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Hydrogen peroxide activates p70^S6k signaling pathway

JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第46期274卷 32596-32602页

作者： Bae, GU Seo, DW Kwon, HK Lee, HY Hong, S Lee, ZW Ha, KS Lee, HW Han, JW Sungkyunkwan Univ Coll Pharm Dept Biochem Suwon 440746 South Korea Sungkyunkwan Univ Coll Life Sci & Nat Resources Dept Genet Engn Suwon 440746 South Korea Konyang Univ Coll Med Dept Pharmacol Nonsan 320711 South Korea Korea Basic Sci Inst Biomol Res Grp Taejon 305333 South Korea

We investigated a possible role of reactive oxygen species (ROS) in p70(S6k) activation, which plays an important role in the progression of cells from G(0)/G(1) to S phase of the cell cycle by translational up-regulation of a family of mRNA transcripts that encode for components of the protein synthetic machinery. Treatment of mouse epidermal cell JB6 with H2O2 generated extracellularly by glucose/glucose oxidase led to the activation of p70(S6k) and p90(Rsk) and to phosphorylation of p42(MAPK)/p44(MAPK) The activation of p70(S6k) and p90(Rsk) was dose-dependent and transient, maximal activities being in extracts treated for 15 and 30 min, respectively. Further characterization of ROS-induced activation of p70S6k using specific inhibitors for p70S6k Signaling pathway, rapamycin, and wortmannin revealed that ROS acted upstream of the rapamycin-sensitive component FRAP/RAFT and wortmannin-sensitive component phosphatidylinositol 3-kinase, because both inhibitors caused the inhibition of ROS-induced p70(S6k) activity. In addition, Ca2+ chelation also inhibited ROS-induced activation of p70S6k, indicating that Ca2+ is a mediator of p70(S6k) activation by ROS. However, down-regulation of 12-O-tetradecanoylphorbol-13-acetate (TPA)-responsive protein kinase C (PKC) by chronic pretreatment with TPA or a specific PHC inhibitor Re-31-8220 did not block the activation of p70S6k by ROS, indicating that the activation of TPA-responsive PHC was not required for stimulation of p70(S6k) activity by H2O2 in JB6 cells. Exposure of JB6 cells to platelet-derived growth factor or epidermal growth factor led to a rapid increase in H2O2, phosphorylation, and activation of p70(S6k), which were antagonized by the pretreatment of catalase. Taken together, the results suggest that ROS act as a messenger in growth factor-induced p70(S6k) signaling pathway.

关键词：雄二烯类/药理学钙/代谢过氧化氢酶/药理学细胞系酶激活表皮生长因子/药理学基因表达调控酶学/药物作用过氧化氢/药理学吲哚类/药理学小鼠近交BALBC 丝裂原激活蛋白激酶类/代谢磷酰化血小板源性生长因子/药理学蛋白激酶C/拮抗剂和抑制剂活性氧/代谢核糖体蛋白质S6激酶类/遗传学核糖体蛋白质S6激酶类/代谢信号传导/药物作用西罗莫司/药理学十四酰佛波乙酯/药理学动物小鼠

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Vinexin forms a signaling complex with Sos and modulates epidermal growth factor-induced c-Jun N-terminal kinase/stress-activated protein kinase activities

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第50期274卷 35933-35937页

作者： Akamatsu, M Aota, S Suwa, A Ueda, K Amachi, T Yamada, KM Akiyama, SK Kioka, N Kyoto Univ Grad Sch Agr Div Appl Life Sci Sakyo Ku Kyoto 6068502 Japan Biomol Engn Res Inst Suita Osaka 565 Japan NIDCR Craniofacial Dev Biol & Regenerat Branch NIH Bethesda MD 20892 USA NIEHS Mol Carcinogenesis Lab NIH Res Triangle Pk NC 27709 USA

Vinexin, a novel protein that plays a hey role in cell spreading and cytoskeletal organization, contains three SH3 domains and binds to vinculin through its first and second SH3 domains. We show here that the third SH3 domain binds to Sos, a guanine nucleotide exchange factor for Pas and Pac, both in vitro and in vivo. Point mutations in the third SH3 domain abolished the vinexin-Sos interaction. Stimulation of NIH/3T3 cells with serum, epidermal growth factor (EGF), or platelet derived growth factor (PDGF) decreased the electro phoretic mobility of Sos and concomitantly inhibited formation of the vinexin-Sos complex. Phosphatase treatment of lysates restored the binding of Sos to vinexin, suggesting that signaling from serum, EGF, or PDGF regulates the vinexin-Sos complex through the Sos phosphorylation. To evaluate the function of vinexin downstream of growth factors, we examined the effects of wild-type and mutant vinexin expression on extracellular signal-regulated kinase (Erk) and c-Jun N-terminal kinase/stress activated protein kinase (JNK/SAPK) activation in response to EGF. Exogenous expression of vinexin beta in NIH/3T3 cells enhanced JNK/SAPK activation but did not affect Erk activation. Moreover mutations in the third SH3 domain abolished EGF activation of JNK/SAPK in a dominant-negative fashion, whereas they slightly stimulated Erk. Together these results suggest that vinexin can selectively modulate EGF-induced signal transduction pathways leading to JNK/SAPK kinase activation.

关键词： 3T3细胞色谱法亲和表皮生长因子/药理学 JNK丝裂原活化蛋白激酶类动力学丝裂原激活蛋白激酶类/代谢肌蛋白质类/化学肌蛋白质类/分离和提纯肌蛋白质类/代谢磷酰化血小板源性生长因子/药理学点突变重组融合蛋白质类/代谢信号传导 SOS蛋白质类/化学 SOS蛋白质类/分离和提纯 SOS蛋白质类/代谢转染 src同源域动物小鼠

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Role of endocytosis in the activation of the extracellular signal-regulated kinase cascade by sequestering and nonsequestering G protein-coupled receptors

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第4期97卷 1489-1494页

作者： Pierce, KL Maudsley, S Daaka, Y Luttrell, LM Lefkowitz, RJ Duke Univ Med Ctr Howard Hughes Med Inst Durham NC 27710 USA Duke Univ Med Ctr Dept Med Durham NC 27710 USA Duke Univ Med Ctr Dept Surg Durham NC 27710 USA Duke Univ Med Ctr Dept Biochem Durham NC 27710 USA

Acting through a number of distinct pathways, many G protein-coupled receptors (GPCRs) activate the extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK) cascade. Recently, it has been shown that in some cases, clathrin-mediated endocytosis is required for GPCR activation of the ERK/MAPK cascade, whereas in others it is not. Accordingly, we compared ERK activation mediated by a GPCR that does not undergo agonist-stimulated endocytosis, the alpha(2A) adrenergic receptor (alpha(2A) AR), with ERK activation mediated by the beta(2) adrenergic receptor (beta(2) AR), which is endocytosed. Surprisingly, we found that in COS-7 cells, ERK activation by the alpha(2A) AR, like that mediated by both the beta(2) AR and the epidermal growth factor receptor (EGFR), is sensitive to mechanistically distinct inhibitors of clathrin-mediated endocytosis, including monodansylcadaverine. a mutant dynamin I, and a mutant beta-arrestin 1. Moreover, we determined that, as has been shown for many other GPCRs, both alpha(2A) and beta(2) AR-mediated ERK activation involves transactivation of the EGFR, Using confocal immunofluorescence microscopy, we found that stimulation of the beta(2) AR, the alpha(2A) AR, or the EGFR each results in internalization of a green fluorescent protein-tagged EGFR. Although beta(2) AR stimulation leads to redistribution of both the beta(2) AR and EGFR, activation of the alpha(2A) AR leads to redistribution of the EGFR but the alpha(2A) AR remains on the plasma membrane. These findings separate GPCR endocytosis from the requirement for clathrin-mediated endocytosis in EGFR transactivation-mediated ERK activation and suggest that it is the receptor tyrosine kinase or another downstream effector that must engage the endocytic machinery.

关键词：肾上腺素能α激动剂/药理学 COS细胞网格蛋白/代谢胞吞作用酶抑制剂表皮生长因子/药理学荧光抗体技术 GTP结合蛋白质类/代谢异丙肾上腺素/药理学丝裂原激活蛋白激酶类/代谢磷酰化喹唑啉类喹恶啉类/药理学受体肾上腺素能α/代谢受体肾上腺素能β/代谢受体细胞表面/代谢转染酪氨酸磷酸化抑制剂/药理学动物

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Constitutive and growth factor-regulated phosphorylation of caveolin-1 occurs at the same site (Tyr-14) in vivo:: Identification of a c-Src/Cav-1/Grb7 signaling cassette

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MOLECULAR ENDOCRINOLOGY 2000年第11期14卷 1750-1775页

作者： Lee, H Volonte, D Galbiati, F Iyengar, P Lublin, DM Bregman, DB Wilson, MT Campos-Gonzalez, R Bouzahzah, B Pestell, RG Scherer, PE Lisanti, MP Yeshiva Univ Albert Einstein Coll Med Dept Mol Pharmacol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Albert Einstein Canc Ctr Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Cell Biol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Pathol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Dev & Mol Biol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Med Bronx NY 10461 USA Washington Univ Sch Med Dept Pathol St Louis MO 63110 USA BD Transduct Labs Lexington KY 40511 USA

Caveolin-1 was first identified as a phosphoprotein in Rous sarcoma virus (RSV)-transformed chicken embryo fibroblasts. Tyrosine 14 is now thought to be the principal site for recognition by c-Src kinase;however, little is known about this phosphorylation event. Here, we generated a monoclonal antibody (mAb) probe that recognizes only tyrosine 14-phosphorylated caveolin-1. Using this approach, we show that caveolin-1 (Y14) is a specific tyrosine kinase substrate that is constitutively phosphorylated in Src- and Abl-transformed cells and transiently phosphorylated in a regulated fashion during growth factor signaling. We also provide evidence that tyrosine-phosphorylated caveolin-1 is localized at the major sites of tyrosine-kinase signaling, i.e. focal adhesions. By analogy with other signaling events, we hypothesized that caveolin-1 could serve as a docking site for pTyr-binding molecules. In support of this hypothesis, we show that phosphorylation of caveolin-1 on tyrosine 14 confers binding to Grb7 (an SH2-domain containing protein) both in vitro and in vivo. Furthermore, we demonstrate that binding of Grb7 to tyrosine 14-phosphorylated caveolin-1 functionally augments anchorage-independent growth and epidermal growth factor (EGF)-stimulated cell migration. We discuss the possible implications of our findings in the context of signal transduction.

关键词： 3T3细胞脂细胞/药物作用氨基酸序列抗体单克隆/药理学细胞质膜微囊/代谢窖蛋白1 细胞质膜微囊蛋白/遗传学细胞质膜微囊蛋白/免疫学细胞质膜微囊蛋白/代谢细胞黏附/生理学细胞分裂/生理学细胞运动/生理学表皮生长因子/药理学 GRB7衔接蛋白质生长物质/代谢胰岛素/代谢胰岛素/药理学脂类代谢小鼠近交BALBC 分子序列数据磷酰化/药物作用蛋白质类/代谢受体表皮生长因子/代谢信号传导酪氨酸/代谢钒酸盐类/药理学 src族激酶类/代谢动物女(雌)性人类小鼠

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Tumor necrosis factor α-mediated insulin resistance, but not dedifferentiation, is abrogated by MEK1/2 inhibitors in 3T3-L1 adipocytes

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MOLECULAR ENDOCRINOLOGY 2000年第10期14卷 1557-1569页

作者： Engelman, JA Berg, AH Lewis, RY Lisanti, MP Scherer, PE Yeshiva Univ Albert Einstein Coll Med Dept Cell Biol Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Ctr Diabet Res & Training Bronx NY 10461 USA Yeshiva Univ Albert Einstein Coll Med Dept Mol Pharmacol Bronx NY 10461 USA

Tumor necrosis factor-alpha (TNF alpha) has been implicated as a contributing mediator of insulin resistance observed in pathophysiological conditions such as obesity, cancer-induced cachexia, and bacterial infections. Previous studies have demonstrated that TNF alpha confers insulin resistance by promoting phosphorylation of serine residues on insulin receptor substrate 1 (IRS-1), thereby diminishing subsequent insulin-induced tyrosine phosphorylation of IRS-1. However, little is known about which signaling molecules are involved in this process in adipocytes and about the temporal sequence of events that ultimately leads to TNF alpha-stimulated IRS-1 serine phosphorylation. In this study, we demonstrate that specific inhibitors of the MAP kinase kinase (MEK)1/2-p42/44 mitogen-activated protein (MAP) kinase pathway restore insulin signaling to normal levels despite the presence of TNF alpha. Additional experiments show that MEK1/2 activity is required for TNF alpha-induced IRS-1 serine phosphorylation, thereby suggesting a mechanism by which these inhibitors restore insulin signaling. We observe that TNF alpha requires 2.5-4 h to markedly reduce insulin-triggered tyrosine phosphorylation of IRS-1 in 3T3-L1 adipocytes. Although TNF alpha activates p42/44 MAP kinase, maximal stimulation is observed within 10-30 min. To our surprise, p42/44 activity returns to basal levels well before IRS-1 serine phosphorylation and insulin resistance are observed. These activation kinetics suggest a mechanism of p42/44 action more complicated than a direct phosphorylation of IRS-1 triggered by the early spike of TNF alpha-induced p42/44 activity. Chronic TNF alpha treatment (>> 72 h) causes adipocyte dedifferentiation, as evidenced by the loss of triglycerides and down-regulation of adipocyte-specific markers. We observe that this longer term TNF alpha-mediated dedifferentiation effect utilizes alternative, p42/44 MAP kinase-independent intracellular pathways. This study suggests th

关键词： 3T3细胞脂细胞/细胞学脂细胞/药物作用茴香霉素/药理学细胞分化/药物作用酶抑制剂/药理学表皮生长因子/药理学类黄酮物质/药理学胰岛素/药理学胰岛素抗药性动力学 MAP激酶激酶1 MAP激酶激酶2 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激酶类/拮抗剂和抑制剂丝裂原激活蛋白激酶类/代谢磷蛋白类/代谢磷酸丝氨酸/代谢磷酸酪氨酸/代谢蛋白质丝氨酸苏氨酸激酶/拮抗剂和抑制剂蛋白酪氨酸激酶类/拮抗剂和抑制剂信号传导肿瘤坏死因子α/药理学动物小鼠

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Growth hormone-induced alteration in ErbB-2 phosphorylation status in 3T3-F442A fibroblasts

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第50期274卷 36015-36024页

作者： Kim, SO Houtman, JCD Jiang, J Ruppert, JI Bertics, PJ Frank, SJ Univ Alabama Birmingham Dept Med Div Endocrinol & Metab Birmingham AL 35294 USA Univ Alabama Birmingham Dept Med Div Hematol Oncol Birmingham AL 35294 USA Univ Alabama Birmingham Dept Cell Biol Birmingham AL 35294 USA Vet Adm Med Ctr Birmingham AL 35294 USA Univ Wisconsin Sch Med Dept Biomol Chem Madison WI 53706 USA

The growth hormone receptor (GHR), a cytokine receptor superfamily member, requires the JAK2 tyrosine kinase for signaling. We now examine functional interactions between growth hormone (GH) and epidermal growth factor (EGF) in 3T3-F442A fibroblasts. Although EGF enhanced ErbB-2 tyrosine phosphorylation, GH, while causing retardation of its migration on SDS-polyacrylamide gel electrophoresis, decreased ErbE-2's tyrosine phosphorylation, GH-induced retardation was reversed by treatment of anti-ErbB-2 precipitates with both alkaline phosphatase and protein phosphatase 2A suggesting that GH induced serine/threonine phosphorylation of ErbB-2. Both GH-induced shift in ErbB-2 migration and GH-induced MAP kinase activation were unaffected by a protein kinase C inhibitor but were blocked by the mitogen-activated protein kinase/extracellular signal-regulated kinase kinase 1 (MEK1) inhibitor, PD98059. Notably, leukemia inhibitory factor, but not interferon-gamma, also promoted ErbB-2 shift and mitogen-activated protein kinase activation. Cotreatment with EGF and GH versus EGF alone resulted in a 35% decline in acute ErbB-2 tyrosine 1248 autophosphorylation, a marked decline (approximately 50%) in DNA synthesis, and substantially decreased cyclin D1 expression. We conclude that in 3T3-F442A cells, 1) the GH-induced decrease in ErbB-2 tyrosine phosphorylation correlates with MEK1/mitogen-activated protein kinase activity and 2) GH antagonizes EGF induced DNA synthesis and cyclin D1 expression in a pattern consistent with its alteration in ErbB-2 phosphorylation status.

关键词： 3T3细胞碱性磷酸酶/代谢抗体细胞周期蛋白D1/遗传学表皮生长因子/药理学基因表达调控/药物作用生长抑制物/药理学人生长激素/药理学白细胞介素6 Janus激酶2 白血病抑制因子淋巴因子/药理学丝裂原激活蛋白激酶类/代谢磷蛋白磷酸酶类/代谢磷酰化磷酸酪氨酸/代谢蛋白质磷酸酶2 蛋白酪氨酸激酶类/代谢原癌基因蛋白质类受体 erbB-2/代谢重组蛋白质类/药理学动物人类小鼠

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A long-term culture of human hepatocytes which show a high growth potential and express their differentiated phenotypes

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第1期256卷 184-191页

作者： Hino, H Tateno, C Sato, H Yamasaki, C Katayama, S Kohashi, T Aratani, A Asahara, T Dohi, K Yoshizato, K Hiroshima Univ Fac Sci Dept Biol Sci Hiroshima 7398526 Japan ERATO JST Yoshizato MorphoMatrix Project Hiroshima 7398526 Japan Hiroshima Univ Sch Med Dept Surg 2 Minami Ku Hiroshima 7340037 Japan Hiroshima Prefectural Inst Ind Sci & Technol Joint Res Project Reg Intens Hiroshima Tissue Regenerat Project Hiroshima 7390046 Japan

The present study succeeded for the first time in cultivating for more than 2 months human normal hepatocytes which showed a high growth potential and expressed their differentiated phenotypes. Constituents of culture medium were critical for this culture, and the medium optimized for their growth contained fresh human serum, fetal bovine serum, Swiss 3T3-cell conditioned medium, L-ascorbic acid a-phosphate, epidermal growth factor, nicotinamide, and dimethyl sulfoxide. Hepatocytes steadily replicated and formed colonies which continued to increase in size up to around 35 days. The number of hepatocytes in the most replicative colonies increased 17-fold during 31 days. Cells in colonies expressed normal differentiated hepatocytic phenotypes for as long as 35 days. These hepatocytes retained normal liver functions at least for 70 days such as to secrete albumin, and to metabolize lidocaine and D-galactose. (C) 1999 Academic Press.

关键词： 3T3细胞白蛋白类/分析白蛋白类/分泌抗坏血酸/类似物和衍生物抗坏血酸/药理学生物学标记/分析血蛋白质类/药理学细胞培养技术/方法细胞分化/药物作用细胞分裂/药物作用细胞大小/药物作用细胞存活/药物作用细胞培养的培养基条件性 DNA/生物合成二甲亚砜/药理学表皮生长因子/药理学半乳糖/代谢利多卡因/代谢肝/细胞学肝/药物作用肝/代谢肝/分泌烟酰胺/药理学时间因素成年人老年人动物女(雌)性人类男(雄)性小鼠中年人

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The effect of cytokines on the proliferation and migration of bovine meniscal cells

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AMERICAN JOURNAL OF SPORTS MEDICINE 1999年第5期27卷 636-643页

作者： Bhargava, MM Attia, ET Murrell, GAC Dolan, MM Warren, RF Hannafin, JA Cornell Univ Med Ctr New York Hosp Hosp Special SurgLab Soft Tissue Res New York NY 10021 USA

We determined the effect of cytokines on the proliferation and migration of cells isolated from the inner-third (white-white), middle-third (red-white), and outer-third (red-red) regions of bovine meniscus. Cells from the outer, or peripheral, region of the meniscus exhibited higher DNA synthesis in the presence of 10% serum compared with cells from the inner or central regions. Recombinant human platelet-derived growth factor-AB, hepatocyte growth factor/scatter factor, and bone morphogenic protein-2 stimulated DNA synthesis of all meniscal cells in a dose-dependent manner, with a two- to threefold maximal stimulation at 10 ng/ml. Cell migration was also stimulated by addition of cytokines. Platelet-derived growth factor and hepatocyte growth factor caused an increase in the migration of cells derived from all three zones, while interleukin-1 selectively stimulated the migration of outer-zone meniscal cells. Epidermal growth factor was much less effective and stimulated the migration of cells in the inner and outer zones by 40% to 50%, while bone morphogenic protein-2 and insulin-like growth factor-1 stimulated the migration of meniscal cells from the middle zone by 40% to 50%. The identification of cytokines that stimulate both the growth and migration of meniscal cells may provide new tools for modulation of meniscal healing.

关键词：骨形态发生蛋白质类/药理学细胞分裂细胞运动细胞培养的软骨细胞/细胞学细胞因子类/药理学 DNA/生物合成剂量效应关系药物表皮生长因子/药理学成纤维细胞生长因子/药理学成纤维细胞/细胞学肝细胞生长因子/药理学胰岛素样生长因子Ⅰ/药理学胰岛素样生长因子Ⅱ/药理学白细胞介素1/药理学半月板胫骨/细胞学血小板源性生长因子/药理学放射性药物/诊断应用重组蛋白质类转化生长因子β/药理学氚/诊断应用动物牛人类

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Impact of bovine oocyte maturation media on oocyte transcript levels, blastocyst development, cell number, and apoptosis

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BIOLOGY OF REPRODUCTION 2000年第2期62卷 355-364页

作者： Watson, AJ De Sousa, P Caveney, A Barcroft, LC Natale, D Urquhart, J Westhusin, ME Univ Western Ontario Dept Obstet & Gynaecol London ON N6A 5C1 Canada Univ Western Ontario Dept Physiol London ON N6A 5C1 Canada Texas A&M Univ Coll Vet Med Dept Vet Physiol & Pharmacol College Stn TX 77843 USA

The objectives were 1) to investigate the effects of oocyte maturation in serum-free and amino acid-supplemented defined media on oocyte transcript levels, blastocyst cell number, and apoptosis;2) to investigate the influence of oocyte maturation culture atmosphere on blastocyst development, total cell number, and apoptosis;and 3) to examine the influence of epidermal growth factor (EGF) during oocyte maturation on blastocyst cell number and apoptosis. The results demonstrate that blastocysts derived from in vitro maturation, fertilization, and embryo culture protocols undergo apoptosis but that apoptotic levels are not greatly influenced by the oocyte maturation environment. Amino acid supplementation of oocyte maturation media was associated with enhanced developmental frequencies, increased blastocyst cell number, and elevated oocyte maternal mRNA levels. Oocyte maturation with supplemented synthetic oviduct rFluid medium (cSOFMaa) resulted in blastocyst cell numbers comparable to those observed with Tissue Culture Medium 199 + newborn calf serum. Blastocyst development was reduced following oocyte maturation under a 5% CO2, 7% O-2, 88% N-2 culture atmosphere. EGF supplementation of oocyte maturation medium resulted in a concentration-dependent increase in blastocyst development but did not influence blastocyst total cell number or apoptosis. Our findings indicate that cSOFMaa medium is an effective base medium for bovine oocyte maturation.

关键词：氨基酸类/药理学细胞凋亡/生理学胚泡/细胞学胚泡/生理学细胞计数着色剂培养基无血清 DNA/化学胚胎和胎儿发育/生理学表皮生长因子/药理学受精体外遗传标记图像处理计算机辅助原位缺口末端标记显微镜检查电视卵母细胞/生长和发育卵母细胞/代谢普罗匹定 RNA 信使/分析 RNA 信使/分离和提纯逆转录聚合酶链反应动物牛女(雌)性

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Vav family proteins couple to diverse cell surface receptors

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MOLECULAR AND CELLULAR BIOLOGY 2000年第17期20卷 6364-6373页

作者： Moores, SL Selfors, LM Fredericks, J Breit, T Fujikawa, K Alt, FW Brugge, JS Swat, W Harvard Univ Sch Med Dept Cell Biol Boston MA 02115 USA Harvard Univ Sch Med Dept Genet Boston MA 02115 USA Harvard Univ Sch Med Ctr Blood Res Boston MA 02115 USA Harvard Univ Sch Med Dept Pediat Childrens Hosp Boston MA 02115 USA Harvard Univ Sch Med Howard Hughes Med Inst Boston MA 02115 USA

Vav proteins are guanine nucleotide exchange factors for Rho family GTPases which activate pathways leading to actin cytoskeletal rearrangements and transcriptional alterations. Vav proteins contain several protein binding domains which can link cell surface receptors to downstream signaling proteins. Vav1 is expressed exclusively in hematopoietic cells and tyrosine phosphorylated in response to activation of multiple cell surface receptors. However, it is not known whether the recently identified isoforms Vav2 and Vav3, which are broadly expressed, can couple,vith similar classes of receptors, nor is it known whether all Vav isoforms possess identical functional activities. We expressed Vav1, Vav2, and Vav3 at equivalent levels to directly compare the responses of the Vav proteins to receptor activation. Although each Vav isoform was tyrosine phosphorylated upon activation of representative receptor tyrosine kinases, integrin, and lymphocyte antigen receptors, we found unique aspects of Vav protein coupling in each receptor pathway. Each Vav protein coprecipitated with activated epidermal growth factor and platelet-derived growth factor (PDGF) receptors, and multiple phosphorylated tyrosine residues on the PDGF receptor were able to mediate Vav2 tyrosine phosphorylation, Integrin-induced tyrosine phosphorylation of Vav proteins was net detected in nonhematopoietic cells unless the protein tyrosine kinase Syk was also expressed, suggesting that integrin activation of Vav proteins may be restricted to cell types that express particular tyrosine kinases. In addition, we found that Vav1, but not Vav2 or Vav3, can efficiently cooperate with T-cell receptor signaling to enhance NFAT dependent transcription, while Vav1 and Vav3, but not Vav2, can enhance NF kappa B dependent transcription. Thus, although each Vav isoform can respond to similar cell surface receptors, there are isoform-specific differences in their activation of downstream signaling pathways.

关键词：氨基酸序列 CHO细胞 COS细胞细胞周期蛋白质类细胞系仓鼠亚科 DNA 互补/代谢表皮生长因子/药理学鸟嘌呤核苷酸交换因子类整合素类/代谢 Jurkat细胞分子序列数据癌基因蛋白质类/化学癌基因蛋白质类/代谢磷酰化血小板源性生长因子/药理学蛋白质结合蛋白质亚型蛋白质结构三级原癌基因蛋白质类/化学原癌基因蛋白质类/代谢原癌基因蛋白质c-vav 受体抗原 B细胞/代谢受体抗原 T细胞/代谢受体细胞表面/代谢序列同源性氨基酸信号传导酪氨酸/代谢动物人类小鼠

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