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EGF receptor signaling stimulates SRC kinase phosphorylation of clathrin, influencing clathrin redistribution and EGF uptake

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CELL 1999年第5期96卷 677-687页

作者： Wilde, A Beattie, EC Lem, L Riethof, DA Liu, SH Mobley, WC Soriano, P Brodsky, FM Univ Calif San Francisco Dept Immunol & Microbiol GW Hooper Fdn San Francisco CA 94143 USA Univ Calif San Francisco Dept Biopharmaceut Sci San Francisco CA 94143 USA Univ Calif San Francisco Dept Pharmaceut Chem San Francisco CA 94143 USA Univ Calif San Francisco Dept Physiol San Francisco CA 94143 USA Univ Calif San Francisco Dept Neurol San Francisco CA 94143 USA Univ Calif San Francisco Dept Anat San Francisco CA 94143 USA Fred Hutchinson Canc Res Ctr Div Basic Sci Seattle WA 98109 USA

Epidermal growth factor (EGF) binding to its receptor causes rapid phosphorylation of the clathrin heavy chain at tyrosine 1477, which lies in a domain controlling clathrin assembly. EGF-mediated clathrin phosphorylation is followed by clathrin redistribution to the cell periphery and is the product of downstream activation of SRC kinase by EGF receptor (EGFR) signaling. In cells lacking SRC kinase, or cells treated with a specific SRC family kinase inhibitor, EGF stimulation of clathrin phosphorylation and redistribution does not occur, and EGF endocytosis is delayed. These observations demonstrate a role for SRC kinase in modification and recruitment of clathrin during ligand-induced EGFR endocytosis and thereby define a novel effector mechanism for regulation of endocytosis by receptor signaling.

关键词：氨基酸序列生物转运网格蛋白/代谢胞吞作用/药物作用表皮生长因子/代谢配体分子序列数据磷酰化/药物作用蛋白质加工转译后/药物作用原癌基因蛋白质pp60(c-src)/代谢受体表皮生长因子/生理学重组融合蛋白质类/代谢肿瘤细胞培养的 src族激酶类/代谢动物牛人类小鼠

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Heparan sulfate proteoglycan isoforms of the CD44 hyaluronan receptor induced in human inflammatory macrophages can function as paracrine regulators of fibroblast growth factor action

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第11期275卷 7964-7974页

作者： Jones, M Tussey, L Athanasou, N Jackson, DG Univ Oxford Nuffield Dept Med MRC Human Immunol UnitInst Mol Med Oxford OX3 9DU England John Radcliffe Hosp Dept Cellular Sci Oxford OX3 9DU England Nuffield Orthopaed Ctr Oxford OX3 7LD England

The CD44 glycoprotein is expressed in multiple isoforms on a variety of cell types where it functions as a receptor for hyaluronan-mediated motility. Recently, interest has centered on CD44 heparan sulfate proteoglycan (HSPG) isoforms because of their potential to sequester heparin-binding growth factors and chemokines. Expression of these isoforms on ectodermal cells has recently been shown to regulate limb morphogenesis via presentation of fibroblast growth factor (FGF) 4/FGF 8 while expression on tumor cells was shown to sequester hepatocyte growth factor and promote tumor dissemination. To date, however, CD44 HSPG expression in tissue macrophages and lymphocytes has not been adequately investigated, despite the fact these cells actively synthesize growth factors and chemokines and indirect evidence that monocyte CD44 sequesters macrophage inflammatory-protein-Ip. Here we show primary human monocytes rather than lymphocytes express CD44 HSPGs, but only following in vitro differentiation to macrophages or activation with the proin-flammatory cytokine interleukin-1 alpha or bacterial lipopolysaccharide. Furthermore, we show these isoforms are preferentially modified with heparan rather than chondroitin sulfate, bind the macrophage-derived growth factors FGF-2, vascular endothelial growth factor, and heparin-binding epidermal growth factor with varying affinities (K-d 25-330 nM) and in the case of FGF-2, can stimulate productive binding to the high affinity tyrosine kinase FGF receptor 1 (FGFR1). In contrast, we find no evidence for significant binding to C-C chemokines. Last, we confirm by immunofluorescent antibody staining that inflamed synovial membrane macrophages express CD44 HSPGs and that expression is greatest in cells containing high FGF-2 levels. These results suggest a paracrine role for macrophage CD44 HSPG isoforms in the regulation of growth factor action during inflammation.

关键词：细胞分化炎症趋化因子类/代谢内皮生长因子/代谢表皮生长因子/代谢成纤维细胞生长因子2/代谢类肝素硫酸蛋白聚糖类/代谢炎症/代谢炎症介导素类/代谢胞间信号肽类和蛋白质类白细胞介素1/代谢淋巴因子/代谢巨噬细胞/细胞学巨噬细胞/免疫学单核细胞/细胞学单核细胞/免疫学旁分泌细胞细胞间通讯蛋白质结合蛋白质亚型/代谢受体蛋白质酪氨酸激酶类/代谢受体成纤维细胞生长因子 1型受体成纤维细胞生长因子/代谢滑膜/免疫学滑膜/病理学血管内皮生长因子A 血管内皮生长因子类人类

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Geldanamycin induces ErbB-2 degradation by proteolytic fragmentation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第34期275卷 26625-26631页

作者： Tikhomirov, O Carpenter, G Vanderbilt Univ Sch Med Dept Biochem Nashville TN 37232 USA Vanderbilt Univ Sch Med Dept Med Nashville TN 37232 USA

Exposure of carcinoma cell lines to the antibiotic geldanamycin induces the degradation of ErbB-2, a coreceptor tyrosine kinase that is frequently overexpressed in certain tumors. Using ErbB-2 mutants expressed as chimeric receptors or green fluorescent protein fusion proteins, we report that the kinase domain of ErbB-2 is essential for geldanamycin-induced degradation. The kinase domain of the related epidermal growth factor receptor was not sensitive to this drug. The data further indicate mechanistic aspects of ErbB-2 degradation by geldanamycin. The data show that exposure to the drug induces at least one cleavage within the cytoplasmic domain of ErbB-2 producing a 135-kDa fragment and a 23-kDa fragment. The latter represents the carboxyl-terminal domain of ErbB-2, whereas the former represents the ectodomain and part of the cytoplasmic domain. Degradation of the carboxyl-terminal fragment is prevented by proteasome inhibitors, whereas degradation of the membrane-anchored 135-kDa ErbB-2 fragment is blocked by inhibitors of the endocytosis-dependent degradation pathway. Confocal microscopy studies confirm a geldanamycin-induced localization of ErbB-2 on intracellular vesicles.

关键词： 3T3细胞苯醌类结合部位 COS细胞电泳聚丙烯酰氨凝胶酶抑制剂/药理学内酰胺类大环肽碎片/代谢蛋白酪氨酸激酶类/拮抗剂和抑制剂醌类/药理学受体表皮生长因子/代谢受体 erbB-2/代谢重组融合蛋白质类/代谢构效关系肿瘤细胞培养的动物女(雌)性人类小鼠

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Ligand discrimination in signaling through an ErbB4 receptor homodimer

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第26期275卷 19803-19807页

作者： Sweeney, C Lai, C Riese, DJ Diamonti, AJ Cantley, LC Carraway, KL Harvard Univ Sch Med Dept Cell Biol Boston MA 02215 USA Harvard Inst Med Beth Israel Deaconess Med Ctr Div Signal Transduct Boston MA 02215 USA Scripps Res Inst Res Inst Dept Neuropharmacol La Jolla CA 92037 USA Purdue Univ Dept Med Chem & Mol Pharmacol W Lafayette IN 47907 USA

The epidermal growth factor (EGF)-like family of growth factors elicits cellular responses by stimulating the dimerization, autophosphorylation, and tyrosine kinase activities of the ErbB family of receptor tyrosine kinases, Although several different EGF-like ligands are capable of binding to a single ErbB family member, it is generally thought that the biological and biochemical responses of a single receptor dimer to different ligands are indistinguishable. To test whether an ErbB receptor dimer is capable of discriminating among ligands we have examined the effect of four EGF-like growth factors on signaling through the ErbB4 receptor homodimer in CEM/HER4 cells, a transfected human T cell line ectopically expressing ErbB4 in an ErbB-null background. Despite stimulating similar levels of gross receptor tyrosine phosphorylation, the EGF-like growth factors betacellulin, neuregulin-1 beta, neuregulin-2 beta, and neuregulin-3 exhibited different biological potencies in a cellular growth assay. Moreover, the different ligands induced different patterns of recruitment of intracellular signaling proteins to the activated receptor and induced differential usage of intracellular kinase signaling cascades. Finally, two-dimensional phosphopeptide mapping of ligand-stimulated ErbB4 revealed that the different growth factors induce different patterns of receptor tyrosine phosphorylation, These results indicate that ErbB4 activation by growth factors is not generic and suggest that individual ErbB receptors can discriminate between different EGF-like ligands within the context of a single receptor dimer. More generally, our observations significantly modify our understanding of signaling through receptor tyrosine kinases and point to a number of possible models for ligand-mediated signal diversification.

关键词：细胞系二聚作用电泳聚丙烯酰氨凝胶生长物质/药理学配体模型生物学磷酸转移酶类/代谢受体表皮生长因子/代谢重组融合蛋白质类/代谢信号传导酪氨酸/代谢人类

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Epidermal growth factor signaling pathway influences retinoid metabolism by reduction of retinyl ester hydrolase activities in normal and malignant keratinocytes

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JOURNAL OF CELLULAR PHYSIOLOGY 2000年第2期183卷 265-272页

作者： Jurukovski, V Simon, M SUNY Stony Brook Dept Oral Biol & Pathol Stony Brook NY 11794 USA SUNY Stony Brook Dept Dermatol Stony Brook NY 11794 USA

The effects of EGFR signaling on retinol metabolism were evaluated in the squamous cell carcinoma cell lines defective in LRAT, In a 24-h incubation, the presence of EGF resulted in a 20-25% increase in retinyl ester accumulation. Assessment of retinol esterification and retinyl ester utilization (hydrolysis), in cell cultures and in cell homogenates, revealed that the increase in retinyl ester mass was the result of a reduction in retinyl ester hydrolysis. When grown in the absence of EGF, the cultures used about 40% of their retinyl esters, compared to about 21% in cultures grown with EGF. Th is effect of EGF was blocked by an EGF receptor-neutralizing antibody, an EGF receptor tyrosine-kinase inhibitor (PD153035), and a specific inhibitor of MEK kinase influencing the mitogen-activated protein kinase (MAPK) cascade (PD98059). Both transcription and translation were required, suggesting that signaling from the EGF receptor through the MAPK cascade controls the expression of modulators or inhibitors of the retinyl ester hydrolase(s). Thus EGFR signaling can alter the intracellular concentration of retinol by suppressing the access to the retinyl ester pool. Similar EGF effects were seen in cultures of normal keratinocytes. (C) 2000 Wiley-Liss, Inc.

关键词：羧酸酯水解酶类/拮抗剂和抑制剂羧酸酯水解酶类/代谢细胞系表皮生长因子/代谢表皮生长因子/药理学基因 ras 角蛋白细胞/药物作用角蛋白细胞/代谢丝裂原激活蛋白激酶类/代谢蛋白质生物合成维生素A酸类/代谢信号传导转录遗传肿瘤细胞培养的维生素A/代谢人类

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Characterization of hPRP4 kinase activation: potential role in signaling

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2000年第2期271卷 456-463页

作者： Huang, Y Deng, TL Winston, BW Univ Calgary Dept Med Calgary AB T2N 4N1 Canada Univ Calgary Dept Biochem & Mol Biol Div Crit Care Med Calgary AB T2N 4N1 Canada Univ Calgary Immunol Res Grp Calgary AB T2N 4N1 Canada Univ Florida Coll Med Dept Biochem & Mol Biol Gainesville FL 32610 USA

Mitogen-activated protein kinases (MAPKs) and cyclin-dependent kinases (CDKs) are important proline-directed Ser/Thr kinases that play distinct roles in cell differentiation and proliferation. hPRP4 (pre-mRNA processing gene), a human homologue of S. pombe Prp4, is a recently isolated CDK-like kinase with homology to MAPKs. Little is known about the mRNA processing function of hPRP4 or about the signaling pathways with which it is associated. hPRP4 is expressed in a variety of human tissues with the highest expression in the brain, lung and liver. In this paper, we characterize the activation of hPRP4 in COS-7 cells and show that hPRP4 also possesses a transcription factor activation function. hPRP4 is activated by epidermal growth factor (EGF) or forskolin treatment, but not tetradecanoyl phorbol acetate (TPA) nor ultraviolet (UV) irradiation. Activated hPRP4 phosphorylates residue Thr-417 on Elk-1 resulting in Elk-l activation. This site of Elk-1 phosphorylation is distinct from that of other MAPKs. Coexpression of hPRP4 with an Elk-1 reporter construct causes trans activation of the reporter. These findings suggest that hPRP4, a CDK-Like kinase related to MAPKs, may play a distinct role in signal transduction in ad dition to its role in mRNA processing. (C) 2000 Academic Press.

关键词：印迹法 RNA COS细胞 DNA结合蛋白质类酶激活表皮生长因子/代谢福司柯林/代谢基因文库萤光素酶类/代谢诱变定点磷酰化沉淀素试验蛋白质丝氨酸苏氨酸激酶/遗传学蛋白质丝氨酸苏氨酸激酶/代谢原癌基因蛋白质类/代谢核糖核蛋白 U4-U6小核/遗传学核糖核蛋白 U4-U6小核/代谢信号传导苏氨酸/代谢组织分布转录因子转染 ets结构域蛋白Elk1 动物人类

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Heparin-binding EGF-like growth factor is up-regulated in the obstructed kidney in a cell- and region-specific manner and acts to inhibit apoptosis

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AMERICAN JOURNAL OF PATHOLOGY 2000年第3期156卷 889-898页

作者： Nguyen, HT Bride, SH Badawy, AB Adam, RM Lin, JQ Orsola, A Guthrie, PD Freeman, MR Peters, CA Childrens Hosp Dept Urol Urol Lab Boston MA 02115 USA Harvard Univ Sch Med Dept Surg Boston MA 02115 USA

The expression of certain growth factors in the epidermal growth factor (EGF) family is altered in response to renal injury. Recent studies have demonstrated that heparin binding EGF-like growth factor (HB-EGF) expression may be cytoprotective in response to apoptotic signals. The purpose of this study was to investigate the potential role of HB-EGF in the upper urinary tract following unilateral ureteral obstruction. We present evidence that: i) ureteral obstruction induced cell-specific but transient activation of HB-EGF gene expression;ii) HB-EGF expression in renal epithelial cells increased under conditions where mechanical deformation, such as that caused by hydronephrotic distension, induces apoptosis,but HB-EGF expression did not increase in renal pelvis smooth muscle cells under identical conditions;and iii) enforced expression of HB-EGF served to protect renal epithelial cells from stretch-induced apoptosis. These results suggest a potential mechanism by which the kidney protects itself from apoptosis triggered by urinary tract obstruction.

关键词：肌动蛋白类/代谢细胞凋亡细胞培养的 DNA碎片裂 DNA引物/化学疾病模型动物表皮生长因子/遗传学表皮生长因子/代谢上皮细胞/代谢上皮细胞/病理学免疫酶技术胞间信号肽类和蛋白质类角蛋白质类/代谢肾皮质/代谢肾皮质/病理学亮氨酰氨肽酶/代谢肌平滑/代谢肌平滑/病理学 RNA 信使/代谢大鼠 Zucker 逆转录聚合酶链反应转染增量调节输尿管梗阻/代谢输尿管梗阻/病理学 γ-谷氨酰转移酶/代谢动物女(雌)性人类小鼠大鼠

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Parathyroid hormone activates mitogen-activated protein kinase in opossum kidney cells

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ENDOCRINOLOGY 1999年第12期140卷 5771-5779页

作者： Cole, JA Univ Missouri Sch Med Dept Pharmacol Columbia MO 65212 USA

Many G protein-coupled receptor agonists activate p42/p44 mitogen-activated protein kinase (MAPK), using signaling pathways that are a function of receptor, G protein-coupled, and effector complement. In opossum kidney (OK) cells, activation of endogenous PTH receptors caused a time- (peak within 15-30 min, sustained for similar to 2 h) and dose-dependent (EC50 similar to 3 X 10(-10) M) activation of MAPK. Immunoblot analysis with an activation- specific MAPK antibody indicated that PTH activated both p42 and p44 MAPK. Epidermal growth factor (EGF) also activated p42 and p44MAPK in a time- (peak at 5 min, return to basal within 2 h) and dose-dependent (EC50 similar to 3 ng/ml) fashion. PTH-dependent MAPK activation was mimicked by the protein kinase C activator (PKC) phorbol myristate acetate (PMA), and the protein kinase A activators 8 bromo-cAMP (8-Br-cAMP) and forskolin but was not affected by pertussis toxin pretreatment. PMA or 8-Br-cAMP pretreatment blocked MAPK activation by reexposure to each kinase activator but caused no significant reduction in MAPK activation by PTH. MAPK activation by PTH, EGF, and 8-Br-cAMP was inhibited by the MAPK kinase inhibitor PD98059 and an EGF receptor (EGFR)-selective inhibitor tyrphostin AG1478. AG1478 also blocked MAPK activation by insulin-like growth factor-1 and platelet-derived growth factor. EGF and PTH caused time- and AG1478-sensitive phosphorylation of the EGFR, but EGFR desensitization did not affect MAPK activation by PTH. EGF, PMA, and low doses of PTH (10(12) to 10(-9) M) stimulated while 8-Br-cAMP and high doses of PTH (10(-8) to 10(-6) M) inhibited [H-3]thymidine uptake. These data demonstrate that PTH activates MAPK and suggest that PKC, protein kinase A, and the EGFR play roles in PTH signaling. The biphasic effect of PTH on DNA synthesis suggests that MAPK activation by the hormone leads to distinct cellular responses.

关键词： 8-溴环腺苷一磷酸/药理学细胞培养的 DNA/生物合成酶激活/药物作用酶抑制剂/药理学表皮生长因子/药理学肾/酶学丝裂原活化蛋白激酶1/代谢丝裂原活化蛋白激酶3 丝裂原激活蛋白激酶类/代谢负鼠甲状旁腺素/药理学磷酰化磷酸酪氨酸/代谢蛋白酪氨酸激酶类/拮抗剂和抑制剂受体表皮生长因子/代谢十四酰佛波乙酯/药理学动物

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Heregulin enhances regenerative proliferation in postnatal rat utricular sensory epithelium after ototoxic damage

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JOURNAL OF NEUROCYTOLOGY 1999年第10-11期28卷 901-912页

作者： Zheng, JL Frantz, G Lewis, AK Sliwkowski, M Gao, WQ Genentech Inc Dept Neurosci San Francisco CA 94080 USA Genentech Inc Dept Pathol San Francisco CA 94080 USA Genentech Inc Dept Mol Oncol San Francisco CA 94080 USA

Hair cell loss due to acoustic and ototoxic damage often leads to hearing and balance impairments. Although a spontaneous event in chicks and lower vertebrates, hair cell replacement occurs at a much lower frequency in mammals presumably due to a very low rate of supporting cell proliferation following injury. We report here that heregulin, a member of the neuregulin family, dramatically enhances proliferation of supporting cells in postnatal rat utricular epithelial sheet cultures after gentamicin treatment, as revealed by bromo-deoxyuridine (BrdU) immunocytochemistry. A dose-dependent study shows that the maximal effects of heregulin are achieved at 3 nM. The mitogenic effects of heregulin are confirmed in utricular whole mount cultures. Autoradiography of the utricular whole mount cultures shows that heregulin also enhances the number of tritiated thymidine-labeled cells within the hair cell layer. TaqMan quantitative RT-PCR analysis and immunocytochemistry reveal that heregulin and its binding receptors (ErbB-2, ErbB-3 and ErbB-4) are expressed in the inner ear sensory epithelium. Of several ligands activating various ErbB receptors, including heregulin, neuregulin-3, beta-cellulin, heparin binding-epidermal growth factor (HB-EGF), transforming growth factor-alpha (TGF-alpha) and EGF, heregulin shows the most potent mitogenic effects on supporting cells. Because neuregulin-3 that signals only through ErbB-4 does not show an effect, these data suggest that activation of the ErbB-2-ErbB-3 heterodimeric complexes, rather than ErbB-4, is critical for the proliferative response in the utricular sensory epithelium. In addition, gentamicin treatment induces an upregulation of heregulin mRNA. Considered together, heregulin may play an important role in hair cell regeneration following ototoxic damage.

关键词：细胞计数/药物作用细胞分裂/药物作用细胞培养的剂量效应关系药物内耳/代谢上皮细胞/细胞学上皮细胞/药物作用上皮细胞/代谢基因表达/药物作用庆大霉素类/药理学毛细胞听觉/细胞学毛细胞听觉/药物作用迷路支持细胞/细胞学迷路支持细胞/药物作用配体有丝分裂原/代谢有丝分裂原/毒性神经调节蛋白1/遗传学神经调节蛋白1/代谢神经调节蛋白1/药理学 RNA 信使/生物合成大鼠 Wistar 受体表皮生长因子/遗传学受体表皮生长因子/代谢受体 erbB-2/遗传学受体 erbB-2/代谢受体 erbB-3/遗传学受体 erbB-3/代谢再生/药物作用再生/生理学球囊和椭圆囊/细胞学球囊和椭圆囊/药物作用球囊和椭圆囊/代谢胸苷/代谢增量调节/药物作用动物大鼠

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Molecular mechanism for the Shp-2 tyrosine phosphatase function in promoting growth factor stimulation of Erk activity

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MOLECULAR AND CELLULAR BIOLOGY 2000年第5期20卷 1526-1536页

作者： Shi, ZQ Yu, DH Park, M Marshall, M Feng, GS Indiana Univ Sch Med Dept Biochem & Mol Biol Indianapolis IN 46202 USA Indiana Univ Sch Med Walther Oncol Ctr Indianapolis IN 46202 USA Walther Canc Inst Indianapolis IN 46202 USA McGill Univ Royal Victoria Hosp Mol Oncol Grp Dept Med Montreal PQ H3A 1A1 Canada McGill Univ Royal Victoria Hosp Mol Oncol Grp Dept Oncol Montreal PQ H3A 1A1 Canada McGill Univ Royal Victoria Hosp Mol Oncol Grp Dept Biochem Montreal PQ H3A 1A1 Canada

We have previously shown that activation of extracellular signal-regulated kinase (Erk) by epidermal growth factor (EGF) treatment was significantly decreased in mouse fibroblast cells expressing a mutant Shp-2 molecule lacking 65 amino acids in the SH2-N domain, Shp-2(Delta 46-110). To address the molecular mechanism for the positive role of Shp-2 in mediating Erk induction, we evaluated the activation of signaling components upstream of Erk in Shp-2 mutant cells, EGF-stimulated Ras, Raf, and Mek activation was significantly attenuated in Shp-2 mutant cells, suggesting that Shp-2 acts to promote Ras activation or to suppress the down-regulation of activated Ras. Biochemical analyses indicate that upon EGF stimulation, Shp-2 is recruited into a multiprotein complex assembled on the Gab1 docking molecule and that Shp-2 seems to exert its biological function by specifically dephosphorylating an unidentified molecule of 90 kDa in the complex. The mutant Shp-2(Delta 46-110) molecule failed to participate in the Gab1-organized complex for dephosphorylation of p90, correlating with a defective activation of the Ras-Raf-Mek-Erk cascade in EGF-treated Shp-2 mutant cells. Evidence is also presented that Shp-2 does not appear to modulate the signal relay from EGF receptor to Ras through the Shc, Grb2, and Sos proteins. These results begin to elucidate the mechanism of Shp-2 function downstream of a receptor tyrosine kinase to promote the activation of the Ras-Erk pathway, with potential therapeutic applications in cancer treatment.

关键词：细胞系表皮生长因子/代谢细胞内信号肽和蛋白质类 MAP激酶信号系统丝裂原激活蛋白激酶类/代谢多蛋白复合物蛋白质酪氨酸磷酸酶非受体11型蛋白酪氨酸磷酸酶非受体6型蛋白质酪氨酸磷酸酶类/代谢信号传导 ras蛋白质类/代谢动物小鼠

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