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排序方式: 共有349条查询结果,搜索用时 31 毫秒
101.
Christo N. Nanev 《Crystal Research and Technology》2015,50(6):451-457
The so‐called bond selection mechanism, BSM (C.N. Nanev, Progress in Crystal Growth and Characterization of Materials, 59 , 133–169, 2013) allows explaining a set of traits in both protein crystal nucleation and growth processes. BSM explanatory and predictive power are enhanced now, when intra‐crystalline repulsive interactions are assumed to act in parallel with the attractive forces, the former arising due to protein surface patch‐to‐patch incompatibility. Shapes of 1D and 2D protein crystals are considered from such a perspective. Using BSM the strong directional kinetic anisotropy in the edge growth rates of 2D protein crystals is tackled. The shapes of near‐critically sized apoferritin crystals and of experimentally grown 3D apoferritin crystals are considered. 相似文献
102.
The Molecular Structure of Alzheimer β‐Amyloid Fibrils Formed in the Presence of Phospholipid Vesicles
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Zheng Niu Weijing Zhao Dr. Zhengfeng Zhang Dr. Fanshu Xiao Xinqi Tang Prof. Jun Yang 《Angewandte Chemie (International ed. in English)》2014,53(35):9294-9297
β‐amyloid (Aβ) fibrils are the major species involved in Alzheimer’s disease (AD). An atomic‐resolution molecular structure of Aβ40 fibrils formed in the presence of lipid vesicles was obtained by using magic angle spinning (MAS) solid‐state NMR spectroscopy. The fibril structures formed in the presence of the lipid vesicles are remarkably different from those formed in solution. These results provide insights into the molecular mechanism of Aβ aggregation in the presence of lipid vesicles. 相似文献
103.
Hong Hee Lee Tae Su Choi Shin Jung C. Lee Jong Wha Lee Junghong Park Dr. Young Ho Ko Prof. Dr. Won Jong Kim Prof. Dr. Kimoon Kim Prof. Dr. Hugh I. Kim 《Angewandte Chemie (International ed. in English)》2014,53(29):7461-7465
Amyloid fibrils are insoluble protein aggregates comprised of highly ordered β‐sheet structures and they are involved in the pathology of amyloidoses, such as Alzheimer’s disease. A supramolecular strategy is presented for inhibiting amyloid fibrillation by using cucurbit[7]uril (CB[7]). CB[7] prevents the fibrillation of insulin and β‐amyloid by capturing phenylalanine (Phe) residues, which are crucial to the hydrophobic interactions formed during amyloid fibrillation. These results suggest that the Phe‐specific binding of CB[7] can modulate the intermolecular interaction of amyloid proteins and prevent the transition from monomeric to multimeric states. CB[7] thus has potential for the development of a therapeutic strategy for amyloidosis. 相似文献
104.
Dr. Christofer Lendel Dr. Morten Bjerring Dr. Anatoly Dubnovitsky Robert T. Kelly Dr. Andrei Filippov Prof. Dr. Oleg N. Antzutkin Prof. Dr. Niels Chr. Nielsen Prof. Dr. Torleif Härd 《Angewandte Chemie (International ed. in English)》2014,53(47):12756-12760
Oligomeric and protofibrillar aggregates formed by the amyloid‐β peptide (Aβ) are believed to be involved in the pathology of Alzheimer’s disease. Central to Alzheimer pathology is also the fact that the longer Aβ42 peptide is more prone to aggregation than the more prevalent Aβ40. Detailed structural studies of Aβ oligomers and protofibrils have been impeded by aggregate heterogeneity and instability. We previously engineered a variant of Aβ that forms stable protofibrils and here we use solid‐state NMR spectroscopy and molecular modeling to derive a structural model of these. NMR data are consistent with packing of residues 16 to 42 of Aβ protomers into hexameric barrel‐like oligomers within the protofibril. The core of the oligomers consists of all residues of the central and C‐terminal hydrophobic regions of Aβ, and hairpin loops extend from the core. The model accounts for why Aβ42 forms oligomers and protofibrils more easily than Aβ40. 相似文献
105.
Characterization of New Specific Copper Chelators as Potential Drugs for the Treatment of Alzheimer’s Disease
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Dr. Michel Nguyen Dr. Anne Robert Dr. Alix Sournia‐Saquet Dr. Laure Vendier Dr. Bernard Meunier 《Chemistry (Weinheim an der Bergstrasse, Germany)》2014,20(22):6771-6785
The non‐controlled redox‐active metal ions, especially copper, in the brain of patients with Alzheimer disease (AD) should be considered at the origin of the intense oxidative damage in the AD brain. Several bis(8‐aminoquinoline) ligands, such as 1 and PA1637, are able to chelate Cu2+ with high affinity, and are specific chelators of copper with respect to iron and zinc. They are able to efficiently extract Cu2+ from a metal‐loaded amyloid. In addition, these tetradentate ligands are specific for the chelation of Cu2+ compared with Cu+. Consequently, the copper ion is easily released from the bis(8‐aminoquinoline) ligand under reductive conditions, and can be trapped again by a protein having some affinity for copper such as human serum albumin (HSA) proteins. In addition, the copper is not efficiently released from [Cu(CQ)2] in reductive conditions. The catalytic production of H2O2 by [Cu2+‐Aβ1?28]/ascorbate is inhibited in vitro by the bis(8‐aminoquinoline) 1 , suggesting that 1 should be able to play a protective role against oxidative damages induced by copper‐loaded amyloids. 相似文献
106.
107.
pH‐Controlled Formation of a Stable β‐Sheet and Amyloid‐like Fibers from an Amphiphilic Peptide: The Importance of a Tailor‐Made Binding Motif for Secondary Structure Formation
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Dr. Poulami Jana Martin Ehlers Elio Zellermann Dr. Krishnananda Samanta Prof. Dr. Carsten Schmuck 《Angewandte Chemie (International ed. in English)》2016,55(49):15287-15291
The new amphiphilic peptide 1 is composed of alternating cyclohexyl side chains and guanidiniocarbonyl pyrrole (GCP) groups. In contrast to analogue 2 , which contains lysine instead of the GCP groups and only exists as a random coil owing to charge repulsion, peptide 1 forms a stable β‐sheet at neutral pH in aqueous medium. The weakly basic GCP groups (pKa≈7) are key for secondary structure formation as they stabilize the β‐sheet through mutual interactions (formation of a “GCP zipper”). The β‐sheets further aggregate into left‐handed helically twisted fibers. However, β‐sheet formation is completely reversible as a function of pH. At low pH (ca. 4), peptide 1 is unstructured (random coil) as all GCP units are protonated. Only round colloidal particles are observed. The amyloid nature of the fibers formed at neutral pH was confirmed by staining experiments with Congo Red and thioflavin T. Furthermore, at millimolar concentrations, peptide 1 forms a stable hydrogel. 相似文献
108.
Recent studies have reported that the cholinergic anti-inflammatory pathway regulates peripheral inflammatory responses via alpha7 nicotinic acetylcholine receptors (alpha7 nAChRs) and that acetylcholine and nicotine regulate the expression of proinflammatory mediators such as TNF-alpha and prostaglandin E2 in microglial cultures. In a previous study we showed that ATP released by beta-amyloid-stimulated microglia induced reactive oxygen species (ROS) production, in a process involving the P2X(7) receptor (P2X(7)R), in an autocrine fashion. These observations led us to investigate whether stimulation by nicotine could regulate fibrillar beta amyloid peptide (1-42) (fAbeta1-42)-induced ROS production by modulating ATP efflux-mediated Ca(2+) influx through P2X(7)R. Nicotine inhibited ROS generation in fAbeta(1-42)-stimulated microglial cells, and this inhibition was blocked by mecamylamine, a non-selective nAChR antagonist, and a-bungarotoxin, a selective alpha7 nAChR antagonist. Nicotine inhibited NADPH oxidase activation and completely blocked Ca(2+) influx in fAbeta(1-42)-stimulated microglia. Moreover, ATP release from fAbeta(1-42)-stimulated microglia was significantly suppressed by nicotine treatment. In contrast, nicotine did not inhibit 2',3'-O-(4-benzoyl)-benzoyl ATP (BzATP)-induced Ca(2+) influx, but inhibited ROS generation in BzATP-stimulated microglia, indicating an inhibitory effect of nicotine on a signaling process downstream of P2X(7)R. Taken together, these results suggest that the inhibitory effect of nicotine on ROS production in fAbeta1-42-stimulated microglia is mediated by indirect blockage of ATP release and by directly altering the signaling process downstream from P2X(7)R. 相似文献
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