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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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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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Dityrosine cross-linking promotes formation of stable α-synuclein polymers -: Implication of nitrative and oxidative stress in the pathogenesis of neurodegenerative synucleinopathies

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第24期275卷 18344-18349页

作者： Souza, JM Giasson, BI Chen, QP Lee, VMY Ischiropoulos, H Childrens Hosp Philadelphia Stokes Res Inst Abramson Ctr 416D Philadelphia PA 19104 USA Univ Penn Med Ctr Dept Biochem & Biophys Philadelphia PA 19104 USA Univ Penn Med Ctr Ctr Neurodegenerat Dis Res Philadelphia PA 19104 USA Univ Penn Med Ctr Dept Pathol & Lab Med Philadelphia PA 19104 USA Univ Republica Fac Med Dept Bioquim Montevideo 11800 Uruguay

Intracellular proteinaceous aggregates are hallmarks of many common neurodegenerative disorders, and recent studies have shown that alpha-synuclein is a major component of several pathological intracellular inclusions, including Lewy bodies in Parkinson's disease (PD) and glial cell inclusions in multiple system atrophy. However, the molecular mechanisms underlying alpha-synuclein aggregation into filamentous inclusions remain unknown. Since oxidative and nitrative stresses are potential pathogenic mediators of PD and other neurodegenerative diseases, we asked if oxidative and/or nitrative events alter alpha-synuclein and induce it to aggregate. Here we show that exposure of human recombinant a-synuclein to nitrating agents (peroxynitrite/CO2 or myeloperoxidase/H2O2/nitrite) induces formation of nitrated alpha-synuclein oligomers that are highly stabilized due to covalent cross-linking via the oxidation of tyrosine to form o,o'-dityrosine. We also demonstrate that oxidation and nitration of pre-assembled alpha-synuclein filaments stabilize these filaments to withstand denaturing conditions and enhance formation of SDS-insoluble, heat-stable high molecular mass aggregates. Thus, these data suggest that oxidative and nitrative stresses are involved in mechanisms underlying the pathogenesis of Lewy bodies and glial cell inclusions in PD and multiple system atrophy, respectively, as well as alpha-synuclein pathologies in other synucleinopathies.

关键词：电泳聚丙烯酰氨凝胶神经组织蛋白质类/代谢神经变性疾病/病因学硝酸盐类/代谢氧化性应激聚合物/代谢重组蛋白质类/代谢突触核蛋白类酪氨酸/类似物和衍生物酪氨酸/代谢 α突触核蛋白人类

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Three isoforms of synaptic scaffolding molecule and their characterization -: Multimerization between the isoforms and their interaction with N-methyl-D-aspartate receptors and SAP90/PSD-95-associated protein

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第4期275卷 2966-2972页

作者： Hirao, K Hata, Y Yao, I Deguchi, M Kawabe, H Mizoguchi, A Takai, Y JCR Pharmaceut Co Ltd Japan Sci & Technol Corp ERATO Takai Biotimer ProjectNishi Ku Kobe Hyogo 6512241 Japan Tokyo Med & Dent Univ Dept Med Biochem Bunkyo Ku Tokyo 1138519 Japan Osaka Univ Grad Sch Med Fac Med Dept Mol Biol & Biochem Suita Osaka 5650871 Japan Kyoto Univ Grad Sch Dept Anat & Neurobiol Kyoto 6068315 Japan

The synaptic scaffolding molecule (S-SCAM) has been identified as a protein interacting with SAP90/PSD-95-associated protein (SAPAP) (also called guanylate kinase-associated protein/hDLG-associated protein). S-SCAM;I has six PDZ (we have numbered them PDZ-0 to -5), two WV, and one guanylate kinase (GK) domains and interacts with N-methyl-D-aspartate (NMDA) receptor via PDZ-5 and SAPAP via the GIC domain. me have identified here shorter isoforms of S-SCAM that start at the 164th or 224th methionine, and we renamed the original one, S-SCAM alpha, the middle one, S-SCAM beta, and the shortest one, SSCAM-gamma. S-SCAM beta and -gamma have five PDZ (PDZ-1 to -5), two WW, and one GK domains. S-SCAM alpha interacted with S-SCAM beta and -gamma through the region containing PDZ-4 and -5. The region containing both of PDZ-4 and -5 is sufficient for the clustering of NMDA receptors and forms a dimer in gel filtration, suggesting that S-SCAM forms multimers via the interaction between the C-terminal PDZ domains and assembles NMDA receptors into clusters. S-SCAM beta P and -gamma also interacted with SAPAP, suggesting that the N-terminal region of the GH domain is not necessary for the interaction. Finally, we have identified the interaction of the PDZ domains of S-SCAM with the GK domain of PSD-95/SAP90. S-SCAM PSD-95/SAP90, and SAPAP are colocalized at least in some part in brain. Therefore, S-SCAM, PSD-95/SAP90, and SA-PAP may form a complex in vivo.

关键词：衔接蛋白质类信号转导氨基酸序列碱基序列生物聚合物 CHO细胞 COS细胞载体蛋白质类/化学载体蛋白质类/代谢小脑/代谢色谱法凝胶仓鼠亚科 DNA引物显微镜检查荧光分子序列数据神经组织蛋白质类/化学神经组织蛋白质类/代谢蛋白质结合蛋白质亚型/化学蛋白质亚型/代谢受体 N-甲基-D-天冬氨酸/代谢视网膜/代谢序列同源性氨基酸动物大鼠

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Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration

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NATURE 1999年第6762期402卷 615-622页

作者： Patrick, GN Zukerberg, L Nikolic, M de la Monte, S Dikkes, P Tsai, LH Harvard Univ Sch Med Dept Pathol Boston MA 02115 USA Howard Hughes Med Inst Boston MA 02115 USA Massachusetts Gen Hosp Dept Pathol Boston MA 02114 USA Massachusetts Gen Hosp E Ctr Canc Charlestown MA 02119 USA Childrens Hosp Dept Neurol Boston MA 02115 USA

Cyclin-dependent kinase 5 (Cdk5) is required for proper development of the mammalian central nervous system. To be activated, Cdk5 has to associate with its regulatory subunit, p35, We have found that p25, a truncated form of p35, accumulates in neurons in the brains of patients with Alzheimer's disease. This accumulation correlates with an increase in Cdk5 kinase activity. Unlike p35, p25 is not readily degraded, and binding of p25 to Cdk5 constitutively activates Cdk5, changes its cellular location and alters its substrate specificity, In vivo the p25/Cdk5 complex hyperphosphorylates tau, which reduces tau's ability to associate with microtubules, Moreover, expression of the p25/Cdk5 complex in cultured primary neurons induces cytoskeletal disruption, morphological degeneration and apoptosis, These findings indicate that cleavage of p35, followed by accumulation of p25, may be involved in the pathogenesis of cytoskeletal abnormalities and neuronal death in neurodegenerative diseases.

关键词： 3T3细胞阿尔茨海默病/酶学阿尔茨海默病/病因学阿尔茨海默病/病理学细胞凋亡脑/酶学 COS细胞克隆分子培养技术细胞周期蛋白依赖激酶5 细胞周期蛋白质依赖激酶类/代谢细胞骨架/代谢细胞骨架/病理学酶激活酶激动剂类/代谢酶稳定性免疫组织化学配对分析神经组织蛋白质类/代谢神经原纤维缠结/酶学神经元/病理学磷酰化大鼠 Sprague-Dawley tau蛋白质类/代谢老年人老年人 80以上动物女(雌)性人类男(雄)性小鼠中年人大鼠

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Regulation of neurabin I interaction with protein phosphatase 1 by phosphorylation

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BIOCHEMISTRY 1999年第39期38卷 12943-12949页

作者： McAvoy, T Allen, PB Obaishi, H Nakanishi, H Takai, Y Greengard, P Nairn, AC Hemmings, HC Cornell Univ Weill Med Coll Dept Anesthesiol New York NY 10021 USA Cornell Univ Weill Med Coll Dept Pharmacol New York NY 10021 USA Rockefeller Univ Mol & Cellular Neurosci Lab New York NY 10021 USA ERATO Japan Sci & Technol Corp Takai Biotimer Project Kobe Hyogo 65122 Japan Osaka Univ Sch Med Dept Mol Biol & Biochem Suita Osaka 565 Japan

Neurabin I is a brain-specific actin-binding protein. Here we show that neurabin I binds protein phosphatase 1 (PP1) and inhibits PP1 activity. Neurabin I interacted with PP1 alpha in an overlay assay, in yeast two-hybrid interaction analysis, and in coprecipitation and co-immunoprecipitation experiments. Neurabin I also copurified with both the alpha and gamma isoforms of PP1. A glutathione S-transferase (GST)-neurabin I fusion protein (residues 318-661) containing the putative PP1 binding domain (residues 456-460) inhibited PP1 activity (K-i = 2.7 +/- 1.2 nM). This fusion protein was also rapidly phosphorylated in vitro by PKA (K-m = 6 mu M) to a stoichiomtry of 1 mol/mol. The phosphorylated residue was identified as serine 461 by HPLC-MS analysis of a tryptic digest. Phosphorylation of GST-neurabin I (residues 318-661) by PKA significantly reduced its binding to PP1 by overlay and by glutathione-Sepharose coprecipitation assays. A 35-fold decrease in inhibitory potency was also observed using a S461E mutant, which mimics phosphorylation of S461. These findings identify a signaling mechanism involving the regulation of PPI activity and localization mediated by the cAMP pathway.

关键词：氨基酸序列脑/酶学脑/代谢环AMP依赖性蛋白激酶类/代谢微丝蛋白质类/代谢分子序列数据神经组织蛋白质类/代谢肽碎片/化学磷蛋白磷酸酶类/化学磷蛋白磷酸酶类/代谢磷酰化沉淀素试验蛋白质磷酸酶1 大鼠 Sprague-Dawley 序列同源性氨基酸动物男(雄)性大鼠

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Phosphorylation of a new brain-specific septin, G-septin, by cGMP-dependent protein kinase

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第14期275卷 10047-10056页

作者： Xue, J Wang, X Malladi, CS Kinoshita, M Milburn, PJ Lengyel, I Rostas, JAP Robinson, PJ Childrens Med Res Inst Cell Signalling Unit Wentworthville NSW 2145 Australia Univ Newcastle Dept Med Biochem Fac Med & Hlth Sci Newcastle NSW 2308 Australia Kyoto Univ Grad Sch Med Dept Mol Oncol Kyoto 606 Japan Australian Natl Univ John Curtin Sch Med Res Canberra ACT 0200 Australia Hungarian Acad Sci Biol Res Ctr Inst Biochem H-6701 Szeged Hungary

The septins are a family of GTPase enzymes, some of which are required for the cytokinesis stage of cell di vision and others of which are associated with exocytosis. me purified and cloned the cDNA for a 40-kDa protein from rat brain that is a substrate for type I cGMP-dependent protein kinase (PKG). The amino acid sequences of two tryptic peptides of P40 showed high homology to the septins. Molecular cloning revealed the 358-amino acid P40 to be a new member of the septin family. P40 was named G-septin, as it is phosphorylated in, vitro by PKG, but relatively poorly by the related cAMP dependent protein kinase and not by protein kinase C, Two splice variants of G-septin (alpha and beta) were found with distinct N and C termini, but a common GTPase domain. G-septin lacks the C-terminal coiled-coil domain characteristic of all other mammalian septins and uniquely has two predicted phosphorylation site motifs for type I PKG. Photoaffinity labeling with [alpha-P-32]GTP confirmed that G-septin is a GTP-binding protein. Northern blotting showed that G-septin mRNA (5.0 kilobases) is highly expressed in brain and undetectable in 12 other tissues, indicating that the G-septins are primarily neuronal proteins. Very low levels of 6.0-, 3.4-, and 2.6-kilobase transcripts were found in testis. Our results reveal a new class of brain-specific septins that may be regulated by PKG in neurons.

关键词：选择性剪接氨基酸序列脑/酶学克隆分子环GMP依赖性蛋白激酶类/代谢 GTP磷酸水解酶类/化学 GTP磷酸水解酶类/遗传学 GTP磷酸水解酶类/代谢遗传变异鸟苷三磷酸/代谢动力学分子序列数据神经组织蛋白质类/化学神经组织蛋白质类/遗传学神经组织蛋白质类/代谢肽碎片/化学磷酰化种系发生蛋白质亚型/化学蛋白质亚型/代谢蛋白激酶类/代谢重组蛋白质类/化学重组蛋白质类/代谢氯苄乙胺序列比对序列同源性氨基酸底物特异性动物人类大鼠

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Production of human CNS neurons from embryonal carcinoma cells using a cell aggregation method

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BIOTECHNIQUES 1999年第5期26卷 946-+页

作者： Cheung, WMW Fu, WY Hui, WS Ip, NY Hong Kong Univ Sci & Technol Dept Biol Clear Water Bay Hong Kong Peoples R China Hong Kong Univ Sci & Technol Biotechnol Res Inst Hong Kong Peoples R China

When treated with retinoic acid (RA), a human embryonal carcinoma (EC) cell line, NTera2 cl.D/1 (NT2), differentiates into several morphologically distinct cell types, which include terminally differentiated postmitotic central nervous system (CNS) neurons. Accumulating evidence has demonstrated the significant potential of NT2 cells in studies related to cancer therapy and neurodegenerative diseases However, preparation of enriched NT2 neurons often requires a lengthy period (co. five,weeks) and depends largely on tedious techniques similar to those used for primary neuronal cultures. Here, we report a rapid protocol for the preparation of these human CNS neurons. Using the method of cell aggregation, enriched NT2 neurons can he obtained in approximately two weeks. We also demonstrated that cell aggregation reduced the time normally required for the induction of neuronal differentiation as revealed by the early expression of neuronal markers. The period of RA treatment could also be reduced if NT2 cells were maintained cls aggregates for a sufficient period of time. Taken together our findings demonstrated that cell aggregation promoted RA-induced neuronal differentiation of NT2 cells and provided a rapid protocol for the efficient production of NT2 neurons. The ability to produce large quantities of human CNS neurons should facilitate future rise of these neurons for basic research and applications in cell therapy.

关键词：生物技术癌胚胎性/病理学细胞集合细胞分化/药物作用中枢神经系统/细胞学中枢神经系统/药物作用中枢神经系统/代谢神经组织蛋白质类/代谢神经突/超微结构神经元/细胞学神经元/药物作用神经元/代谢时间因素维甲酸/药理学肿瘤细胞培养的人类

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Constitutive phosphorylation of the Parkinson's disease associated α-synuclein

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第1期275卷 390-397页

作者： Okochi, M Walter, J Koyama, A Nakajo, S Baba, M Iwatsubo, T Meijer, L Kahle, PJ Haass, C Univ Munich Adolf Butenandt Inst Dept Biochem D-80336 Munich Germany Univ Tokyo Grad Sch Pharmaceut Sci Dept Neuropathol & Neurosci Tokyo 1130033 Japan Showa Univ Sch Pharmaceut Sci Biol Chem Lab Tokyo Japan CNRS Biol Stn F-29682 Roscoff France

alpha-Synuclein has been implicated in the pathogenesis of Parkinson's disease, since rare autosomal dominant mutations are associated with early onset of the disease and alpha-synuclein was found to be a major constituent of Lewy bodies. We have analyzed alpha-synuclein expression in transfected cell lines. In pulse-chase experiments alpha-synuclein appeared to be stable over long periods (t(1/2) 54 h) and no endoproteolytic processing was observed. alpha-Synuclein was constitutively phosphorylated in human kidney 293 cells as well as in rat pheochromocytoma PC12 cells. In both cell lines phosphorylation was highly sensitive to phosphatases, since okadaic acid markedly stabilized phosphate incorporation. Phosphoamino acid analysis revealed that phosphorylation occurred predominantly on serine. Using site-directed mutagenesis we have identified a major phosphorylation site at serine 129 within the C-terminal domain of alpha-synuclein. An additional site, which was phosphorylated less efficiently, was mapped to serine 87. The major phosphorylation site was located within a consensus recognition sequence of casein kinase 1 (CK-1). In vitro experiments and two-dimensional phosphopeptide mapping provided further evidence that serine 129 was phosphorylated by CK-1 and CK-2. Moreover, phosphorylation of serine 129 was reduced in vivo upon inhibition of CK-1 or CK-2. These data demonstrate that alpha-synuclein is constitutively phosphorylated within its C terminus and may indicate that the function of alpha-synuclein is regulated by phosphorylation/dephosphorylation.

关键词：氨基酸序列抗体特异性脑化学酪蛋白激酶Ⅱ 酪蛋白激酶类分子序列数据诱变定点神经组织蛋白质类/遗传学神经组织蛋白质类/免疫学神经组织蛋白质类/代谢 PC12细胞帕金森病/代谢磷蛋白类/遗传学磷蛋白类/免疫学磷蛋白类/代谢磷酰化蛋白激酶抑制剂蛋白激酶类/代谢蛋白质丝氨酸苏氨酸激酶/拮抗剂和抑制剂蛋白质丝氨酸苏氨酸激酶/代谢丝氨酸/遗传学突触核蛋白类 α突触核蛋白动物人类大鼠

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EHSH1/intersectin, a protein that contains EH and SH3 domains and binds to dynamin and SNAP-25 -: A protein connection between exocytosis and endocytosis?

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第26期274卷 18446-18454页

作者： Okamoto, M Schoch, S Südhof, TC Univ Texas SW Med Ctr Howard Hughes Med Inst Ctr Basic Neurosci Dallas TX 75235 USA Univ Texas SW Med Ctr Dept Mol Genet Dallas TX 75235 USA

In yeast two-hybrid screens for proteins that bind to SNAP-25 and may be involved in exocytosis, we isolated a protein called EHSH1 (for ER domain/SH3 domain-containing protein). Cloning of full-length cDNAs revealed that EHSH1 is composed of an N-terminal region with two EH domains, a central region that is enriched in lysine, leucine, glutamate, arginine, and glutamine (KLERQ domain), and a C-terminal region comprised of five SH3 domains. The third SH3 domain is alternatively spliced, Data bank searches demonstrated that EHSH1 is very similar to Xenopus and human intersectins and to human SH3P17. In addition, we identified expressed sequence tags that encode a second isoform of EHSH1, called EHSH2. EHSH1 is abundantly expressed in brain and at lower levels in all other tissues tested. In binding studies, we found that the central KLERQ domain of EHSH1 binds to recombinant or native brain SNAP-25 and SNAP-23, The C-terminal SH3 domains, by contrast, quantitatively interact with dynamin, a protein involved in endocytosis. Dynamin strongly binds to the alternatively spliced central SH3 domain (SH3C) and the two C-terminal SH3 domains (SH3D and SH3E) but not to the N-terminal SH3 domains (SH3A and SH3B), Immunoprecipitations confirmed that both dynamin and SNAP-25 are complexed to EHSH1 in brain, Our data suggest that EHSH1/intersectin may be a novel adaptor protein that couples endocytic membrane traffic to exocytosis. The ability of multiple SH3 domains in EHSH1 to bind to dynamin suggests that EHSH1 can cluster several dynamin molecules in a manner that is regulated by alternative splicing.

关键词：衔接蛋白质类膜泡运输氨基酸序列载体蛋白质类/化学载体蛋白质类/代谢果蝇属果蝇蛋白质类动力蛋白质类胞吞作用胞吐作用 GTP磷酸水解酶类/代谢基因文库膜蛋白质类分子序列数据神经组织蛋白质类/代谢蛋白质结合突触体相关蛋白质25 爪蟾属 src同源域动物人类小鼠大鼠

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