosine kinase activity inhibition is considered a promising therapeutic strategy for the treatment of cancer. Many small-molecule inhibitors of EGFR tyrosine kinase (EGFR-TK), from medicinally privileged molecules to commercial drugs, have been overviewed. Particular attention has been paid to the structure of the molecule and its mechanism of action if reported. Subsequent classification of the molecules under discussion has been carried out. Both natural and synthetic

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Heo, Jung Sun, Yun Jung Lee, and Ho Jae Han. "EGF stimulates proliferation of mouse embryonic stem cells: involvement of Ca2+ influx and p44/42 MAPKs." American Journal of Physiology-Cell Physiology 290, no. 1 (2006): C123—C133. http://dx.doi.org/10.1152/ajpcell.00142.2005.

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We examined the effect of EGF on the proliferation of mouse embryonic stem (ES) cells and their related signal pathways. EGF increased [3H]thymidine and 5-bromo-2′-deoxyuridine incorporation in a time- and dose-dependent manner. EGF stimulated the phosphorylation of EGF receptor (EGFR). Inhibition of EGFR tyrosine kinase with AG-1478 or herbimycin A, inhibition of PLC with neomycin or U-73122, inhibition of PKC with bisindolylmaleimide I or staurosporine, and inhibition of L-type Ca2+ channels with nifedipine or methoxyverapamil prevented EGF-induced [3H]thymidine incorporation. PKC-α, -βI, -γ

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Jaszewski, Richard, Ahmed Khan, Fazlul H. Sarkar, et al. "Folic acid inhibition of EGFR-mediated proliferation in human colon cancer cell lines." American Journal of Physiology-Cell Physiology 277, no. 6 (1999): C1142—C1148. http://dx.doi.org/10.1152/ajpcell.1999.277.6.c1142.

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Although accumulating evidence suggests a chemopreventive role for folic acid in colon cancer, the regulation of this process in unknown. We hypothesize that supplemental folic acid exerts its chemopreventive role by inhibiting mucosal hyperproliferation, an event considered to be central to the initiation of carcinogenesis in the gastrointestinal tract. The present investigation examines the effect of supplemental folic acid on proliferation of Caco-2 and HCT-116 colon cancer cell lines. Furthermore, because certain tyrosine kinases, particularly epidermal growth factor receptor (EGFR), play

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von Achenbach, Caroline, Vincent Blot, William Weiss, and Michael Weller. "CSIG-06. DEPATUXIZUMAB MAFODOTIN (ABT-414)-INDUCED GLIOBLASTOMA CELL DEATH REQUIRES EGFR OVEREXPRESSION, BUT NOT PHOSPHORYLATION." Neuro-Oncology 21, Supplement_6 (2019): vi45. http://dx.doi.org/10.1093/neuonc/noz175.177.

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Abstract Glioblastomas commonly (40%) exhibit epidermal growth factor receptor (EGFR) amplification, half of these tumors carry the EGFRvIII deletion variant characterized by an in-frame deletion of exons 2–7, resulting in constitutive EGFR activation. Although EGFR tyrosine kinase inhibitors had only modest effects in glioblastoma, novel therapeutic agents targeting amplified EGFR or EGFRvIII continue to be developed. Depatuxizumab mafodotin (ABT-414) is an antibody drug conjugate consisting of the monoclonal antibody 806 and, as its toxic payload, monomethyl auristatin F, designed to target

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Park, Jin H., Yingting Liu, Mark A. Lemmon, and Ravi Radhakrishnan. "Erlotinib binds both inactive and active conformations of the EGFR tyrosine kinase domain." Biochemical Journal 448, no. 3 (2012): 417–23. http://dx.doi.org/10.1042/bj20121513.

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Erlotinib and gefitinib, tyrosine kinase inhibitors used to block EGFR (epidermal growth factor receptor) signalling in cancer, are thought to bind only the active conformation of the EGFR-TKD (tyrosine kinase domain). Through parallel computational and crystallographic studies, we show in the present study that erlotinib also binds the inactive EGFR-TKD conformation, which may have significant implications for its use in EGFR-mutated cancers.

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GALLET, Carole, Stéphanie BLAIE, Sylviane LÉVY-TOLEDANO, and Aïda HABIB. "Epidermal-growth-factor receptor and metalloproteinases mediate thromboxane A2-dependent extracellular-signal-regulated kinase activation." Biochemical Journal 371, no. 3 (2003): 733–42. http://dx.doi.org/10.1042/bj20021030.

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The signalling pathways that link G-protein-coupled receptors to mitogen-activated protein kinases involve receptor and non-receptor tyrosine kinases and protein kinase C (PKC). We explored the pathways that are implicated in the thromboxane (TX) A2-dependent activation of extracellular-signal-regulated protein kinase (ERK) and the role of the two TX receptor (TP) isoforms, TPα and TPβ. ERK activation by IBOP, a TX analogue, was dependent on epidermal-growth-factor receptor (EGFR) in TPα- or TPβ-transfected cells and in human aortic smooth muscle cells (hASMCs), since AG1478, a selective inhib

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Chadwick, Wayne, Alex Keselman, Sung-Soo Park, et al. "Repetitive Peroxide Exposure Reveals Pleiotropic Mitogen-Activated Protein Kinase Signaling Mechanisms." Journal of Signal Transduction 2011 (December 19, 2011): 1–15. http://dx.doi.org/10.1155/2011/636951.

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Oxidative stressors such as hydrogen peroxide control the activation of many interconnected signaling systems and are implicated in neurodegenerative disease etiology. Application of hydrogen peroxide to PC12 cells activated multiple tyrosine kinases (c-Src, epidermal growth factor receptor (EGFR), and Pyk2) and the serine-threonine kinase ERK1/2. Peroxide-induced ERK1/2 activation was sensitive to intracellular calcium chelation and EGFR and c-Src kinase inhibition. Acute application and removal of peroxide allowed ERK1/2 activity levels to rapidly subside to basal serum-deprived levels. Usin

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Kuwada, Scott K., Kirk A. Lund, Xiu Fen Li, et al. "Differential signaling and regulation of apical vs. basolateral EGFR in polarized epithelial cells." American Journal of Physiology-Cell Physiology 275, no. 6 (1998): C1419—C1428. http://dx.doi.org/10.1152/ajpcell.1998.275.6.c1419.

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Overexpression of the epidermal growth factor receptors (EGFR) in polarized kidney epithelial cells caused them to appear in high numbers at both the basolateral and apical cell surfaces. We utilized these cells to look for differences in the regulation and signaling of apical vs. basolateral EGFR. Apical and basolateral EGFR were biologically active and mediated EGF-induced cell proliferation to similar degrees. Receptor downregulation and endocytosis were less efficient at the apical surface, resulting in prolonged EGF-induced tyrosine kinase activity at the apical cell membrane. Tyrosine ph

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Yoshioka, Hiroshige, Terufumi Kato, Isamu Okamoto, et al. "Therapies after first-line afatinib in patients with EGFRm+ NSCLC in Japan: retrospective analysis of LUX-Lung 3." Future Oncology 16, no. 4 (2020): 49–60. http://dx.doi.org/10.2217/fon-2019-0659.

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Aim: Acquired resistance to EGFR tyrosine kinase inhibitors is inevitable in non-small-cell lung cancer. To inform subsequent treatment decisions, we retrospectively assessed therapies following afatinib in Japanese patients from LUX-Lung 3. Patients & methods: LUX-Lung 3 was a randomized, open-label, Phase III study of afatinib versus cisplatin/pemetrexed in treatment-naive patients with EGFR mutation-positive ( EGFRm+) advanced lung adenocarcinoma. Results: Among 47 Japanese patients who discontinued first-line afatinib, 91/81/62% received ≥one/two/three subsequent therapies. The most co

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Kan, Yagmur, YiTing Paung, Markus A. Seeliger, and W. Todd Miller. "Domain Architecture of the Nonreceptor Tyrosine Kinase Ack1." Cells 12, no. 6 (2023): 900. http://dx.doi.org/10.3390/cells12060900.

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The nonreceptor tyrosine kinase (NRTK) Ack1 comprises a distinct arrangement of non-catalytic modules. Its SH3 domain has a C-terminal to the kinase domain (SH1), in contrast to the typical SH3-SH2-SH1 layout in NRTKs. The Ack1 is the only protein that shares a region of high homology to the tumor suppressor protein Mig6, a modulator of EGFR. The vertebrate Acks make up the only tyrosine kinase (TK) family known to carry a UBA domain. The GTPase binding and SAM domains are also uncommon in the NRTKs. In addition to being a downstream effector of receptor tyrosine kinases (RTKs) and integrins,

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Thomas, Rintu, Shivangi Srivastava, Rajasekhara Reddy Katreddy, Jason Sobieski, and Zhang Weihua. "Kinase-Inactivated EGFR Is Required for the Survival of Wild-Type EGFR-Expressing Cancer Cells Treated with Tyrosine Kinase Inhibitors." International Journal of Molecular Sciences 20, no. 10 (2019): 2515. http://dx.doi.org/10.3390/ijms20102515.

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Inhibiting the tyrosine kinase activity of epidermal growth factor receptor (EGFR) using small molecule tyrosine kinase inhibitors (TKIs) is often ineffective in treating cancers harboring wild-type EGFR (wt-EGFR). TKIs are known to cause dimerization of EGFR without altering its expression level. Given the fact that EGFR possesses kinase-independent pro-survival function, the role of TKI-inactivated EGFR in cancer cell survival needs to be addressed. In this study, using wt-EGFR-expressing cancer cells A549 (lung), DU145 (prostate), PC3 (prostate), and MDA-MB-231 (breast), we characterized th

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Smithberger, Erin, Abigail Shelton, Madison Butler, et al. "CSIG-10. GENOTYPE – KINOME GUIDED DEVELOPMENT OF PRECISION EGFR-TARGETED THERAPEUTICS FOR GLIOBLASTOMA." Neuro-Oncology 22, Supplement_2 (2020): ii29. http://dx.doi.org/10.1093/neuonc/noaa215.122.

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Abstract Glioblastoma (GBM) is an aggressive primary brain tumor with poor survival and limited treatment options. However, it is an attractive candidate for precision therapeutic approaches due to the frequency of amplification and/or activating mutations in the epidermal growth factor receptor (EGFR) gene and the availability of several brain penetrant second- and third-generation EGFR tyrosine kinase inhibitors (TKI). We used comprehensive molecular profiling of a panel of genetically engineered mouse astrocyte models to examine whether mutational profiles, particularly EGFR and PTEN status

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Santiskulvong, Chintda, James Sinnett-Smith, and Enrique Rozengurt. "EGF receptor function is required in late G1 for cell cycle progression induced by bombesin and bradykinin." American Journal of Physiology-Cell Physiology 281, no. 3 (2001): C886—C898. http://dx.doi.org/10.1152/ajpcell.2001.281.3.c886.

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We examined the role of epidermal growth factor (EGF) receptor (EGFR) tyrosine kinase activation in G protein-coupled receptor (GPCR) agonist-induced mitogenesis in Swiss 3T3 and Rat-1 cells. Addition of EGFR tyrosine kinase inhibitors (e.g., tyrphostin AG-1478) abrogated bombesin-induced extracellular signal-regulated kinase (ERK) activation in Rat-1 cells but not in Swiss 3T3 cells, indicating the importance of cell context in determining the role of EGFR in ERK activation. In striking contrast, treatment with tyrphostin AG-1478 markedly (∼70%) inhibited DNA synthesis induced by bombesin in

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Wayne, Chad M., Heng-Yu Fan, Xiaodong Cheng, and JoAnne S. Richards. "Follicle-Stimulating Hormone Induces Multiple Signaling Cascades: Evidence that Activation of Rous Sarcoma Oncogene, RAS, and the Epidermal Growth Factor Receptor Are Critical for Granulosa Cell Differentiation." Molecular Endocrinology 21, no. 8 (2007): 1940–57. http://dx.doi.org/10.1210/me.2007-0020.

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Abstract FSH regulates ovarian granulosa cell differentiation not only by activating adenylyl cyclase and protein kinase A (PKA) but also by other complex mechanisms. Using primary rat granulosa cell cultures, we provide novel evidence that FSH rapidly activates two small GTP-binding proteins RAP1 and RAS. FSH activation of RAP1 requires cAMP-mediated activation of exchange factor activated by cAMP/RAPGEF3 whereas FSH activation of RAS and downstream signaling cascades involves multiple factors. Specifically, FSH activation of RAS required Rous sarcoma oncogene (SRC) family tyrosine kinase (SF

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Creeden, Justin F., Khaled Alganem, Ali S. Imami, et al. "Kinome Array Profiling of Patient-Derived Pancreatic Ductal Adenocarcinoma Identifies Differentially Active Protein Tyrosine Kinases." International Journal of Molecular Sciences 21, no. 22 (2020): 8679. http://dx.doi.org/10.3390/ijms21228679.

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Pancreatic cancer remains one of the most difficult malignancies to treat. Minimal improvements in patient outcomes and persistently abysmal patient survival rates underscore the great need for new treatment strategies. Currently, there is intense interest in therapeutic strategies that target tyrosine protein kinases. Here, we employed kinome arrays and bioinformatic pipelines capable of identifying differentially active protein tyrosine kinases in different patient-derived pancreatic ductal adenocarcinoma (PDAC) cell lines and wild-type pancreatic tissue to investigate the unique kinomic net

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Cybulsky, A. V., P. R. Goodyer, and A. J. McTavish. "Epidermal growth factor receptor activation in developing rat kidney." American Journal of Physiology-Renal Physiology 267, no. 3 (1994): F428—F436. http://dx.doi.org/10.1152/ajprenal.1994.267.3.f428.

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Epidermal growth factor (EGF) binding increases in late-gestational rat kidney and then falls toward basal adult levels postnatally during the 1st wk. We report that the increase in EGF binding is accompanied by an increase in EGF receptor (EGFR) protein and activation of EGFR tyrosine kinase. Multiple proteins were endogenously tyrosine phosphorylated in kidney membranes from fetal rats, and the phosphorylation pattern was similar in rats ranging from 16 to 21 days of gestation. Tyrosine phosphorylation was, however, almost undetectable in 12-wk adult rat kidneys (controls). Among the phospho

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Harandi, Amir, Aisha S. Zaidi, Abigail M. Stocker, and Damian A. Laber. "Clinical Efficacy and Toxicity of Anti-EGFR Therapy in Common Cancers." Journal of Oncology 2009 (2009): 1–14. http://dx.doi.org/10.1155/2009/567486.

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Epidermal growth factor receptor (EGFR) is a cell surface molecule and member of the ErbB family of receptor tyrosine kinases. Its activation leads to proliferation, antiapoptosis, and metastatic spread, making inhibition of this pathway a compelling target. In recent years, an increasing number of clinical trials in the management of solid malignancies have become available indicating the clinical efficacy of anti-EGFR monoclonal antibodies and oral small molecule tyrosine kinase inhibitors (TKIs). This review addresses frequently used EGFR inhibitors, summarizes clinical efficacy data of the

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Ishikawa, Kouki, Atsuki Nara, Kunihiro Matsumoto, and Hiroshi Hanafusa. "EGFR-dependent phosphorylation of leucine-rich repeat kinase LRRK1 is important for proper endosomal trafficking of EGFR." Molecular Biology of the Cell 23, no. 7 (2012): 1294–306. http://dx.doi.org/10.1091/mbc.e11-09-0780.

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Ligand-induced activation of the epidermal growth factor receptor (EGFR) initiates trafficking events that relocalize the receptors from the cell surface to intracellular endocytic compartments. We recently reported that leucine-rich repeat kinase 1 (LRRK1) is involved in the trafficking of EGFR from early to late endosomes. In this study, we demonstrate that EGFR regulates the kinase activity of LRRK1 via tyrosine phosphorylation and that this is required for proper endosomal trafficking of EGFR. Phosphorylation of LRRK1 at Tyr-944 results in reduced LRRK1 kinase activity. Mutation of LRRK1 T

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Fang, K. S., E. Ionides, G. Oster, R. Nuccitelli, and R. R. Isseroff. "Epidermal growth factor receptor relocalization and kinase activity are necessary for directional migration of keratinocytes in DC electric fields." Journal of Cell Science 112, no. 12 (1999): 1967–78. http://dx.doi.org/10.1242/jcs.112.12.1967.

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Human keratinocytes migrate towards the negative pole in DC electric fields of physiological strength. This directional migration is promoted by epidermal growth factor (EGF). To investigate how EGF and its receptor (EGFR) regulate this directionality, we first examined the effect of protein tyrosine kinase inhibitors, including PD158780, a specific inhibitor for EGFR, on this response. At low concentrations, PD158780 inhibited keratinocyte migration directionality, but not the rate of migration; at higher concentrations, it reduced the migration rate as well. The less specific inhibitors, gen

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Hirata, Masashi, Masahiro Sakaguchi, Chikako Mochida, et al. "Lidocaine Inhibits Tyrosine Kinase Activity of the Epidermal Growth Factor Receptor and Suppresses Proliferation of Corneal Epithelial Cells." Anesthesiology 100, no. 5 (2004): 1206–10. http://dx.doi.org/10.1097/00000542-200405000-00024.

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Background Although lidocaine is recognized as an excellent topical corneal analgesic, its toxic effect on corneal epithelial cells limits its use during corneal epithelial wound healing. Mechanism of the impairment of corneal reepithelialization with lidocaine, however, has not been evaluated. The authors' previous study revealed that lidocaine inhibits the activity of tyrosine kinase receptors through the interaction with specific amino acid sequences around autophosphorylation sites, including acidic, basic, and aromatic amino acids. Epidermal growth factor receptor (EGFR), a tyrosine kinas

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Oksvold, Morten P., Henrik S. Huitfeldt, Anne Carine Østvold, and Ellen Skarpen. "UV induces tyrosine kinase-independent internalisation and endosome arrest of the EGF receptor." Journal of Cell Science 115, no. 4 (2002): 793–803. http://dx.doi.org/10.1242/jcs.115.4.793.

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We have compared the activation and trafficking of epidermal growth factor receptor (EGFR) induced by UV light and EGF. Tyrosine phosphorylation of EGFR was not detected in UV-exposed cells by immunoblotting of whole cell lysates or EGFR immunoprecipitates with antibodies specific for each of the five activated autophosphorylation sites of EGFR. In addition, EGFR of UV-irradiated cells did not demonstrate increased 32P-incorporation. However, UV-exposed cells demonstrated a gel mobility shift of EGFR, which was not abolished by alkaline phosphatase treatment. UV-exposure did not induce dimeris

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Cabart, Mathilde, Judith Raimbourg, Lisenn Lalier, Jaafar Bennouna, and Francois Vallette. "Optimisation of EGFR TKI efficiency in the therapeutic scheme of EGFR wild-type lung cancer." Journal of Clinical Oncology 31, no. 15_suppl (2013): e18532-e18532. http://dx.doi.org/10.1200/jco.2013.31.15_suppl.e18532.

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e18532 Background: EGFR tyrosine kinase inhibitors (EGFR TKI) have improved the therapeutic care of lung cancer patients but only a small sub-population of patients, namely those harboring EGFR-mutated tumors, benefit from this therapy. The observation that EGFR TKI enhance prognosis and quality of life in all patients when used as second line or maintenance treatment impelled us into the search of potential markers of the optimal introduction kinetics of EGFR TKI in the therapeutic scheme. Methods: We used lung cancer cell lines harboring either wild-type or mutated EGFR (NCI-H1650, NCI-H1975

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Dogan, Izzet, Nijat Khanmammadov, Anıl Yıldız, et al. "Predictors of response in EGFR-mutant metastatic non-small cell lung cancer patients treated with tyrosine kinase inhibitors." Journal of Cancer Research and Therapeutics 19, no. 7 (2023): 1945–49. http://dx.doi.org/10.4103/jcrt.jcrt_877_22.

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ABSTRACT Background: The goal of the study was to evaluate the efficacy of tyrosine kinase inhibitors in patients with epidermal growth factor receptor (EGFR)-mutant metastatic non-small cell cancer and to determine the factors that predict objective response. Materials and Methods: In the study, data from metastatic non-small cell lung cancer patients with EGFR mutations treated with tyrosine kinase inhibitors were retrospectively reviewed. Factors predicting objective response were evaluated with logistic regression analysis. Results: The study evaluated the data of 105 patients. The most co

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Li, Hongbing, Paloma I. Palomo-Jiménez, María José Ruano, and Antonio Villalobo. "Signal transduction and regulation of the epidermal growth factor receptor." Electronic Journal of Pathology and Histology 6, no. 1 (2000): 07. https://doi.org/10.3233/eph-2000-6_1_07.

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The epidermal growth factor receptor (EGFR) is a plasma membrane tyrosine kinase that belongs, together with other three related members, to the ErbB family of receptors. These receptors share a large group of polypeptide ligands, that induce homodimerization or heterodimerization among themselves, and the activation of their intrinsic tyrosine kinases followed by their transphosphorylation. The active phosphorylated receptors generate a series of signaling events conducted to initiate cell proliferation, differentiation and/or antiapoptotic responses. In this short review it will be analysed

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Fedi, P., J. H. Pierce, P. P. di Fiore, and M. H. Kraus. "Efficient coupling with phosphatidylinositol 3-kinase, but not phospholipase C gamma or GTPase-activating protein, distinguishes ErbB-3 signaling from that of other ErbB/EGFR family members." Molecular and Cellular Biology 14, no. 1 (1994): 492–500. http://dx.doi.org/10.1128/mcb.14.1.492-500.1994.

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Recombinant expression of a chimeric EGFR/ErbB-3 receptor in NIH 3T3 fibroblasts allowed us to investigate cytoplasmic events associated with ErbB-3 signal transduction upon ligand activation. An EGFR/ErbB-3 chimera was expressed on the surface of NIH 3T3 transfectants as two classes of receptors possessing epidermal growth factor (EGF) binding affinities comparable to those of the wild-type EGF receptor (EGFR). EGF induced autophosphorylation in vivo of the chimeric receptor and DNA synthesis of EGFR/ErbB-3 transfectants with a dose response similar to that of EGFR transfectants. However, the

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Fedi, P., J. H. Pierce, P. P. di Fiore, and M. H. Kraus. "Efficient coupling with phosphatidylinositol 3-kinase, but not phospholipase C gamma or GTPase-activating protein, distinguishes ErbB-3 signaling from that of other ErbB/EGFR family members." Molecular and Cellular Biology 14, no. 1 (1994): 492–500. http://dx.doi.org/10.1128/mcb.14.1.492.

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Recombinant expression of a chimeric EGFR/ErbB-3 receptor in NIH 3T3 fibroblasts allowed us to investigate cytoplasmic events associated with ErbB-3 signal transduction upon ligand activation. An EGFR/ErbB-3 chimera was expressed on the surface of NIH 3T3 transfectants as two classes of receptors possessing epidermal growth factor (EGF) binding affinities comparable to those of the wild-type EGF receptor (EGFR). EGF induced autophosphorylation in vivo of the chimeric receptor and DNA synthesis of EGFR/ErbB-3 transfectants with a dose response similar to that of EGFR transfectants. However, the

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Yen, Hsin-Yung, Ying-Chih Liu, Nai-Yu Chen, et al. "Effect of sialylation on EGFR phosphorylation and resistance to tyrosine kinase inhibition." Proceedings of the National Academy of Sciences 112, no. 22 (2015): 6955–60. http://dx.doi.org/10.1073/pnas.1507329112.

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Epidermal growth factor receptor (EGFR) is a heavily glycosylated transmembrane receptor tyrosine kinase. Upon EGF-binding, EGFR undergoes conformational changes to dimerize, resulting in kinase activation and autophosphorylation and downstream signaling. Tyrosine kinase inhibitors (TKIs) have been used to treat lung cancer by inhibiting EGFR phosphorylation. Previously, we demonstrated that EGFR sialylation suppresses its dimerization and phosphorylation. In this report, we further investigated the effect of sialylation on the phosphorylation profile of EGFR in TKI-sensitive and TKI-resistant

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McClelland, C. M., and W. J. Gullick. "Identification of surrogate markers for determining drug activity using proteomics." Biochemical Society Transactions 31, no. 6 (2003): 1488–90. http://dx.doi.org/10.1042/bst0311488.

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In a high proportion of human carcinomas overexpression of the EGFR (epidermal growth factor receptor), a receptor tyrosine kinase, represents a potential target for cancer treatment. EGFR is induced to dimerize through ligand binding which activates the tyrosine kinase activity of the receptor. This catalyses the transfer of ATP's γ-phosphate to hydroxyl groups of tyrosine residues on the receptor, creating binding sites that recruit downstream signalling proteins. New drugs, SMTKIs (small-molecule tyrosine kinase inhibitors), have been designed to inhibit the tyrosine kinase activity of the

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Liu, Lei, Jerrold R. Turner, Yingjie Yu, et al. "Differential expression of EGFR during early reparative phase of the gastric mucosa between young and aged rats." American Journal of Physiology-Gastrointestinal and Liver Physiology 275, no. 5 (1998): G943—G950. http://dx.doi.org/10.1152/ajpgi.1998.275.5.g943.

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Aging is associated with decreased reparative ability of the gastric mucosa. Our recent data suggest a role for epidermal growth factor receptor (EGFR) in the mucosal reparative processes. Thus we examined changes in EGFR tyrosine kinase activity as well as expression and subcellular localization of EGFR and its ligand transforming growth factor-α (TGF-α) in the gastric mucosa of young (4-mo-old) and aged (24-mo-old) Fischer 344 male rats during the early reparative phase after acute injury induced by 2 M NaCl. Within 240 min of injury, significant epithelial restitution was observed in the ga

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Noch, E., I. Alnahhas, L. Palma, and L. Cantley. "P13.18 Inhibition of epidermal growth factor receptor and platelet-derived growth factor receptor-alpha exerts synergistic efficacy in glioblastoma." Neuro-Oncology 23, Supplement_2 (2021): ii36. http://dx.doi.org/10.1093/neuonc/noab180.125.

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Abstract BACKGROUND Despite our understanding of the genetic changes that precipitate gliomagenesis, targeted therapy has failed in glioblastoma (GBM) with median survival not significantly improved over the past two decades. Epidermal growth factor receptor (EGFR) alterations, including amplification and activating mutations, are among the most common genetic changes in GBM, occurring in more than half of cases. EGFR is located on Chr. 7, and Chr. 7 gain is one of the earliest events precipitating gliomagenesis. Various EGFR inhibitors, including tyrosine kinase inhibitors, monoclonal antibod

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Minnelli, Cristina, Laura Cianfruglia, Emiliano Laudadio, Giovanna Mobbili, Roberta Galeazzi, and Tatiana Armeni. "Effect of Epigallocatechin-3-Gallate on EGFR Signaling and Migration in Non-Small Cell Lung Cancer." International Journal of Molecular Sciences 22, no. 21 (2021): 11833. http://dx.doi.org/10.3390/ijms222111833.

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The epidermal growth factor receptor (EGFR) is one of the most well-studied molecular targets in non-small cell lung cancer (NSCLC) and tyrosine kinase inhibitors have been shown to be effective in the treatment of advanced NSCLC. Nevertheless, the efficacy of tyrosine kinase inhibitors could be compromised by additional mutations in EGFR and compensatory activations of other pathways. Epigallocatechin-3-gallate (EGCG), the main bioactive molecule in green tea, acts as a tyrosine kinase inhibitor toward cancer cells overexpressing EGFR (wild-type). However, little information has been reported

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Hawash, Mohammed. "Advances in Cancer Therapy: A Comprehensive Review of CDK and EGFR Inhibitors." Cells 13, no. 19 (2024): 1656. http://dx.doi.org/10.3390/cells13191656.

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Protein kinases have essential responsibilities in controlling several cellular processes, and their abnormal regulation is strongly related to the development of cancer. The implementation of protein kinase inhibitors has significantly transformed cancer therapy by modifying treatment strategies. These inhibitors have received substantial FDA clearance in recent decades. Protein kinases have emerged as primary objectives for therapeutic interventions, particularly in the context of cancer treatment. At present, 69 therapeutics have been approved by the FDA that target approximately 24 protein

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Chen, P., K. Gupta, and A. Wells. "Cell movement elicited by epidermal growth factor receptor requires kinase and autophosphorylation but is separable from mitogenesis." Journal of Cell Biology 124, no. 4 (1994): 547–55. http://dx.doi.org/10.1083/jcb.124.4.547.

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The EGF receptor (EGFR) upon activation signals increased cell movement. However, the domains within the receptor, and the pathway which trigger movement are undefined. We expressed EGFR mutants at physiologic levels in receptor-devoid NR6 cells to investigate this biologic response. The receptors possessed kinase activity and underwent autophosphorylation as predicted by primary amino acid sequence. EGF-induced cell motility was assessed in vitro by excess migration into an acellular area and colony scatter in the presence of saturating concentrations of EGF. Wild-type (WT)-EGFR signaled incr

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Watty, Mega, Rezi Riadhi Syahdi, and Arry Yanuar. "DATABASE COMPILATION AND VIRTUAL SCREENING OF SECONDARY METABOLITES DERIVED FROM MARINE FUNGI AS EPIDERMAL GROWTH FACTOR RECEPTOR TYROSINE ABSTRACT KINASE INHIBITORS." Asian Journal of Pharmaceutical and Clinical Research 10, no. 17 (2017): 142. http://dx.doi.org/10.22159/ajpcr.2017.v10s5.23118.

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Objective: Epidermal growth factor receptor (EGFR), a transmembrane protein with cytoplasmic kinase activity, transduces growth factor signaling from the extracellular space to the cell. EGFR downstream signaling increases proliferation and reduces apoptosis. Agents that are targeted at intracellular tyrosine kinase are tyrosine kinase inhibitor small molecules, which have a mechanism of action that affects adenosine triphosphate binding to the receptor. The exploration of bioactive compounds from marine materials, including marine fungi, has become a major interest lately for anticancer treat

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