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A nuclear factor, ASC-2, as a cancer-amplified transcriptional coactivator essential for ligand-dependent transactivation by nuclear receptors in vivo

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第48期274卷 34283-34293页

作者： Lee, SK Anzick, SL Choi, JE Bubendorf, L Guan, XY Jung, YK Kallioniemi, OP Kononen, J Trent, JM Azorsa, D Jhun, BH Cheong, JH Lee, YC Meltzer, PS Lee, JW NHGRI Canc Genet Branch NIH Bethesda MD 20892 USA Pusan Natl Univ Coll Pharm Pusan 609735 South Korea Kwangju Inst Sci & Technol Dept Life Sci Kwangju 500303 South Korea Chonnam Natl Univ Ctr Ligand & Transcript Kwangju 500757 South Korea Chonnam Natl Univ Hormone Res Ctr Kwangju 500757 South Korea

Many transcription coactivators interact with nuclear receptors in a ligand- and C-terminal transactivation function (AF2)-dependent manner. We isolated a nuclear factor (designated ASC-2) with such properties by using the ligand-binding domain of retinoid X receptor as a bait in a yeast two-hybrid screening. ASC-2 also interacted with other nuclear receptors, including retinoic acid receptor, thyroid hormone receptor, estrogen receptor alpha, and glucocorticoid receptor, basal factors TFIIA and TBP, and transcription integrators CBP/p300 and SRC-1. In transient cotransfections, ASC-2, either alone or in conjunction with CBP/p300 and SRC-1, stimulated ligand dependent transactivation by wild type nuclear receptors but not mutant receptors lacking the AF2 domain. Consistent with an idea that ASC-2 is essential for the nuclear receptor function in vivo, microinjection of anti-ASC-2 antibody abrogated the ligand-dependent transactivation of retinoic acid receptor, and this repression was fully relieved by coinjection of ASC-2-expression vector. Surprisingly, ASC-2 was identical to a gene previously identified during a search for genes amplified and overexpressed in breast and other human cancers. From these results, we concluded that ASC-2 is a bona fide transcription coactivator molecule of nuclear receptors, and its altered expression may contribute to the development of cancers.

关键词：氨基酸序列克隆分子基因扩增基因表达基因表达调控肿瘤组蛋白酰基转移酶细胞内信号肽和蛋白质类配体分子序列数据肿瘤/遗传学核蛋白质类/遗传学核蛋白质类/代谢核受体共激活因子1 核受体共激活因子类卵母细胞/代谢蛋白质结合受体胞质和核/遗传学受体胞质和核/代谢受体胞质和核/生理学重组融合蛋白质类/遗传学重组融合蛋白质类/代谢序列比对反式激活因子类/遗传学反式激活因子类/代谢反式激活因子类/生理学转录因子/遗传学转录因子/代谢转录因子/生理学转录激活/遗传学肿瘤细胞培养的双杂交系统技术爪蟾属动物人类

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A conserved nuclear receptor consensus sequence (DR-4) mediates transcriptional activation of the chicken CYP2H1 gene by phenobarbital in a hepatoma cell line

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13362-13369页

作者： Handschin, C Meyer, UA Univ Basel Bioctr Dept Pharmacol Neurobiol CH-4056 Basel Switzerland

Phenobarbital-responsive DNA elements were identified in the 5'-flanking region of the chicken CYP2H1 gene by in reporter gene assays in a chicken hepatoma cell line (leghorn male hepatoma (LMH)), A 264-base pair (bp) enhancer sequence (phenobarbital-responsive unit (PBRU)) responded to phenobarbital and a variety of phenobarbital-type inducers. Analysis of putative transcription factor binding sites within the 264-bp element revealed a nuclear receptor half-site repeat (DR-4) neighboring a putative nuclear factor-1 site. This motif resembles phenobarbital response elements in the flanking regions of three phenobarbital-inducible genes, rat CYP2B2, mouse Cyp2b10 and human CYP2B6. Activation of the 264-bp element was eliminated after site-directed mutagenesis of the DR-4 hexamer half-sites. Evidence for evolutionary conservation of this recognition site was indicated by activation in LMH cells of a mouse Cyp2b10 phenobarbital-responsive enhancer by the same spectrum of inducers that activate the CYP2H1 264-bp PBRU. Inhibition of this activation by okadaic acid may explain the reported inhibitory effects on induction of CYP2B1/2 and Cyp2b10 by this phosphatase inhibitor. We show that this inhibition occurs directly on the 264-bp PBRU, whereas the proximal promoter of CYP2H1 is induced by okadaic acid in reporter gene assays. These experiments exploit the unique phenobarbital inducibility of the hepatoma-derived cell line LMH.

关键词：碱基序列保守序列细胞色素P450酶系统/遗传学兴奋性氨基酸拮抗剂/药理学基因表达调控酶学/药物作用基因表达调控肿瘤/药物作用肝肿瘤实验性/遗传学分子序列数据苯巴比妥/药理学受体胞质和核/遗传学序列比对转录激活/药物作用肿瘤细胞培养的动物人类男(雄)性小鼠大鼠

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The interaction of calmodulin with alternatively spliced isoforms of the type-I inositol trisphosphate receptor

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第4期275卷 2305-2311页

作者： Lin, C Widjaja, J Joseph, SK Thomas Jefferson Univ Sch Med Dept Pathol & Cell Biol Philadelphia PA 19107 USA

A 592-amino acid segment of the regulatory domain of the neuronal type-I inositol 1,4,5-trisphosphate receptor (IP3R) isoform (type-I long, amino acids1314-1905) and the corresponding 552-amino acid alternatively spliced form present in peripheral tissues (type-I short, amino acids 1693-1733 deleted) were expressed as glutathione S-transferase fusion proteins. These domains encompass a putative calmodulin (CaM) binding domain and two protein kinase A phosphorylation sites. Both long and short fusion proteins retained the ability to bind CaM in a Ca2+-dependent manner as measured by CaM-Sepharose chromatography or a dansyl-CaM fluorescence assay. Both assays indicated that the short fusion protein bound twice the amount of CaM than the long form at saturating concentrations of CaM. In addition, the binding of the short form to CaM-Sepharose was inhibited by phosphorylation with protein kinase A, whereas the binding of the long form was unaffected. Full-length cDNAs encoding type-I long, type-I short, and type-III IP3R isoforms were expressed in COS cells, and the Ca2+ sensitivity of [H-3]IP, binding to permeabilized cells was measured. The type-I long isoform was more sensitive to Ca2+ inhibition (IC50 = 0.55 mu M) than the type-I short (IC50 = 5.7 mu M) Or the type-III isoform (IC50 = 3 mu M). In agreement with studies on the fusion proteins, the full-length type-I short bound more CaM-Sepharose, and this binding was inhibited to a greater extent by protein kinase A phosphorylation than the type-I long IP3R. Although type-III IP(3)Rs did not bind directly to CaM-Sepharose, hetero-oligomers of type-I/III DP,Rs retained the ability to interact with CaM. We conclude that the deletion of the SII splice site in the type-I IP3R results in the differential regulation of the alternatively spliced isoforms by Ca2+, CaM, and protein kinase A.

关键词：选择性剪接结合部位生物聚合物 COS细胞钙/代谢钙通道/遗传学钙通道/代谢钙调蛋白/代谢细胞培养的肌醇1 4 5-三磷酸受体配体磷酰化蛋白质亚型/遗传学蛋白质亚型/代谢受体胞质和核/遗传学受体胞质和核/代谢重组融合蛋白质类/代谢转染动物大鼠

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Degradation of the peroxisome proliferator-activated receptor γ is linked to ligand-dependent activation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第24期275卷 18527-18533页

作者： Hauser, S Adelmant, G Sarraf, P Wright, HM Mueller, E Spiegelman, BM Dana Farber Canc Inst Boston MA 02115 USA Harvard Univ Sch Med Dept Cell Biol Boston MA 02115 USA

The nuclear hormone receptor peroxisome proliferator-activated receptor (PPAR) gamma is a ligand-activated transcription factor that regulates several crucial biological processes such as adipogenesis, glucose homeostasis, and cell growth. It is also the functional receptor for a new class of insulin-sensitizing drugs, the thiazolidinediones, now widely used in the treatment of type 2 diabetes mellitus. Here we report that PPAR gamma protein levels are significantly reduced in adipose cells and fibroblasts in response to specific ligands such as thiazolidinediones. Studies with several doses of different ligands illustrate that degradation of PPAR gamma correlates well with the ability of ligands to activate this receptor. However, analyses of PPAR gamma mutants show that, although degradation does not strictly depend on the transcriptional activity of the receptor, it is dependent upon the ligand-gated activation function 2 (AF2) domain. Proteasome inhibitors inhibited the down-regulation of PPAR gamma and ligand activation enhanced the ubiquitination of this receptor. These data indicate that, although ligand binding and activation of the AF2 domain increase the transcriptional function of PPAR gamma, these same processes also induce ubiquitination and subsequent degradation of this receptor by the proteasome.

关键词： 3T3细胞脂细胞/代谢半胱氨酸内肽酶类/代谢电泳聚丙烯酰氨凝胶配体多酶复合物/代谢蛋白酶体内肽酶复合物 RNA 信使/代谢受体胞质和核/遗传学受体胞质和核/代谢反式激活(遗传学) 转录因子/遗传学转录因子/代谢转染动物小鼠

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Peroxisomal targeting signal-1 receptor protein PEX5 from Leishmania donovani -: Molecular, biochemical, and immunocytochemical characterization

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13637-13644页

作者： Jardim, A Liu, W Zheleznova, E Ullman, B Oregon Hlth & Sci Univ Dept Biochem & Mol Biol Portland OR 97201 USA

The human pathogens of the Leishmania and Trypanosoma genera compartmentalize glycolytic and other key metabolic pathways in unique subcellular microbodies called glycosomes, organelles related to the peroxisomes of mammals and yeast. The molecular machinery that carries out the specific targeting of glycosomal proteins to the organelle has not been characterized, although the bulk of glycosomal proteins contain the COOH-terminal tripeptide glycosomal peroxisomal targeting signal-1 (PTS-1) similar to the mammalian and fungal peroxisomal targeting signal. To characterize the mechanisms of glycosomal targeting, the gene encoding PEX5, designated LdPEX5, has been isolated from Leishmania donovani. LdPEX5 encodes a 625-amino acid protein with a molecular mass of 69.7 kDa. Like its homologs in yeast and humans, LdPEX5 predicts a protein with seven copies of a tetratricopeptide repeat in its COOH-terminal half proposed to mediate PTS-1 binding and three copies of a WXXX(Y/F) motif in its NH2 terminus conjectured to be essential for protein translocation into the organelle. LdPEX5 was overexpressed in Escherichia coli and purified to homogeneity for binding experiments and generation of antibodies. Recombinant LdPEX5 bound xanthine phosphoribosyltransferase (XPRT), a PTS-1 containing glycosomal protein with a K-D of 4.2 nM, but did not bind an XPRT in which the PTS-1 had been deleted. Moreover, binding studies with the COOH-terminal half of the LdPEX5 confirmed that this portion of the PEX5 protein was capable of binding the XPRT PTS-1 with an affinity of 17.3 nM. Confocal microsocopy revealed that LdPEX5 was predominantly in the cytosolic milieu, and genetic analysis implied that LdPEX5 was an essential gene.

关键词：氨基酸序列克隆分子杜氏利什曼原虫/代谢分子序列数据受体胞质和核/分析受体胞质和核/遗传学受体胞质和核/代谢序列比对序列分析动物人类

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Role of PPARγ in regulating a cascade expression of cyclin-dependent kinase inhibitors, p18(INK4c) and p21(Waf1/Cip1), during adipogenesis

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第24期274卷 17088-17097页

作者： Morrison, RF Farmer, SR Boston Univ Sch Med Dept Biochem Boston MA 02118 USA

Molecular mechanisms coupling growth arrest and cell differentiation were examined during adipogenesis, Data are presented that document a cascade expression of members of two independent families of cyclin-dependent kinase inhibitors that define distinct states of growth arrest during 3T3-L1 preadipocyte differentiation. Exit from the cell cycle into a pre-differentiation state of post-mitotic growth arrest was characterized by significant increases in p21 and p27, During onset of irreversible growth arrest associated with terminal differentiation, the level of p21 declined with a concomitant, dramatic increase in p18 and a sustained level of p27, The expression of p18 and p21, regulated at the level of protein and mRNA accumulation, was directly coupled to differentiation. Stable cell lines were engineered to express adipogenic transcription factors to examine the active role of trans-acting elements in regulating these cell cycle inhibitors. Ectopic expression of peroxisome proliferator-activated receptor (PPAR) gamma in non-precursor fibroblastic cell lines resulted in conversion to adipocytes and a coordinated increase in p18 and p21 mRNA and protein expression in a PPAR gamma ligand-associated manner. These data demonstrate a role for PPAR gamma in mediating the differentiation-dependent cascade expression of cyclin-dependent kinase inhibitors, thereby providing a molecular mechanism coupling growth arrest and adipocyte differentiation.

关键词： 3T3细胞脂细胞/细胞学 CCAAT增强子结合蛋白类载体蛋白质类/代谢细胞周期细胞周期蛋白质类细胞分化周期素依赖激酶抑制剂p18 周期素依赖激酶抑制剂p21 细胞周期蛋白质依赖激酶类/拮抗剂和抑制剂细胞周期蛋白类/代谢 DNA结合蛋白质类/生物合成酶抑制剂基因表达调控小鼠近交BALBC 模型生物学核蛋白质类/生物合成 RNA 信使/代谢受体胞质和核/遗传学受体胞质和核/代谢重组蛋白质类/代谢转录因子/遗传学转录因子/代谢转录遗传肿瘤抑制蛋白质类动物小鼠

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Retina-specific nuclear receptor: A potential regulator of cellular retinaldehyde-binding protein expressed in retinal pigment epithelium and Mailer glial cells

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 1999年第26期96卷 15149-15154页

作者： Chen, F Figueroa, DJ Marmorstein, AD Zhang, Q Petrukhin, K Caskey, CT Austin, CP Merck Res Labs Dept Human Genet West Point PA 19486 USA

In an effort to identify nuclear receptors important in retinal disease, we screened a retina cDNA library for nuclear receptors. Here we describe the identification of a retina-specific nuclear receptor (RNR) from both human and mouse. Human RNR is a splice variant of the recently published photoreceptor cell-specific nuclear receptor [Kobayashi, M., Takezawa, S., Hara, K,, Yu, R. T,, Umesono, Y,, Agata, K., Taniwaki, M., Yasuda, K, & Umesono, K. (1999) Proc. Natl. Acad. Sci. USA 96, 4814-4819] whereas the mouse RNR is a mouse ortholog. Northern blot and reverse transcription-PCR analyses of human mRNA samples demonstrate that RNR is expressed exclusively in the retina, with transcripts of approximate to 7.5 kb, approximate to 3.0 kb, and approximate to 2.3 kb by Northern blot analysis. In situ hybridization with multiple probes on both primate and mouse eye sections demonstrates that RNR is expressed in the retinal pigment epithelium and in Muller glial cells. By using the Gal4 chimeric receptor/reporter cotransfection system, the ligand binding domain of RNR was found to repress transcriptional activity in the absence of exogenous ligand, Gel mobility shift assays revealed that RNR can interact with the promoter of the cellular retinaldehyde binding protein gene in the presence of retinoic acid receptor (RAR) and/or retinoid X receptor (RXR), These data raise the possibility that RNR acts to regulate the visual cycle through its interaction with cellular retinaldehyde binding protein and therefore may be a target for retinal diseases such as retinitis pigmentosa and age-related macular degeneration.

关键词：选择性剪接载体蛋白质类/生物合成克隆分子基因表达调控猕猴分子序列数据神经胶质/代谢孤儿核受体眼色素上皮/代谢启动区遗传蛋白质结合受体胞质和核/遗传学受体胞质和核/代谢视网膜/代谢序列分析 DNA 组织分布转录因子转染动物人类小鼠

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The acute phase response is associated with retinoid X receptor repression in rodent liver

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第21期275卷 16390-16399页

作者： Beigneux, AP Moser, AH Shigenaga, JK Grunfeld, C Feingold, KR Univ Calif San Francisco Dept Vet Affairs Med Ctr Dept Med Metab Sect 111FMed Serv San Francisco CA 94121 USA

The acute phase response (APR) is associated with decreased hepatic expression of many proteins involved in lipid metabolism. The nuclear hormone receptors peroxisome proliferator-activated receptor alpha (PPAR alpha) and liver X receptor (LXR) play key roles in regulation of hepatic lipid metabolism. Because heterodimerization with RXR is crucial for their action, we hypothesized that a decrease in RXR may be one mechanism to coordinately down-regulate gene expression during APR. We demonstrate that lipopolysaccharide (LPS) induces a rapid, dose-dependent decrease in RXR alpha, RXR beta, and RXR gamma proteins in hamster liver. Maximum inhibition was observed at 4 h for RXR alpha (62%) and RXR beta (50%) and at 2 h for RXR gamma (61%). These decreases were associated with a marked reduction in RXR alpha, RXR beta, and RXR gamma mRNA levels. Increased RNA degradation is likely responsible for the repression of RXR, because LPS did not decrease RXR beta and RXR gamma transcription and only marginally inhibited (38%) RXR alpha transcription. RXR repression was associated with decreased LXR alpha and PPAR alpha mRNA levels and reduced ***, *** and *** binding activities in nuclear extracts. Furthermore, LPS markedly decreased both basal and Wy-14,643-induced expression of acyl-CoA synthetase, a well characterized PPAR alpha target. The reduction in hepatic RXR levels alone or in association with other nuclear hormone receptors could be a mechanism for coordinately inhibiting the expression of multiple genes during the APR.

关键词：急相反应/遗传学急相反应/代谢仓鼠亚科细胞因子类/药理学 DNA结合蛋白质类二聚作用基因表达调控/药物作用脂多糖类/药理学肝/代谢金仓鼠 RNA 信使/代谢受体胞质和核/遗传学受体胞质和核/代谢受体维甲酸/遗传学受体维甲酸/代谢维甲类X受体时间因素转录因子/遗传学转录因子/代谢动物男(雄)性

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Peroxisome proliferator-activated receptor α negatively regulates the vascular inflammatory gene response by negative cross-talk with transcription factors NF-κB and AP-1

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第45期274卷 32048-32054页

作者： Delerive, P De Bosscher, K Besnard, S Vanden Berghe, W Peters, JM Gonzalez, FJ Fruchart, JC Tedgui, A Haegeman, G Staels, B Inst Pasteur Dept Atherosclerose U325 INSERM F-59019 Lille France Univ Lille 2 Fac Pharm F-59000 Lille France Univ Ghent Mol Biol Lab B-9000 Ghent Belgium VIB B-9000 Ghent Belgium INSERM U141 F-75745 Paris 10 France NCI Dept Mol Carcinogenesis NIH Bethesda MD 20892 USA

Interleukin-6 (IL-6) is a pleiotropic cytokine, whose plasma levels are elevated in inflammatory diseases such as atherosclerosis. We have previously reported that peroxisome proliferator-activated receptor alpha (PPAR alpha) Ligands (fibrates) lower elevated plasma concentrations of IL-6 in patients with atherosclerosis and inhibit IL-1-stimulated IL-6 secretion by human aortic smooth muscle cells (SMC). Here, we show that aortic explants isolated from PPAR alpha-null mice display an exacerbated response to inflammatory stimuli, such as li popolysaccharide (LPS), as demonstrated by increased IL-6 secretion. Furthermore, fibrate treatment represses IL-6 mRNA levels in LPS-stimulated aortas of PPAR alpha wild-type, but not of PPAR alpha-null mice, demonstrating a role for PPAR alpha in this fibrate action. in human aortic SMC, fibrates inhibit IL-1-induced IL-6 gene expression. Furthermore, activation of PPAR alpha represses both c-Jun- and p65-induced transcription of the human IL-6 promoter. Transcriptional interference between PPAR alpha and both c-Jun and p65 occurs reciprocally, since c-Jun and p65 also inhibit PPAR alpha-mediated activation of a PPAR response element-driven promoter. This transcriptional interference occurs independent of the promoter context as demonstrated by cotransfection experiments using PPAR alpha, p65, and c-Jun Gal4 chimeras. Overexpression of the transcriptional coactivator cAMP-responsive element-binding protein-binding protein (CBP) does not relieve PPAR alpha-mediated transcriptional repression of p65 and c-Jun, Finally, glutathione S-transferase pull-down experiments demonstrate that PPAR alpha physically interacts with c-dun, p65, and CBP. Altogether these data indicate that fibrates inhibit the vascular inflammatory response via PPAR alpha by interfering with the NF-kappa B and AP-1 transactivation capacity involving direct protein-protein interaction with p65 and c-Jun.

关键词： COS细胞 cAMP反应元件结合蛋白质/代谢减量调节白细胞介素1/药理学白细胞介素6/遗传学脂多糖类/药理学 NF-κB/生理学静脉炎/遗传学启动区遗传受体胞质和核/遗传学受体胞质和核/生理学转录因子AP-1/生理学转录因子/遗传学转录因子/生理学转录遗传转染动物人类男(雄)性小鼠

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Function of GATA transcription factors in preadipocyte-adipocyte transition

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SCIENCE 2000年第5489期290卷 134-138页

作者： Tong, Q Dalgin, G Xu, HY Ting, CN Leiden, JM Hotamisligil, GS Harvard Univ Sch Publ Hlth Div Biol Sci Boston MA 02115 USA Harvard Univ Sch Publ Hlth Dept Nutr Boston MA 02115 USA

Genes that control the early stages of adipogenesis remain largely unknown. Here, we show that murine GATA-2 and GATA-3 are specifically expressed in white adipocyte precursors and that their down-regulation sets the stage for terminal differentiation. Constitutive GATA-2 and GATA-3 expression suppressed adipocyte differentiation and trapped cells at the preadipocyte stage. This effect is mediated, at least in part, through the direct suppression of peroxisome proliferator-activated receptor gamma. GATA-3-deficient embryonic stem cells exhibit an enhanced capacity to differentiate into adipocytes, and defective GATA-2 and GATA-3 expression is associated with obesity. Thus, GATA-2 and GATA-3 regulate adipocyte differentiation through molecular control of the preadipocyte-adipocyte transition.

关键词： 3T3细胞脂细胞/细胞学脂细胞/代谢脂肪组织/细胞学脂肪组织/代谢脂肪组织棕色/细胞学脂肪组织棕色/代谢细胞分化细胞培养的 DNA结合蛋白质类/化学 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/代谢 GATA2转录因子 GATA3转录因子基因表达突变肥胖症/遗传学肥胖症/代谢启动区遗传受体胞质和核/遗传学受体胞质和核/代谢干细胞/细胞学反式激活因子类/化学反式激活因子类/遗传学反式激活因子类/代谢转录因子/化学转录因子/遗传学转录因子/代谢转录遗传锌指动物小鼠

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