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The PDZ protein TIP-1 interacts with the Rho effector rhotekin and is involved in Rho signaling to the serum response element

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第43期275卷 33962-33968页

作者： Reynaud, C Fabre, S Jalinot, P Ecole Normale Super Lyon CNRS UMR 5665 Lab Biol Mol & Cellulaire F-69364 Lyon 07 France

The human T-cell lymphotrophic virus, type 1 Tax protein can interact via its C terminus with various proteins including a PDZ domain. In this work, one of them, TIP-1, is characterized as a cytoplasmic 14-kDa protein mainly corresponding to one PDZ domain. A two-hybrid screen performed with TIP-1 as bait showed that it interacts with the human homologue of rhotekin that was previously identified in mice as a Rho effector. Both human and mouse rhotekins exhibit at their C termini the sequence QSPV-COOH that matches the X(S/T)XV-COOH consensus known for proteins recognizing PDZ domains. Mutation of the serine and valine residues to alanine impairs interaction of rhotekin with TIP-I. Transient expression experiments with a reporter construct including the c-Fos serum response element (SRE) showed that coexpression of TIP-I with the constitutively active RhoA.V14 mutant and human rhotekin caused a strong activation of the SRE. A negative mutant of Rho, RhoA.N19, was unable to cooperate with TIP-1 and rhotekin, The positive effect of TIP-I was also lost when the C terminus of rhotekin was mutated. These data show that the complex of active Rho with its effector rhotekin bound to TIP-1 produces in the cytoplasm a signal that triggers strong activation of the SRE.

关键词：氨基酸序列 COS细胞载体蛋白质类/生理学克隆分子 DNA结合蛋白质类/生理学基因表达调控谷氨酰胺酶 HeLa细胞细胞内信号肽和蛋白质类 Lim激酶类分子序列数据蛋白激酶类蛋白质丝氨酸苏氨酸激酶/生理学蛋白质类/遗传学蛋白质类/生理学反应元件 ρAGTP结合蛋白质/生理学动物人类

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Interaction of linker for activation of T cells with multiple adapter proteins in platelets activated by the glycoprotein VI-selective ligand, convulxin

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第43期275卷 33427-33434页

作者： Asazuma, N Wilde, JI Berlanga, O Leduc, M Leo, A Schweighoffer, E Tybulewicz, V Bon, C Liu, SK McGlade, CJ Schraven, B Watson, SP Univ Oxford Dept Pharmacol Oxford OX1 3QT England Heidelberg Univ Inst Immunol D-69120 Heidelberg Germany Inst Pasteur Unite Venens F-75724 Paris 15 France Univ Toronto Hosp Sick Children Res Inst Dept Med Biophys Toronto ON M5G 1X8 Canada Natl Inst Med Res Div Cellular Immunol London NW7 1AA England

The snake venom toxin convulxin activates platelets through the collagen receptor glycoprotein VI (GPVI)/Fc receptor gamma -chain (FcR gamma -chain) complex leading to tyrosine phosphorylation and activation of the tyrosine Syk and phospholipase C gamma2 (PLC gamma2), In the present study, we demonstrate that convulxin is a considerably more powerful agonist than collagen or the GPVI-selective collagen-related peptide (CRP), Confirmation that the response to convulxin is mediated solely via Syk was provided by studies on Syk-deficient platelets. The increase in phosphorylation of the FcR gamma -chain is associated with marked increases in tyrosine phosphorylation of downstream proteins including Syk, linker for activation of T cells (LAT), SLP-76, and PLC gamma2, The transmembrane adapter LAT coprecipitates with SLP-76 and PLC gamma2, as well as with a number of other adapter proteins, some of which have not been previously described in platelets, including Cbl, Grb2, Gads, and SKAP-HOM. Cads is constitutively associated with SLP-76 and is probably the protein bridging its association with LAT, There was no detectable association between Grb2 and SLP-76 in control or stimulated cells, suggesting that the interaction of LAT with Grb2 is present in a separate complex to that of LAT Gads SLP-76. These results show that the trimeric convulxin stimulates a much greater phosphorylation of the FcR gamma -chain and subsequent downstream responses relative to CRP and collagen, presumably because of its ability to cause a greater degree of cross-linking of GPVI, The adapter LAT appears to play a critical role in recruiting a number of other adapter proteins to the surface membrane in response to activation of GPVI, presumably at sites of glycolipid-enriched microdomains, enabling an organized signaling cascade that leads to platelet activation.

关键词：衔接蛋白质类信号转导血小板/药物作用血小板/代谢载体蛋白质类/生理学胶原/药理学响尾蛇毒液类/药理学环AMP受体蛋白质/药理学 GRB2衔接蛋白质整合素类/代谢细胞内信号肽和蛋白质类外源凝集素类 C型膜蛋白质类磷蛋白类/生理学磷酰化蛋白质类/生理学受体胶原受体 IgG/生理学 C型磷脂酶类/生理学人类

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Solution structure of BID, an intracellular amplifier of apoptotic signaling

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CELL 1999年第5期96卷 615-624页

作者： Chou, JJ Li, HL Salvesen, GS Yuan, JY Wagner, G Harvard Univ Comm Higher Degrees Biophys Cambridge MA 02138 USA Harvard Univ Sch Med Dept Biol Chem & Mol Pharmacol Boston MA 02115 USA Harvard Univ Sch Med Dept Cell Biol Boston MA 02115 USA Burnham Inst La Jolla CA 92037 USA

We report the solution structure of BID, an intracellular cross-talk agent that can amplify FAS/TNF apoptotic signal through the mitochondria death pathway after Caspase 8 cleavage. BID contains eight alpha helices where two central hydrophobic helices are surrounded by six amphipathic ones. The fold resembles pore-forming bacterial toxins and shows similarity to BCL-X-L although sequence homology to BCL-X-L is limited to the 16-residue BH3 domain. Furthermore, we modeled a complex of BCL-X-L and BID by aligning the BID and BAK BH3 motifs in the known BCL-X-L-BAK BH3 complex. Additionally, we show that the overall structure of BID is preserved after cleavage by Caspase 8. We propose that BID has both BH3 domain-dependent and -independent modes of action in inducing mitochondrial damage.

关键词：氨基酸序列抗原 CD95/生理学细胞凋亡/生理学与BH3相互作用的凋亡激活蛋白质载体蛋白质类/化学载体蛋白质类/生理学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/代谢二聚作用酶激活磁共振波谱学线粒体/生理学模型分子分子序列数据蛋白质构象蛋白质多聚化蛋白质结构三级原癌基因蛋白质c-bcl-2/化学重组融合蛋白质类/化学序列比对序列同源性氨基酸信号传导/生理学溶液构效关系 bcl-X蛋白质人类

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Endophilin/SH3p4 is required for the transition from early to late stages in clathrin-mediated synaptic vesicle endocytosis

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NEURON 1999年第1期24卷 143-154页

作者： Ringstad, N Gad, H Löw, P Di Paolo, G Brodin, L Shupliakov, O De Camilli, P Karolinska Inst Dept Neurosci Nobel Inst Neurophysiol S-17177 Stockholm Sweden Yale Univ Sch Med Howard Hughes Med Inst New Haven CT 06510 USA Yale Univ Sch Med Dept Cell Biol New Haven CT 06510 USA

Endophilin/SH3p4 is a protein highly enriched in nerve terminals that binds the GTPase dynamin and the polyphosphoinositide phosphatase synaptojanin, two proteins implicated in synaptic vesicle endocytosis. We show here that antibody-mediated disruption of endophilin function in a tonically stimulated synapse leads to a block in the invagination of clathrin-coated pits adjacent to the active zone and therefore to a block of synaptic vesicle recycling. Mle also show that in a cell-free system, endophilin is not associated with clathrin coats and is a functional partner of dynamin. Our findings suggest that endophilin is part of a biochemical machinery that acts in trans to the clathrin coat from early stages to vesicle fission.

关键词：衔接蛋白质类信号转导氨基酸序列抗体/药理学秀丽新小杆线虫/遗传学载体蛋白质类/拮抗剂和抑制剂载体蛋白质类/化学载体蛋白质类/生理学无细胞系统网格蛋白/生理学有被小窝细胞膜/生理学动力蛋白质类胞吞作用 GTP磷酸水解酶类/生理学七鳃鳗显微镜检查电子分子序列数据脊髓/化学突触/超微结构突触小泡/代谢突触小泡/超微结构 src同源域动物大鼠

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Inhibition of myogenesis by depletion of the glycogen-associated regulatory subunit of protein phosphatase-1 in rat skeletal muscle cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第34期275卷 26102-26108页

作者： Ragolia, L Zuo, Q Begum, N Winthrop Univ Hosp Diabet Res Lab Mineola NY 11501 USA SUNY Stony Brook Sch Med Stony Brook NY 11794 USA

In this study, we examined the role of the glycogen-associated regulatory subunit of protein phosphatase-l (PP-1(G)) in L6 rat skeletal muscle cell myogenesis. The level of PP-1(G) was depleted by transfection with an inducible antisense oriented PP-1(G) gene. Western blot analysis of the PP-1(G)-depleted cell line revealed a >90% depletion of PP-1(G) protein and a 45% reduction in cellular PP-1 activity and abolished the ability of L6 myoblasts to differentiate into multinucleated myotubes. PP-1(G)-depleted cells also exhibited a marked reduction in the expression of the differentiation marker myogenin as well as creatine kinase. After 7 days in culture, PP-1(G)-depleted cells sustained myoblast levels of inhibitor of differentiation-a, whereas control L6 cells had a severely lower inhibitor of differentiation-a level and progressed into myotubes. Myoblasts were unable to exit the cell cycle, as measured by the impaired induction of p27 cyclin-dependent kinase inhibitor, a >2-fold increase in DNA synthesis, and elevated levels of phosphorylated retinoblastoma protein (pRb). Replacement of the PP-1(G) gene restored PP-1(G) protein expression, PP-1 enzymatic activity, and the ability to differentiate into myotubes. We conclude that PP-1(G) plays a definite role in L6 myogenesis via its regulation of PP-1 catalytic activity.

关键词：载体蛋白质类/遗传学载体蛋白质类/生理学细胞系肌酸激酶/代谢 DNA复制动力学肌肉发育肌骨骼/酶学肌骨骼/生长和发育寡脱氧核糖核苷酸类反义/代谢磷酰化视网膜母细胞瘤蛋白质/代谢转染动物大鼠

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Normal blood pressure and plasma renin activity in mice lacking the renin-binding protein, a cellular renin inhibitor

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第20期275卷 15357-15362页

作者： Schmitz, C Gotthardt, M Hinderlich, S Leheste, JR Gross, V Vorum, H Christensen, EI Luft, FC Takahashi, S Willnow, TE Max Delbruck Ctr Mol Med D-13125 Berlin Germany Free Univ Berlin Dept Mol Biol & Biochem D-13125 Berlin Germany Humboldt Univ Franz Volhardt Clin D-13125 Berlin Germany Aarhus Univ Dept Med Biochem DK-8000 Aarhus C Denmark Aarhus Univ Dept Cell Biol DK-8000 Aarhus C Denmark Akita Res Inst Food & Brewing Akita 0101623 Japan

In renal extracts, some renin is present as "high molecular weight renin," a heterodimeric complex of renin with the 46-kDa renin-binding protein (RnBP), also known as N-acyl-D-glucosamine a-epimerase. Because RnBP specifically inhibits renin activity, the protein was proposed to play an important role in the regulation of the renin-angiotensin system (RAS), Using gene targeting, we have generated mice lacking RnBP and tested this hypothesis in vivo. In particular, we analyzed biosynthesis, secretion, and activity of renin and other components of the RAS in mice lacking RnBP, Despite extensive investigations, we were unable to detect any major effects of RnBP deficiency on the plasma and renal RAS or on blood pressure regulation. Contrary to previous hypotheses, we conclude that RnBP does not play a significant role in the regulation of renin activity in plasma or kidney, However, RnBP knockout mice excrete an abnormal pattern of carbohydrates in the urine, indicating a role of the protein in renal carbohydrate metabolism.

关键词：血压/生理学碳水化合物差向异构酶类/缺乏碳水化合物差向异构酶类/遗传学碳水化合物差向异构酶类/代谢载体蛋白质类/遗传学载体蛋白质类/生理学西拉普利/药理学酶前体/血液基因表达肾/代谢小鼠基因敲除器官特异性参考值肾素/血液肾素/遗传学动物男(雄)性小鼠

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The MAPK kinase kinase TAK1 plays a central role in coupling the interleukin-1 receptor to both transcriptional and RNA-targeted mechanisms of gene regulation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第5期276卷 3508-3516页

作者： Holtmann, H Enninga, J Kälble, S Thiefes, A Dörrie, A Broemer, M Winzen, R Wilhelm, A Ninomiya-Tsuji, J Matsumoto, K Resch, K Kracht, M Hannover Med Sch Inst Pharmacol D-30625 Hannover Germany Nagoya Univ Grad Sch Sci Dept Mol Biol Nagoya Aichi 4648602 Japan

Mechanisms of fulminant gene induction during an inflammatory response were investigated using expression of the chemoattractant cytokine interleukin-8 (IL-8) as a model. Recently we found that coordinate activation ofNF-kappaB and c-Jun N-terminal protein kinase (JNK) is required for strong IL-8 transcription, whereas the p38 MAP kinase (MAPK) pathway stabilizes the IL-8 mRNA It is unclear how these pathways are coupled to the receptor for IL-1, an important physiological inducer of IL-8. Expression of the MAP kinase kinase kinase (MAPKKK) TAK1 together with its coactivator TAB1 in HeLa cells activated all three pathways and was sufficient to induce IL-8 formation, NF-kappaB + JNK2-mediated transcription from a minimal IL-8 promoter, and p38 MAPK-mediated stabilization of a reporter mRNA containing IL-8-derived regulatory mRNA sequences. Expression of a kinase-inactive mutant of TAK1 largely blocked IL-1-induced transcription and mRNA stabilization, as well as formation of endogenous IL-8. Truncated TAB1, lacking the TAK1 binding domain, or a TAK1-derived peptide containing a TAK1 autoinhibitory domain were also efficient in inhibition. These data indicate that the previously described three-pathway model of IL-8 induction is operative in response to a physiological stimulus, IL-1, and that the MAPKKK TAK1 couples the IL-1 receptor to both transcriptional and RNA-targeted mechanisms mediated by the three pathways.

关键词：衔接蛋白质类信号转导载体蛋白质类/遗传学载体蛋白质类/生理学酶激活基因表达调控/生理学珠蛋白类/遗传学珠蛋白类/代谢 HeLa细胞白细胞介素8/生物合成白细胞介素8/遗传学细胞内信号肽和蛋白质类 JNK丝裂原活化蛋白激酶类 MAP激酶激酶4 MAP激酶激酶激酶类/遗传学 MAP激酶激酶激酶类/生理学丝裂原激活蛋白激酶激酶类/代谢丝裂原激活蛋白激酶类/代谢突变 NF-κB/代谢 RNA稳定性 RNA 信使/代谢受体白细胞介素1/生理学受体白细胞介素8A/遗传学受体白细胞介素8A/代谢转录遗传/生理学 p38丝裂原活化蛋白激酶类人类

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Disruption of the sarcoglycan-sarcospan complex in vascular smooth muscle: A novel mechanism for cardiomyopathy and muscular dystrophy

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CELL 1999年第4期98卷 465-474页

作者： Coral-Vazquez, R Cohn, RD Moore, SA Hill, JA Weiss, RM Davisson, RL Straub, V Barresi, R Bansal, D Hrstka, RF Williamson, R Campbell, KP Univ Iowa Coll Med Howard Hughes Med Inst Dept Physiol & Biophys Iowa City IA 52242 USA Univ Iowa Coll Med Dept Neurol Iowa City IA 52242 USA Univ Iowa Coll Med Dept Pathol Iowa City IA 52242 USA Univ Iowa Coll Med Dept Obstet & Gynecol Iowa City IA 52242 USA Dept Vet Affairs Iowa City IA 52242 USA Univ Iowa Dept Anat & Cell Biol Iowa City IA 52242 USA Univ Iowa Dept Internal Med Iowa City IA 52242 USA

To investigate mechanisms in the pathogenesis of cardiomyopathy associated with mutations of the dystrophin-glycoprotein complex, we analyzed genetically engineered mice deficient for either alpha-sarcoglycan (Sgca) or delta-sarcoglycan (Sgcd). We found that only Sgcd null mice developed cardiomyopathy with focal areas of necrosis as the histological hallmark in cardiac and skeletal muscle. Absence of the sarcoglycan-sarcospan (SG-SSPN) complex in skeletal and cardiac membranes was observed in both animal models. Loss of vascular smooth muscle SG-SSPN complex was only detected in Sgcd null mice and associated with irregularities of the coronary vasculature. Administration of a vascular smooth muscle relaxant prevented onset of myocardial necrosis. Our data indicate that disruption of the SG-SSPN complex in vascular smooth muscle perturbs vascular function, which initiates cardiomyopathy and exacerbates muscular dystrophy.

关键词：心肌病扩张型/遗传学心肌病扩张型/代谢心肌病扩张型/病理学载体蛋白质类/生理学冠状血管/病理学细胞支架蛋白质类/缺乏细胞支架蛋白质类/遗传学细胞支架蛋白质类/生理学大分子物质膜糖蛋白类/缺乏膜糖蛋白类/遗传学膜糖蛋白类/生理学膜蛋白质类/生理学小鼠基因敲除肌平滑血管/代谢肌平滑血管/病理学肌营养不良动物/遗传学肌营养不良动物/代谢肌营养不良动物/病理学心肌/病理学坏死肿瘤蛋白质类肌聚糖类动物小鼠

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Inherited human Caspase 10 mutations underlie defective lymphocyte and dendritic cell apoptosis in autoimmune lymphoproliferative syndrome type II

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CELL 1999年第1期98卷 47-58页

作者： Wang, J Zheng, LX Lobito, A Chan, FKM Dale, J Sneller, M Yao, X Puck, JM Straus, SE Lenardo, MJ NIAID Immunol Lab NIH Bethesda MD 20892 USA NIAID Clin Invest Lab NIH Bethesda MD 20892 USA NIAID Immunoregulat Lab NIH Bethesda MD 20892 USA Natl Human Genome Res Inst Genet & Mol Biol Branch NIH Bethesda MD 20892 USA NCI Pathol Lab NIH Bethesda MD 20892 USA

Caspases are cysteine proteases that mediate programmed cell death in phylogenetically diverse multicellular organisms. We report here two kindreds with autoimmune lymphoproliferative syndrome (ALPS) type II, characterized by abnormal lymphocyte and dendritic cell homeostasis and immune regulatory defects, that harbor independent missense mutations in Caspase 10. These encode amino acid substitutions that decrease caspase activity and interfere with death receptor-induced apoptosis, particularly that stimulated by Pas ligand and TRAIL. These results provide evidence that inherited nonlethal caspase abnormalities cause pleiotropic apoptosis defects underlying autoimmunity in ALPS type II.

关键词：衔接蛋白质类信号转导氨基酸取代抗原 CD95/生理学细胞凋亡凋亡调节蛋白质类自身免疫疾病/酶学自身免疫疾病/遗传学自身免疫疾病/免疫学乳腺肿瘤载体蛋白质类/生理学半胱氨酸天冬氨酸蛋白酶10 半胱氨酸天冬氨酸蛋白酶/遗传学细胞培养的 DNA引物树突细胞/病理学树突细胞/生理学 Fas配体蛋白质 Fas相关死亡结构域蛋白质 HeLa细胞内环境稳定淋巴细胞/病理学淋巴细胞/生理学淋巴组织增殖性疾病/酶学淋巴组织增殖性疾病/遗传学淋巴组织增殖性疾病/免疫学膜糖蛋白类/生理学突变误义重组蛋白质类/代谢逆转录聚合酶链反应 TNF相关凋亡诱导配体转染肿瘤坏死因子α/生理学儿童女(雌)性人类

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The MRP2/cMOAT transporter and arsenic-glutathione complex formation are required for biliary excretion of arsenic

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第43期275卷 33404-33408页

作者： Kala, SV Neely, MW Kala, G Prater, CI Atwood, DW Rice, JS Lieberman, MW Baylor Coll Med Dept Pathol Houston TX 77030 USA Baylor Coll Med Dept Cellular & Mol Biol Houston TX 77030 USA Univ Texas MD Anderson Canc Ctr Dept Expt Therapeut Houston TX 77030 USA

Worldwide, millions of people are exposed to arsenic in drinking water that exceeds the World Health Organization standard of 10 mug/liter by as much as 50-300-fold, yet little is known about the molecular basis for arsenic excretion. Here me show that transport of arsenic into bile depends on the MRP2/cMOAT transporter and that glutathione is obligatory for such transport, Using reversed phase liquid chromatography/mass spectrometry, we demonstrate that two arsenic-glutathione complexes not previously identified in vivo, arsenic tri-glutathione and methylarsenic diglutathione, account for most of the arsenic in the bile. The structure of the compounds was also confirmed by nuclear magnetic resonance spectroscopy, Our findings may help explain the increased susceptibility of malnourished human populations to arsenic.

关键词：阴离子转运蛋白质类砷/代谢砷剂/代谢胆汁/代谢生物转运载体蛋白质类/生理学谷胱甘肽/类似物和衍生物谷胱甘肽/代谢磁共振波谱学大鼠 Wistar 动物大鼠

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