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SOX9 enhances aggrecan gene promoter/enhancer activity and is up-regulated by retinoic acid in a cartilage-derived cell line, TC6

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第15期275卷 10738-10744页

作者： Sekiya, I Tsuji, K Koopman, P Watanabe, H Yamada, Y Shinomiya, K Nifuji, A Noda, M Tokyo Med & Dent Univ Inst Med Res Dept Mol Pharmacol Chiyoda Ku Tokyo 1010062 Japan Tokyo Med & Dent Univ Dept Orthopaed Surg Tokyo 101 Japan Univ Queensland Ctr Cellular & Mol Biol Brisbane Qld 4072 Australia NIDCR Dev Biol Lab NIH Bethesda MD 20892 USA

SOX9 is a transcription factor that plays a key role in chondrogenesis, Aggrecan is one of the major structural components in cartilage;however, the molecular mechanism of aggrecan gene regulation has not yet been fully elucidated, TC6 is a clonal chondrocytic cell line derived from articular cartilage, The purpose of this study was to examine whether SOX9 modulates aggrecan gene expression and to further identify molecules that regulate Sox9 expression in TC6 cells. SOX9 overexpression in TC6 cells enhanced by similar to 3-fold the transcriptional activity of the AgCAT-8 construct containing S-kilobase (kb) promoter/first exon/first intron fragments of the aggrecan gene. SOX9 enhancement of aggrecan promoter activity was lost when we deleted a 4.5-kb fragment from the 3'-end of the 8-kb fragment corresponding to the region including the first intron, In TC6 cells, SOX9 enhanced the transcriptional activity of a reporter construct containing the Sry/Sox consensus sequence >10-fold. SOX9 enhancement of aggrecan gene promoter activity and SOX9 transactivation through the Sry/Sox consensus sequence were not observed in osteoblastic osteosarcoma cells (ROS17/2.8), indicating the dependence on the cellular background. Northern blot analysis indicated that TC6 cells constitutively express Sox9 mRNA at relatively low levels. To examine regulation of Sox9 gene expression, we investigated the effects of calciotropic hormones and cytokines, Among these, retinoic acid (RA) specifically enhanced Sox9 mRNA expression in TC6 cells. The basal levels of Sox9 expression and its enhancement by RA were observed similarly at both permissive (33 degrees C) and nonpermissive (39 degrees C) temperatures. Furthermore, RA treatment enhanced the transcriptional activity of a reporter construct containing the Sry/Sox consensus sequence in TC6 cells. Moreover, RA treatment also enhanced the transcriptional activity of another reporter construct containing the enhancer region of the type II pro

关键词：软骨蛋白聚糖类碱性磷酸酶/遗传学软骨/代谢细胞系增强子元件遗传学细胞外基质蛋白质类基因表达调控/药物作用高迁移率族蛋白质类/生理学外源凝集素类 C型启动区遗传蛋白聚糖类/遗传学 SOX9转录因子类转录因子/生理学转录遗传/药物作用维甲酸/药理学增量调节动物小鼠

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Site-specific incorporation of nucleoside analogs by HIV-1 reverse transcriptase and the template grip mutant P157S - Template interactions influence substrate recognition at the polymerase active site

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第1期275卷 359-366页

作者： Klarmann, GJ Smith, RA Schinazi, RF North, TW Preston, BD Univ Utah Dept Biochem Eccles Inst Human Genet Salt Lake City UT 84112 USA Univ Utah Dept Radiat Oncol Eccles Inst Human Genet Salt Lake City UT 84112 USA Univ Utah Huntsman Canc Inst Salt Lake City UT 84112 USA Emory Univ Sch Med Dept Pediat Decatur GA 30033 USA Emory Univ Sch Med Georgia Vet Affairs Res Ctr AIDS & HIV Invect Decatur GA 30033 USA Univ Calif Davis Ctr Comparat Med Davis CA 95616 USA

Studies of drug-resistant reverse transcriptases (RTs) reveal the roles of specific structural elements and amino acids in polymerase function. To characterize better the effects of RT/template interactions on dNTP substrate recognition, we examined the sensitivity of human immunodeficiency virus type 1 (HIV-1) RT containing a new mutation in a "template grip" residue (P157S) to the 5'-triphosphates of (-)-beta-2',3'-dideoxy-3'-thiacytidine (3TC), (-)-beta-2',3'-dideoxy-5-fluoro-3'-thiacytidine (FTC), and 3'-azido-3'-deoxythymidine (AZT). A primer extension assay was used to monitor quantitatively drug monophosphate incorporation opposite each of multiple target sites. Wild-type and P157S RTs had similar catalytic activities and processivities on heteropolymeric RNA and DNA templates. When averaged over multiple template sites, P157S RT was 2-7-fold resistant to the 5'-triphosphates of 3TC, FTC, and AZT, Each drug triphosphate inhibited polymerization more efficiently on the DNA template compared with an RNA template of identical sequence. Moreover, chain termination by 3TC and FTC was strongly influenced by template sequence context. Incorporation of FTC and 3TC monophosphate varied up to 10-fold opposite 7 different G residues in the DNA template, and the P157S mutation altered this site specificity. In summary, these data identify Pro(157) as an important residue affecting nucleoside analog resistance and suggest that interactions between RT and the template strand influence dNTP substrate recognition at the RT active site. Our findings are discussed within the context of the HIV-1 RT structure.

关键词：催化域胞苷三磷酸/类似物和衍生物胞苷三磷酸/代谢胞苷三磷酸/药理学双脱氧核苷酸类剂量效应关系药物抗药性 HIV逆转录酶/药物作用 HIV逆转录酶/遗传学 HIV逆转录酶/代谢 HIV-1/酶学拉米夫定/类似物和衍生物突变脯氨酸/遗传学逆转录酶抑制剂/代谢逆转录酶抑制剂/药理学硫代核苷类/代谢噻吩类胸腺嘧啶核苷酸类/代谢胸腺嘧啶核苷酸类/药理学转录遗传/药物作用扎昔他宾/类似物和衍生物扎昔他宾/代谢齐多夫定/类似物和衍生物齐多夫定/代谢齐多夫定/药理学

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Activation of guanine nucleotide-binding proteins and induction of endothelial tissue-type plasminogen activator gene transcription by alcohol

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第17期274卷 12055-12060页

作者： Miyamoto, A Yang, SX Laufs, U Ruan, XL Liao, JK Brigham & Womens Hosp Dept Med Div Cardiovasc Boston MA 02115 USA Harvard Univ Sch Med Boston MA 02115 USA Kagoshima Univ Dept Vet Pharmacol Kagoshima 8900065 Japan

The mechanism by which moderate alcohol ingestion lowers the risk of cardiovascular disease is unknown but may be due, in part, to the ability of alcohol to increase the level of tissue-type plasminogen activator (t-PA), Human endothelial cells were treated with low concentrations of ethanol (0.25-25 mM, 0-24 h), which are associated with moderate alcohol consumption. Although treatment with ethanol alone did not affect t-PA gene transcription or mRNA expression, it augmented isoproterenol (LSO)-stimulated t-PA gene transcription and mRNA levels by 3.4- and 2.8-fold, respectively, and decreased plasminogen activator inhibitor-1 mRNA levels by 65%. These effects of ethanol correlated with 2.5- and 6.9-fold increases in ISO-stimulated cyclic AMP levels and 4x-cyclic AMP response element heterologous promoter activity, respectively. To determine whether alcohol-induced changes in agonist-stimulated cyclic AMP levels were because of modulation of guanine nucleotide-binding proteins (G proteins), we assessed the effects of ethanol on G alpha(s) and G alpha(i2). Although ethanol did not affect the expression of G alpha(s) or G alpha(i2), it increased ISO-stimulated G alpha(s) GTPase and GTP binding activity by 2.2 and 2.9-fold and decreased UK14304-stimulated G alpha(i2) GTPase and GTP binding activity by 38 and 80%, These results indicate that treatment with relatively low concentrations of ethanol enhances agonist-stimulated cyclic AMP-dependent t-PA gene transcription in vascular endothelial cells through differential modulation of G protein.

关键词：细胞培养的环AMP/代谢内皮血管/细胞学内皮血管/药物作用内皮血管/酶学酶激活乙醇/药理学 GTP磷酸水解酶类/代谢 GTP结合蛋白质类/代谢基因表达调控酶学/药物作用纤溶酶原激活物抑制物1/遗传学启动区遗传 RNA 信使/遗传学信号传导组织型纤溶酶原激活物/遗传学转录遗传/药物作用动物牛人类

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Transforming growth factor-β1 (TGF-β1) and TGF-β2 decrease expression of CD36, the type B scavenger receptor, through mitogen-activated protein kinase phosphorylation of peroxisome proliferator-activated receptor-γ

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第2期275卷 1241-1246页

作者： Han, JH Hajjar, DP Tauras, JM Feng, JW Gotto, AM Nicholson, AC Cornell Univ Weill Med Coll Dept Pathol New York NY 10021 USA Cornell Univ Weill Med Coll Ctr Vasc Biol New York NY 10021 USA

CD36, the macrophage type B scavenger receptor, binds and internalizes oxidized low density lipoprotein, a hey event in the development of macrophage foam cells within atherosclerotic lesions. Expression of CD36 in monocyte/macrophages is dependent on differentiation status and exposure to soluble mediators. In this study, we investigated the effect of transforming growth factor-beta 1 (TGF-beta 1) and TGF-beta 2 on the expression of CD36 in macrophages, Treatment of phorbol ester-differentiated THP-1 macrophages with TGF-beta 1 or TGF-beta 2 significantly decreased expression of CD36 mRNA and surface protein. TGF-beta 1/TGF-beta 2 also inhibited CD36 mRNA expression induced by oxidized low density lipoprotein and 15-deoxy Delta(12,14) prostaglandin J(2), a peroxisome proliferator-activated receptor (PPAR)-gamma ligand, suggesting that the TGF-beta 1/TGF-beta 2 down-regulated CD36 expression by inactivating PPAR-gamma-mediated signaling. TGF-beta 1/TGF-beta 2 increased phosphorylation of both mitogen-activated protein (MAP) kinase and PPAR-gamma, whereas NAP kinase inhibitors reversed suppression of CD36 wand inhibited PPAR-gamma phosphorylation induced by TGF-beta 1/TGF-beta 2. Finally, MAP kinase inhibitors alone increased expression of CD36 mRNA and surface protein but had no effect on PPAR-gamma protein levels, Our data demonstrate for the first time that TGF-beta 1 and TGF-beta 2 decrease expression of CD36 by a mechanism involving phosphorylation of MAP kinase, subsequent MAP kinase phosphorylation of PPAR-gamma, and a decrease in CD36 gene transcription by phosphorylated PPAR-gamma.

关键词：细胞分化/药物作用细胞系 DNA结合蛋白质类/代谢基因表达调控/药物作用基因表达调控/免疫学巨噬细胞/免疫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/代谢磷酰化 RNA 信使/遗传学受体胞质和核/代谢十四酰佛波乙酯/药理学转录因子/代谢转录遗传/药物作用转化生长因子β/药理学人类

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Inhibition of proliferation and apoptosis by the transcriptional repressor Mad1 -: Repression of Fas-induced caspase-8 activation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第14期275卷 10413-10420页

作者： Gehring, S Rottmann, S Menkel, AR Mertsching, J Krippner-Heidenreich, A Lüscher, B Hannover Med Sch Inst Mol Biol D-30625 Hannover Germany

Mad1 is a member of the Myc/Max/Mad network of transcriptional regulators that play a central role in the control of cellular behavior. Mad proteins are thought to antagonize Myc functions at least in part by repressing gene transcription. To systematically examine the function of Mad1 in growth control and during apoptosis, we have generated U2OS cell clones that express Mad1 under a tetracyline-regulatable promoter (UTA-Mad1). Mad1 was induced rapidly and efficiently, localized to the nucleus, and bound to DNA as a heterodimer with Max. The induction of Mad1 reduced cellular growth and, more profoundly, inhibited colony formation of UTA-Mad1 cells. Conditioned medium neutralized this inhibitory effect implying that Mad1 function is regulated by extracellular signals. In addition Mad1 interfered with Fas-, TRAIL-, and UV-induced apoptosis, which coincided with a reduced activation of caspase-8 during Fas-mediated apoptosis in response to Mad1 expression. Furthermore, microinjection of Mad1-expressing plasmids into fibroblasts inhibited apoptosis induced by the oncoproteins c-Myc and E1A. Thus, Mad1 not only interferes with cellular proliferation but also with apoptosis, which defines a novel aspect of Mad1 function.

关键词： 3T3细胞细胞凋亡/生理学细胞凋亡/辐射效应凋亡调节蛋白质类 COS细胞载体蛋白质类半胱氨酸天冬氨酸蛋白酶8 半胱氨酸天冬氨酸蛋白酶9 半胱氨酸天冬氨酸蛋白酶/遗传学细胞集合细胞周期蛋白质类细胞分裂/生理学细胞分裂/辐射效应细胞系成纤维细胞基因表达调控/药物作用膜糖蛋白类/生理学核蛋白质类癌基因磷蛋白类/遗传学磷蛋白类/代谢重组蛋白质类/代谢阻遏蛋白质类/遗传学阻遏蛋白质类/代谢 TNF相关凋亡诱导配体四环素/药理学转录遗传/药物作用转染肿瘤细胞培养的肿瘤坏死因子α/生理学紫外线动物人类小鼠

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Ecdysone agonist inducible transcription in transgenic tobacco plants

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PLANT JOURNAL 1999年第1期19卷 97-106页

作者： Martinez, A Sparks, C Hart, CA Thompson, J Jepson, I Zeneca Agrochem Jealotts Hill Res Stn Bracknell RG42 6ET Berks England

A novel chemical-induced gene regulatory system for plants consisting of two molecular components is described. The first, or regulatory, cassette comprises a chimeric receptor composed of the hinge and ligand binding domains of the Heliothis virescens ecdysone receptor and the transactivation domain of the Herpes simplex VP16 protein fused to the DNA binding domain and transactivation of a mammalian glucocorticoid receptor. The second component, a reporter cassette, contains six copies of the glucocorticoid response element (GRE) fused to the minimal 35SCaMV promoter and P-glucuronidase. The system uses a commercially available non-steroidal ecdysone agonist, RH5992 (tebufenozide), as an inducer. Activation of gene expression is shown in both tobacco transient protoplasts and transgenic plants. The response is ligand dependent and is modulated by the change in minimal promoter context. The system is capable of inducing transgene activity up to 420-fold corresponding to 150% of the activity observed with positive controls (35SCaMV:GUS).

关键词：碱基序列花椰菜花叶病毒属/遗传学 DNA引物地塞米松/药理学蜕皮激素/激动剂基因报告葡糖醛酸糖苷酶/遗传学肼类/药理学分子序列数据植物基因修饰植物有毒启动区(遗传学) 受体糖皮质激素/遗传学烟草/遗传学转录遗传/药物作用

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The p56^lck-interacting protein p62 stimulates transcription via the SV40 enhancer

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第26期274卷 18278-18284页

作者： Rachubinski, RA Marcus, SL Capone, JP McMaster Univ Dept Biochem Hamilton ON L8N 3Z5 Canada Univ Alberta Dept Cell Biol Edmonton AB T6G 2H7 Canada

p62 is a recently identified ubiquitin-binding, cytosolic phosphoprotein that interacts with several signal transduction molecules including the tyrosine kinase p56(lck) and the protein kinase C-zeta, p62 is therefore suggested to serve an important role in signal transduction in the cell, although the physiological function of p62 remains undefined. Here we demonstrate by transient transfection assays that p62 stimulates the transcription of reporter genes linked to the simian virus 40 (SV40) enhancer. A putative p62-responsive element was localized to the B domain of the distal 72-base pair repeat of the SV40 enhancer. p62 was unable to bind this element in vitro, nor was it able to activate transcription when directly tethered to a promoter, suggesting that p62 stimulates transcription via an indirect mechanism. Stimulation of transcription mediated by p62 was dependent on its amino-terminal region, which is also necessary for interaction with cell surface signaling molecules. These findings indicate that p62 may link extracellular signals directly to transcriptional responses, and identify the SV40 enhancer as a downstream target for signal transduction pathways in which p62 participates.

关键词：衔接蛋白质类信号转导碱基序列结合部位 COS细胞载体蛋白质类/药理学增强子元件遗传学即早蛋白质类/药理学分子序列数据蛋白质类猴病毒40/遗传学构效关系转录因子转录遗传/药物作用转录激活动物人类小鼠

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A phosphatidylinositol 3-kinase/p70 ribosomal S6 protein kinase pathway is required for the regulation by insulin of the p85α regulatory subunit of phosphatidylinositol 3-kinase gene expression in human muscle cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第48期274卷 34005-34010页

作者： Roques, M Vidal, H Univ Lyon 1 Fac Med Rene Laennec INSERM U449 F-69372 Lyon 08 France

Insulin acutely up-regulates p85 alpha phosphatidylinositol 3-kinase (p85 alpha PI 3-K) mRNA levels in human skeletal muscle (Laville, M., Auboeuf, D., Khalfallah, Y., Vega, N., Riou, J, P., and Vidal, H. (1996) J. Clin. Invest. 98, 43-49), In the present work, we attempted to elucidate the mechanism of action of insulin in primary cultures of human muscle cells. Insulin (10(-7) M, 6 h of incubation) induced a a-fold increase in p85aPI3-K mRNA abundances (118 +/- 12 versus 233 +/- 35 amol/mu g total RNA, n = 5, p < 0.01) without changing the expression levels of insulin receptor, IRS-1, glycogen synthase, and Glut 4 mRNAs in differentiated myotubes from healthy subjects. The effect is most probably due to a transcriptional activation of the p85 alpha PI 3-K gene because the half-life of the mRNA was not affected by insulin treatment (4.0 +/- 0.8 versus 3.1 +/- 0.4 h), PD98059 (50 mu M) did not modify the insulin response but increased p85 alpha PI 3-K mRNA levels in the absence of insulin, suggesting that the mitogen-activated protein kinase pathway exerts a negative effect on p85 alpha PI 3-K mRNA expression in the absence of the hormone. On the other hand, the insulin effect was totally abolished by LY294002 (10 mu M) and rapamycin (50 nM). In addition, overexpression of a constitutively active protein kinase B increased p85 alpha PI 3-K mRNA levels. These results indicate that the phosphatidylinositol 3-kinase/PKB/p70S6 kinase pathway is required for the stimulation by insulin of p85 alpha PI 3-K gene expression in human muscle cells.

关键词：细胞培养的色酮类/药理学更生霉素/药理学剂量效应关系药物酶抑制剂/药理学类黄酮物质/药理学基因表达调控酶学/药物作用糖原合成酶/遗传学胰岛素/药理学胰岛素受体底物蛋白质类吗啉类/药理学肌骨骼/细胞学肌骨骼/药物作用肌骨骼/酶学磷酸肌醇3-激酶类/遗传学磷酸肌醇3-激酶类/代谢磷蛋白类/遗传学蛋白质合成抑制药/药理学蛋白质丝氨酸苏氨酸激酶原癌基因蛋白质类/遗传学原癌基因蛋白质类/生理学原癌基因蛋白质c-akt RNA 信使/药物作用 RNA 信使/遗传学 RNA 信使/代谢受体胰岛素/遗传学重组融合蛋白质类/遗传学重组融合蛋白质类/生理学调控序列核酸核糖体蛋白质S6激酶类/遗传学核糖体蛋白质S6激酶类/代谢信号传导西罗莫司/药理学转录遗传/药物作用成年人人类中年人

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Interdependent SMAD and JNK signaling in transforming growth factor-β-mediated transcription

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第52期274卷 37413-37420页

作者： Engel, ME McDonnell, MA Law, BK Moses, HL Vanderbilt Univ Vanderbilt Ingram Canc Ctr Sch Med Nashville TN 37232 USA Vanderbilt Univ Sch Med Dept Cell Biol Nashville TN 37232 USA

SMAD and JNK cascades are essential components of the transforming growth factor-beta (TGF-beta) signaling machinery and are implicated in common transcriptional responses. However, the relationship of these pathways to one another downstream of the TGF-beta receptor complex is unknown. We show that JNK is rapidly activated by TGF-beta in a SMAD-independent manner and phosphorylates Smad3 outside its -SSXS motif. Smad3 phosphorylation by JNK facilitates both its activation by the TGF-beta receptor complex and its nuclear accumulation. JNK regulates SMAD- and TGF-beta-mediated transcriptional responses, yet JNK activators only partially stimulate transcriptional responses characteristic of TGF-beta without coincident SMAD pathway activation. These results suggest an interdependent relationship between the JNK and SMAD pathways in TGF-beta-mediated transcription.

关键词：细胞培养的 DNA结合蛋白质类/生理学 JNK丝裂原活化蛋白激酶类 MAP激酶激酶4 丝裂原活化蛋白激酶3 丝裂原激活蛋白激酶激酶类/生理学丝裂原激活蛋白激酶类/生理学磷酰化纤溶酶原激活物抑制物1/生物合成 Smad2蛋白质 Smad3蛋白质反式激活因子类/生理学转录遗传/药物作用转化生长因子β/药理学 ρAGTP结合蛋白质/生理学

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Platelet-derived growth factor induces interleukin-6 transcription in osteoblasts through the activator protein-1 complex and activating transcription factor-2

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第10期274卷 6783-6789页

作者： Franchimont, N Durant, D Rydziel, S Canalis, E St Francis Hosp & Med Ctr Res Dept Worcester MA 01605 USA St Francis Hosp & Med Ctr Dept Med Worcester MA 01605 USA Univ Connecticut Sch Med Farmington CT 06030 USA

Platelet-derived growth factor (PDGF) BE, a mitogen that stimulates bone resorption, increases the expression of interleukin-6 (IL-6), a cytokine that induces osteoclast recruitment. The mechanisms involved in IL-6 induction by PDGF BE are poorly understood. We examined the effect of PDGF BE on IL-6 expression in cultures of osteoblasts from fetal rat calvariae (Ob cells). PDGF BE increased IL-6 mRNA and heterogeneous nuclear RNA levels, the rate of transcription, and the activity of base pairs (bp) -2906 to +20 IL-6 promoter fragments transiently transfected into Ob cells. Deletion analysis revealed two responsive regions, one containing an activator protein-1 (AP-1) site located between bp -276 and -257, and a second, less well defined, downstream of -257. Targeted mutations of a cyclic AMP-responsive element (CRE), and nuclear factor-IL-6 and nuclear factor-kappa B binding sites in a bp -257 to +20 IL-6 construct that was transfected into Ob cells, revealed that the CRE also contributed to IL-6 promoter induction by PDGF BE. Electrophoretic mobility shift assay revealed AP-1 and CRE nuclear protein complexes that were enhanced by PDGF BE. Supershift assays revealed binding of Jun and Fos to AP-1 and CRE sequences and binding of activating transcription factor-a to CRE. In conclusion, PDGF BE induces IL-6 transcription in osteoblasts by regulating nuclear proteins of the AP-1 complex and activating transcription factor-2.

关键词：转录激活因子2 cAMP反应元件结合蛋白质/遗传学 cAMP反应元件结合蛋白质/代谢白细胞介素6/生物合成白细胞介素6/遗传学成骨细胞/代谢血小板源性生长因子/药理学 RNA 信使/分析 RNA 信使/生物合成信号传导/药物作用信号传导/遗传学转录因子AP-1/遗传学转录因子AP-1/代谢转录因子/遗传学转录因子/代谢转录遗传/药物作用动物大鼠

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