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Science 24 March 1995: Vol. 267. no. 5205, pp. 1782 - 1788 DOI: 10.1126/science.7892601
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Articles
Science, Vol 267, Issue 5205, 1782-1788
Copyright © 1995 by American Association for the Advancement of Science
Tyrosine kinase inhibition: an approach to drug development
A Levitzki
and
A Gazit
Department of Biological Chemistry, Alexander Silberman Institute of Life Sciences, Hebrew University of Jerusalem, Israel.
Protein tyrosine kinases (PTKs) regulate cell proliferation, cell differentiation, and signaling processes in the cells of the immune system. Uncontrolled signaling from receptor tyrosine kinases and intracellular tyrosine kinases can lead to inflammatory responses and to diseases such as cancer, atherosclerosis, and psoriasis. Thus, inhibitors that block the activity of tyrosine kinases and the signaling pathways they activate may provide a useful basis for drug development. This article summarizes recent progress in the development of PTK inhibitors and demonstrates their potential use in the treatment of disease.
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Toxicol. Sci.
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- Epidermal Growth Factor Receptor-deficient Mice Have Delayed Primary Endochondral Ossification Because of Defective Osteoclast Recruitment.
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- Cytokine-Induced Activation of Signal Transducer and Activator of Transcription in Photoreceptor Precursors Regulates Rod Differentiation in the Developing Mouse Retina.
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J. Neurosci.
24, 9779-9788
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- Involvement of Tumor Necrosis Factor Receptor-associated Protein 1 (TRAP1) in Apoptosis Induced by {beta}-Hydroxyisovalerylshikonin.
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- Development of an Autocrine Neuregulin Signaling Loop with Malignant Transformation of Human Breast Epithelial Cells.
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Cancer Res.
64, 7078-7085
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- Adhesion-Mediated Squamous Cell Carcinoma Survival through Ligand-Independent Activation of Epidermal Growth Factor Receptor.
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Am. J. Pathol.
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- Tyrphostin AGL-2043 eluting stent reduces neointima formation in porcine coronary arteries.
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Cardiovasc Res
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- Calmodulin-mediated Activation of Akt Regulates Survival of c-Myc-overexpressing Mouse Mammary Carcinoma Cells.
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- DNA Topoisomerase I As One of the Cellular Targets of Certain Tyrphostin Derivatives.
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Mol. Pharmacol.
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- The AG1478 tyrosine kinase inhibitor is an effective suppressor of leiomyoma cell growth.
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Hum. Reprod.
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- Signal transduction of betacellulin in growth and migration of vascular smooth muscle cells.
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Am J Physiol Cell Physiol
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- Imaging Phosphorylation Dynamics of the Epidermal Growth Factor Receptor.
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- Akt Phosphorylation and Gefitinib Efficacy in Patients With Advanced Non-Small-Cell Lung Cancer.
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J Natl Cancer Inst
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- Plexin-B1/RhoGEF-mediated RhoA activation involves the receptor tyrosine kinase ErbB-2.
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- Transactivation of the Insulin-Like Growth Factor-I Receptor by Angiotensin II Mediates Downstream Signaling from the Angiotensin II Type 1 Receptor to Phosphatidylinositol 3-Kinase.
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Endocrinology
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- Regional Differences in Tyrosine Kinase Receptor Signaling Components Determine Differential Growth Patterns in the Human Lens.
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Invest. Ophthalmol. Vis. Sci.
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- A Multicenter Phase I Gene Therapy Clinical Trial Involving Intraperitoneal Administration of E1A-Lipid Complex in Patients with Recurrent Epithelial Ovarian Cancer Overexpressing HER-2/neu Oncogene.
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- The role of ADAM protease in the tyrosine kinase-mediated trigger mechanism of ischemic preconditioning.
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- Epigallocatechin-3-gallate Inhibits Epidermal Growth Factor Receptor Signaling Pathway: EVIDENCE FOR DIRECT INHIBITION OF ERK1/2 AND AKT KINASES.
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- Evidence That Tyrphostins AG10 and AG18 Are Mitochondrial Uncouplers That Alter Phosphorylation-dependent Cell Signaling.
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- Activation of STAT Signaling Pathways and Induction of Suppressors of Cytokine Signaling (SOCS) Proteins in Mammalian Lens by Growth Factors.
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- Transforming growth factor-{alpha} directly augments histidine decarboxylase and vesicular monoamine transporter 2 production in rat enterochromaffin-like cells.
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Am J Physiol Gastrointest Liver Physiol
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- Gs Protein-coupled Receptor Agonists Induce Transactivation of the Epidermal Growth Factor Receptor in T84 Cells: IMPLICATIONS FOR EPITHELIAL SECRETORY RESPONSES.
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- Apigenin Induces Apoptosis through Proteasomal Degradation of HER2/neu in HER2/neu-overexpressing Breast Cancer Cells via the Phosphatidylinositol 3-Kinase/Akt-dependent Pathway.
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