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Syne-1, a dystrophin- and klarsicht-related protein associated with synaptic nuclei at the neuromuscular junction

JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第41期275卷 31986-31995页

作者： Apel, ED Lewis, RM Grady, RM Sanes, JR Washington Univ Sch Med Dept Anat & Neurobiol St Louis MO 63110 USA Washington Univ Sch Med Dept Pediat St Louis MO 63110 USA

We describe a novel protein, Syne-1, that is associated with nuclear envelopes in skeletal, cardiac, and smooth muscle cells. Syne-1 contains multiple spectrin repeats similar to those found in dystrophin and utrophin, as well as a domain homologous to the carboxyl-terminal of Klarsicht, a protein associated with nuclei and required for a subset of nuclear migrations in Drosophila. In adult skeletal muscle fibers, levels of Syne-1 are highest in the nuclei that lie beneath the postsynaptic membrane at: the neuromuscular junction. These nuclei are transcriptionally specialized, expressing genes for synaptic components at higher levels than extrasynaptic nuclei in the same cytoplasm. Syne-1 is the first protein found to be selectively associated with synaptic nuclei. Syne-1 becomes concentrated in synaptic nuclei postnatally. It remains synaptically enriched following denervation or degeneration/regeneration, and is also present at high levels in the central nuclei of dystrophic myotubes. The location and structure of Syne-1 suggest that it may participate in the migration of myonuclei in myotubes and/or their anchoring at the postsynaptic apparatus. Finally, we identify a homologous gene, syne-2, that is expressed in an overlapping but distinct pattern.

关键词：选择性剪接/遗传学氨基酸序列细胞系果蝇蛋白质类肌营养不良蛋白/化学荧光抗体技术基因表达谱昆虫蛋白质类/化学膜转运蛋白质类微丝蛋白质类分子序列数据肌纤维骨骼/细胞学肌纤维骨骼/代谢肌蛋白质类/化学肌蛋白质类/遗传学肌蛋白质类/代谢神经组织蛋白质类/化学神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经肌肉接头/化学神经肌肉接头/细胞学神经肌肉接头/代谢核被膜/化学核蛋白质类/化学核蛋白质类/遗传学核蛋白质类/代谢沉淀素试验蛋白质结合蛋白质亚型/化学蛋白质亚型/遗传学蛋白质亚型/代谢 RNA 信使/遗传学 RNA 信使/代谢受体蛋白质酪氨酸激酶类/化学受体蛋白质酪氨酸激酶类/遗传学受体蛋白质酪氨酸激酶类/代谢受体胆碱能序列比对双杂交系统技术动物人类小鼠

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Neurodegeneration prevented by lentiviral vector delivery of GDNF in primate models of Parkinson's disease

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SCIENCE 2000年第5492期290卷 767-773页

作者： Kordower, JH Emborg, ME Bloch, J Ma, SY Chu, YP Leventhal, L McBride, J Chen, EY Palfi, S Roitberg, BZ Brown, WD Holden, JE Pyzalski, R Taylor, MD Carvey, P Ling, ZD Trono, D Hantraye, P Déglon, N Aebischer, P Rush Presbyterian St Lukes Med Ctr Dept Neurol Sci Chicago IL 60612 USA Rush Presbyterian St Lukes Med Ctr Dept Pharmacol Chicago IL 60612 USA Univ Lausanne Sch Med Div Surg Res Lausanne Switzerland Univ Lausanne Sch Med Gene Therapy Ctr Lausanne Switzerland Univ Wisconsin Dept Med Phys Madison WI 53706 USA Univ Wisconsin Dept Radiol Madison WI 53706 USA Univ Geneva Fac Med Dept Genet & Microbiol Geneva Switzerland Serv Hosp Frederic Joliot CEA Dept Rech Med Direct Rech MedCNRSUnite Rech Associe 2210 Orsay France Ecole Polytech Fed Lausanne Swiss Fed Inst Technol CH-1015 Lausanne Switzerland

Lentiviral delivery of glial cell Line-derived neurotrophic factor (Lenti-GDNF) was tested for its trophic effects upon degenerating nigrostriatal neurons in nonhuman primate models of Parkinson's disease (PD). We injected lenti-GDNF into the striatum and substantia nigra of nonlesioned aged rhesus monkeys or young adult rhesus monkeys treated 1 week prior with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Extensive GDNF expression with anterograde and retrograde transport was seen in all animals. In aged monkeys, Lenti-GDNF augmented dopaminergic function. In MPTP-treated monkeys, lenti-GDNF reversed functional deficits and completely prevented nigrostriatal degeneration. Additionally, Lenti-GDNF injections to intact rhesus monkeys revealed Long-term gene expression (8 months). In MPTP-treated monkeys, lenti-GDNF treatment reversed motor deficits in a hand-reach task. These data indicate that GDNF delivery using a Lentiviral vector system can prevent nigrostriatal degeneration and induce regeneration in primate models of PD and might be a viable therapeutic strategy for PD patients.

关键词： 1-甲基-4-苯基-1 2 3 6-四氢吡啶衰老抗原 CD/分析二羟苯丙氨酸/类似物和衍生物二羟苯丙氨酸/代谢疾病模型动物多巴胺/代谢基因表达遗传载体胶质细胞源性神经营养因子慢病毒属/遗传学猕猴新纹状体/代谢新纹状体/病理学神经变性/预防和控制神经生长因子类神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经组织蛋白质类/治疗应用神经元/酶学帕金森病/代谢帕金森病/病理学帕金森病/病理生理学帕金森病/治疗帕金森障碍/代谢帕金森障碍/病理学帕金森障碍/病理生理学帕金森障碍/治疗精神运动性行为黑质/代谢黑质/病理学酪氨酸单氧化酶/代谢动物女(雌)性

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The SH3 domains of endophilin and amphiphysin bind to the proline-rich region of synaptojanin 1 at distinct sites that display an unconventional binding specificity

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第45期274卷 32001-32007页

作者： Cestra, G Castagnoli, L Dente, L Minenkova, O Petrelli, A Migone, N Hoffmüller, U Schneider-Mergener, J Cesareni, G Univ Rome Dept Biol I-00133 Rome Italy Humboldt Univ Univ Frankfurt Charite D-10117 Berlin Germany Univ Turin Dipartimento Genet Biol & Biochim I-10126 Turin Italy

The proline-rich domain of synaptojanin 1, a synaptic protein with phosphatidylinositol phosphatase activity, binds to amphiphysin and to a family of recently discovered proteins known as the SH3p4/8/13, the SH3-GL, or the endophilin family. These interactions are mediated by SH3 domains and are believed to play a regulatory role in synaptic vesicle recycling, We have precisely mapped the target peptides on human synaptojanin that are recognized by the SH3 domains of endophilins and amphiphysin and proven that they are distinct. By a combination of different approaches, selection of phage displayed peptide libraries, substitution analyses of peptides synthesized on cellulose membranes, and a peptide scan spanning a 252-residue long synaptojanin fragment, we have concluded that amphiphysin binds to two sites, PIRPSR and PTIPPR, whereas endophilin has a distinct preferred binding site, PKRPPPPR, The comparison of the results obtained by phage display and substitution analysis permitted the identification of proline and arginine at positions 4 and 6 in the PIRPSR and PTIPPR target sequence as the major determinants of the recognition specificity mediated by the SH3 domain of amphiphysin I. More complex is the structural rationalization of the preferred endophilin ligands where SH3 binding cannot be easily interpreted in the framework of the "classical" type I or type II SH3 binding models. Our results suggest that the binding repertoire of SH3 domains may be more complex than originally predicted.

关键词：衔接蛋白质类信号转导氨基酸序列结合部位结合竞争性载体蛋白质类/代谢酶联免疫吸附测定分子序列数据神经组织蛋白质类/代谢肽库磷酸单酯水解酶类/代谢脯氨酸/代谢 src同源域人类

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Hsc70 chaperones clathrin and primes it to interact with vesicle membranes

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第12期275卷 8439-8447页

作者： Jiang, RF Gao, BC Prasad, K Greene, LE Eisenberg, E NHLBI Cell Biol Lab Sect Cell Physiol NIH Bethesda MD 20892 USA

When Hsc70 uncoats clathrin-coated vesicles in an auxilin- and ATP dependent reaction, a single round of rapid uncoating occurs followed by very slow steady-state uncoating. We now show that this biphasic time course occurs because Hsc70 sequentially forms two types of complex with the dissociated clathrin triskelions. The first round of clathrin uncoating is driven by formation of a pre steady-state assembly protein (AP)-clathrin-Hsc70-ADP complex. Then, following exchange of ADP with ATP, a steady-state AP-clathrin-Hsc70-ATP complex forms that ties up Hsc70, preventing further uncoating, This steady-state complex forms only during uncoating in the presence of APs;in the absence of APs, Hsc70 rapidly dissociates from the uncoated clathrin and continues to carry out uncoating, Whether it is complexed with ATP or ADP, the steady-state complex has very different properties from the pre-steady-state complex in that it cannot be immunoprecipitated by anti-clathrin antibodies and is readily dissociated by fast protein liquid chromatography. Remarkably, when the steady-state complex is incubated with uncoated vesicle membranes in ATP, the pre steady state complex reforms, suggesting that the clathrin triskelions in the steady-state complex rebind to the membranes and are again uncoated by Hsc70. We propose that Hsc70 not only uncoats clathrin but also chaperones it to prevent it from inappropriately polymerizing in the cell cytosol and primes it to reform clathrin coated pits.

关键词：衔接蛋白质类膜泡运输腺苷二磷酸/代谢腺苷三磷酸/代谢载体蛋白质类/代谢网格蛋白/代谢有被小泡/代谢胞吞作用/生理学 HSC70热休克蛋白质类 HSP70热休克蛋白质类模型生物学分子伴侣/代谢神经组织蛋白质类/代谢磷蛋白类/代谢蛋白质结合动物牛

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Multiple interactions between receptor protein-tyrosine phosphatase (RPTP) α and membrane-distal protein-tyrosine phosphatase domains of various RPTPs

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第17期275卷 12446-12452页

作者： Blanchetot, C den Hertog, J Netherlands Inst Dev Biol Hubrecht Lab NL-3584 CT Utrecht Netherlands

Receptor protein-tyrosine phosphatase (RPTP) alpha belongs to the large family of receptor protein-tyrosine phosphatases containing two tandem phosphatase domains. Most of the catalytic activity is retained in the first, membrane-proximal domain (RPTP alpha-D1), and little is known about the function of the second, membrane distal domain (RPTP alpha-D2). We investigated whether proteins bound to RPTP alpha using the two-hybrid system and found that the second domain of RPTP sigma interacted with the juxtamembrane domain of RPTP alpha, We confirmed this interaction by co-immunoprecipitation experiments. Furthermore, RPTP alpha not only interacted with RPTP sigma-D2 but also with RPTP alpha-D2, LAR-D2, RPTP delta-D2, and RPTP mu-D2, members of various RPTP subfamilies, although with different affinities. In the yeast two-hybrid system and in glutathione S-transferase pull-down assays, we show that the RPTP-D2s interacted directly with the wedge structure of RPTP alpha-D1 that has been demonstrated to be involved in inactivation of the RPTP alpha-D1/RPTP alpha-D1 homodimer, The interaction was specific because the equivalent wedge structure in LAR was unable to interact with RPTP alpha-D2 or LAR-D2. In vitro, we show that other interaction sites exist as well, including the C terminus of RPTP alpha-D2. The observation that RPTP alpha, but not LAR, bound to multiple RPTP-D2s with varying affinities suggests a specific mechanism of cross-talk between RPTPs that may regulate their biological function.

关键词： COS细胞细胞系谷胱甘肽转移酶/代谢神经组织蛋白质类/代谢沉淀素试验蛋白质结合蛋白质结构三级蛋白质酪氨酸磷酸酶类/代谢受体样蛋白质酪氨酸磷酸酶类 2类受体样蛋白质酪氨酸磷酸酶类 4类受体样蛋白质酪氨酸磷酸酶类 5类受体细胞表面重组融合蛋白质类/代谢转染双杂交系统技术动物人类

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Functional regulation of γ-aminobutyric acid transporters by direct tyrosine phosphorylation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第31期275卷 23986-23991页

作者： Law, RM Stafford, A Quick, MW Univ Alabama Birmingham Dept Neurobiol Birmingham AL 35294 USA

Tyrosine phosphorylation regulates multiple cell signaling pathways and functionally modulates a number of ion channels and receptors, Neurotransmitter transporters, which act to clear transmitter from the synaptic cleft, are regulated by multiple second messenger pathways that exert their effects, at least in part, by causing a redistribution of the transporter protein to or from the cell surface. To test the hypothesis that tyrosine phosphorylation affects transporter function and to determine its mechanism of action, we examined the regulation of the rat brain gamma-aminobutyric acid (GABA) transporter GAT1 expressed endogenously in hippocampal neurons and expressed heterologously in Chinese hamster ovary cells. Inhibitors of tyrosine kinases decreased GABA uptake;inhibitors of tyrosine phosphatases increased GABA uptake. The decrease in uptake seen with tyrosine kinase inhibitors was correlated with a decrease in tyrosine phosphorylation of GAT1 and resulted in a redistribution of the transporter from the cell surface to intracellular locations. A mutant GAT1 construct that was refractory to tyrosine phosphorylation could not be regulated by tyrosine kinase inhibitors. Activators of protein kinase C, which are known to cause a redistribution of GAT1 from the cell surface, were additive to the effects of tyrosine kinase inhibitors suggesting that multiple signaling pathways control transporter redistribution. Application of brain-derived neurotrophic factor, which activates receptor tyrosine kinases, up-regulated GAT1 function suggesting one potential trigger for the cellular regulation of GAT1 signaling by tyrosine phosphorylation, These data support the hypothesis that transporter expression and function is controlled by the interplay of multiple cell signaling cascades.

关键词：动物新生生物转运/药物作用脑源性神经营养因子/药理学载体蛋白质类/遗传学载体蛋白质类/代谢细胞区室化 GABA质膜转运蛋白质类海马/细胞学海马/代谢膜蛋白质类/遗传学膜蛋白质类/代谢膜转运蛋白质类突变神经组织蛋白质类/代谢神经元/细胞学神经元/代谢有机阴离子转运子磷酰化蛋白酪氨酸激酶类/拮抗剂和抑制剂蛋白酪氨酸激酶类/代谢信号传导酪氨酸增量调节 γ氨基丁酸/代谢动物大鼠

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ESE-1 is a novel transcriptional mediator of inflammation that interacts with NF-κB to regulate the inducible nitric-oxide synthase gene

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JOURNAL OF BIOLOGICAL CHEMISTRY 2001年第5期276卷 3302-3309页

作者： Rudders, S Gaspar, J Madore, R Voland, C Grall, F Patel, A Pellacani, A Perrella, MK Libermann, TA Oettgen, P Harvard Univ Sch Med Inst Med Boston MA 02115 USA Beth Israel Deaconess Med Ctr New England Baptist Bone & Joint Inst Boston MA 02115 USA Beth Israel Deaconess Med Ctr Div Cardiol Boston MA 02115 USA Brigham & Womens Hosp Dept Med Boston MA 02115 USA

Inflammation is a hallmark of several vascular diseases. The nuclear factor kappaB (NF-kappaB) transcription factors are dimeric proteins involved in the activation of a large number of genes in response to inflammatory stimuli. We report the involvement of a novel member of the ETS transcription factor, ESE-1, in mediating vascular inflammation. ESE-1 is induced in response to inflammatory cytokines and lipopolysaccharide in vascular smooth muscle cells, endothelial cells, and cells of the monocyte-macrophage lineage. This induction occurs within hours of stimulation and is mediated by NF-kappaB transactivation of the ESE-1 promoter. We have identified the inducible form of nitric-oxide synthase (NOS2) as a putative target for ESE-1, ESE-1 can bind to the p50 subunit of NF-kappaB, and cotransfection of ESE-1 with the p50 and p65 subunits of NF-kappaB synergistically enhances transactivation of the NOS2 promoter by ESE-1, An ESE-1-binding site within the NOS2 promoter has been identified, the site-directed mutagenesis of which completely abolishes the ability of ESE-1 to transactivate the NOS2 promoter. Finally, in a mouse model of endotoxemia, associated with acute vascular inflammation, ESE-1 is strongly expressed in vascular endothelium and smooth muscle cells. In summary, ESE-1 represents a novel mediator of vascular inflammation.

关键词：结合部位钙结合蛋白质类细胞培养的细胞因子类/药理学 DNA结合蛋白质类炎症/代谢炎症介导素类/代谢炎症介导素类/生理学膜糖蛋白类/代谢突变 NF-κB/代谢 NF-κB/生理学神经组织蛋白质类/代谢一氧化氮合酶/代谢一氧化氮合酶Ⅱ型蛋白质结构三级原癌基因蛋白质类突触结合蛋白质Ⅰ 突触结合蛋白质类反式激活因子类/遗传学反式激活因子类/代谢反式激活因子类/生理学转录因子血管疾病/代谢人类

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Class C Vps protein complex regulates vacuolar SNARE pairing and is required for vesicle docking/fusion

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MOLECULAR CELL 2000年第3期6卷 661-671页

作者： Sato, TK Rehling, P Peterson, MR Emr, SD Univ Calif San Diego Sch Med Div Cellular & Mol Med La Jolla CA 92093 USA Univ Calif San Diego Sch Med Howard Hughes Med Inst La Jolla CA 92093 USA

In yeast, the Class C Vps protein complex (C-Vps complex), composed of Vps11, Vps16, Vps18, and Vps33, functions in Golgi-to-vacuole protein transport. In this study, we characterized and purified this complex and identified its interaction with the syntaxin homolog Vam3. Vam3 pairs with the SNAP-25 homolog Vam7 and VAMP homolog Vti1 to form SNARE complexes during vesicle docking/fusion with the vacuole. The C-Vps complex does not bind to Vam3-Vti1-Vam7 paired SNARE complexes but instead binds to unpaired Vam3. Antibodies to a component of this complex inhibited in vitro vacuole-to-vacuole fusion. Furthermore, temperature-conditional mutations in the Class C VPS genes destabilized Vam3-Vti1-Vam7 pairing. Therefore, we propose that the C-Vps complex associates with unpaired (activated) Vam3 to mediate the assembly of trans-SNARE complexes during both vesicle docking/fusion and vacuole-to-vacuole fusion.

关键词：衔接蛋白质类膜泡运输载体蛋白质类胞质小泡/代谢大肠杆菌真菌蛋白质类/遗传学真菌蛋白质类/代谢基因表达/生理学高尔基体/代谢膜融合/生理学膜蛋白质类/遗传学膜蛋白质类/代谢 Munc18蛋白质类神经组织蛋白质类/遗传学神经组织蛋白质类/代谢蛋白质转运/生理学 Qa-SNARE蛋白质类 SNARE蛋白质类酿酒酵母蛋白质类突触体相关蛋白质25 空泡/代谢膜泡运输蛋白质类酵母菌

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Regulation of complex formation of POB1/epsin/adaptor protein complex 2 by mitotic phosphorylation

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第24期275卷 18399-18406页

作者： Kariya, K Koyama, S Nakashima, S Oshiro, T Morinaka, K Kikuchi, A Hiroshima Univ Sch Med Dept Biochem Minami Ku Hiroshima 7348551 Japan

RalBP1 and POB1, the downstream molecules of small GTP-binding protein Pal, are involved in receptor-mediated endocytosis together with Epsin and Eps15. The regulation of assembly of the complex of these proteins wits examined. RalBP1, POB1, Epsin, and Eps15 formed a complex with alpha-adaptin of AP-2 in Chinese hamster ovary cells, but the formation was reduced in mitotic phase. RalBP1, POB1, Epsin, and Eps15 were all phosphorylated in mitotic phase. The phosphorylated forms of POB1 and Epsin were recognized by the antibody MPM2, which is known to detect mitotic phosphoproteins. POB1 and Epsin were phosphorylated by p34(cdc2) kinase in vitro. Their phosphorylation sites (Ser(411) of POB1 and Ser(357) Of Epsin) were determined. Phosphorylated Epsin and Epsin(S357D) formed a complex with alpha-adaptin less efficiently than wild type Epsin. Although the EH domain of POB1 bound directly to Epsin, phosphorylation of Epsin inhibited the binding. Furthermore, Epsin(S357D) but not Epsin(S357A) lost the effect of Epsin on the insulin-dependent endocytosis, These results suggest that phosphorylation of Epsin in mitotic phase inhibits receptor-mediated endocytosis by disassembly of its complex with POB1 and alpha-adaptin.

关键词：衔接蛋白质类膜泡运输 CHO细胞载体蛋白质类/遗传学载体蛋白质类/代谢共有序列仓鼠亚科 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/代谢胞吞作用胰岛素/代谢大分子物质有丝分裂诱变定点神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经肽类/遗传学神经肽类/代谢磷蛋白类/遗传学磷蛋白类/代谢磷酰化信号传导构效关系膜泡运输蛋白质类 ralGTP结合蛋白质类/生理学动物

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Inhibiting caspase cleavage of huntingtin reduces toxicity and aggregate formation in neuronal and nonneuronal cells

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第26期275卷 19831-19838页

作者： Wellington, CL Singaraja, R Ellerby, L Savill, J Roy, S Leavitt, B Cattaneo, E Hackam, A Sharp, A Thornberry, N Nicholson, DW Bredesen, DE Hayden, MR Univ British Columbia Ctr Mol Med & Therapeut Vancouver BC V5Z 4H4 Canada Buck Ctr Res Aging Novato CA 94945 USA Merck Frosst Ctr Therapeut Res Dept Biochem & Mol Biol Pointe Claire PQ H9R 4P8 Canada Univ Milan Inst Pharmacol Sci I-20133 Milan Italy Johns Hopkins Univ Sch Med Dept Psychiat & Behav Sci Baltimore MD 21287 USA Merck Res Labs Dept Enzymol Rahway NJ 07065 USA

Huntington's disease is a neurodegenerative disorder caused by CAG expansion that results in expansion of a polyglutamine tract at the extreme N terminus of huntingtin (htt). htt with polyglutamine expansion is proapoptotic in different cell types. Here, we show that caspase inhibitors diminish the toxicity of htt, Additionally, we define htt itself as an important caspase substrate by generating a site-directed htt mutant that is resistant to caspase-3 cleavage at positions 513 and 530 and to caspase-6 cleavage at position 586, In contrast to cleavable htt, caspase-resistant htt with an expanded polyglutamine tract has reduced toxicity in apoptotically stressed neuronal and nonneuronal cells and forms aggregates at a much reduced frequency. These results suggest that inhibiting caspase cleavage of htt may therefore be of potential therapeutic benefit in Huntington's disease.

关键词：氨基酸序列细胞凋亡/药物作用细胞凋亡/遗传学结合部位印迹法蛋白质致癌物/药理学半胱氨酸天冬氨酸蛋白酶3 半胱氨酸天冬氨酸蛋白酶6 半胱氨酸天冬氨酸蛋白酶/拮抗剂和抑制剂半胱氨酸天冬氨酸蛋白酶/代谢细胞系酶激活/遗传学荧光抗体技术分子序列数据诱变神经组织蛋白质类/遗传学神经组织蛋白质类/代谢神经组织蛋白质类/毒性神经元/代谢核蛋白质类/遗传学核蛋白质类/代谢核蛋白质类/毒性肽类/代谢质粒/代谢他莫昔芬/药理学时间因素转染动物人类大鼠

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