記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Neuropharmacology  

Exquisitely-regulated synaptic transmission and plasticity underlie higher brain functions such as learning and memory. PSD-95, a member of the MAGUK family, scaffolds an array of postsynaptic proteins including AMPA and NMDA receptors, and plays essential roles in excitatory synaptic transmission and postsynaptic organization. Epilepsy-related secreted protein LGI1 and its receptor ADAM22 represent major constituent elements of the PSD-95-containing synaptic protein complex in the brain. Recent studies begin to reveal a trans-synaptic configuration of the LGI1–ADAM22 complex and its pivotal role in AMPA and NMDA receptor-mediated synaptic transmission through regulating MAGUKs. Especially interesting is that without the association with LGI1–ADAM22, PSD-95 cannot potentiate AMPA receptor-mediated synaptic transmission. Here, we review roles of LGI1–ADAM22 in synaptic function, and discuss its modes of action on the MAGUK regulation: as (i) a trans-synaptic hub, (ii) an extracellular scaffold, and (iii) an allosteric activator. We also highlight patho-physiological roles of the LGI1–ADAM22–MAGUK linkage in synaptic disorders such as epilepsy and autoimmune limbic encephalitis.

DOI： 10.1016/j.neuropharm.2021.108628

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記述言語：日本語   出版者・発行元：日本電気泳動学会  

<p>パルミトイル化修飾は1970年代に報告された脂質修飾で，3量体Gタンパク質αや低分子量Gタンパク質HRas，シナプス足場タンパク質PSD-95等の細胞膜局在を決定する．パルミトイル化修飾は可逆性を有する唯一の脂質修飾であり，シグナル伝達における重要性が示唆されてきた．この10年余りで，パルミトイル化・脱パルミトイル化酵素が明らかになり，プロテオミクス解析によりパルミトイル化タンパク質が数千種類存在することが分かってきた．本稿では，最近，私共が開発したパルミトイル化状態（量比とパルミトイル化部位数）の定量法“APEGS法”について紹介する．APEGS法は，(1) 様々な生物試料に応用でき，(2) 精製を必要とせず（高収率），(3) 調べたい任意のタンパク質に適用可能であり，(4) パルミトイル化動態を定量できる，という点で極めて有用な手法である．</p>

DOI： 10.2198/electroph.65.41

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Wiley  

<jats:title>Abstract</jats:title><jats:p>A 7‐year‐old neutered female domestic shorthaired cat born in Poland and then moved to Japan presented to the local clinic with recent onset of convulsive cluster seizures and status epilepticus. Magnetic resonance imaging revealed bilateral swelling of the hippocampus with T2 hyperintensity and contrast enhancing image, suggesting hippocampal necrosis. The cat completely recovered after treatment with antiepileptic drugs (AED) and administration of prednisolone (1 mg/kg PO q24h for 4 days and tapered). However, cluster seizures reoccurred and developed into status epilepticus despite increasing doses of AED. Although the convulsions were resolved by other AEDs, stupor and renal failure developed, and the cat was euthanized. Pathological findings were consistent with hippocampal necrosis. Immunological analysis for leucine‐rich glioma inactivated 1 (LGI1) autoantibodies was negative, but antibodies against DCC (deleted in colorectal carcinoma) known as netrin‐1 receptor were found. This report describes a case of feline autoimmune limbic encephalitis and hippocampal necrosis that were presumably associated with DCC autoantibodies.</jats:p>

DOI： 10.1111/jvim.15492

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Nature Communications  

Epilepsy is a common brain disorder throughout history. Epilepsy-related ligand-receptor complex, LGI1-ADAM22, regulates synaptic transmission and has emerged as a determinant of brain excitability, as their mutations and acquired LGI1 autoantibodies cause epileptic disorders in human. Here, we report the crystal structure of human LGI1-ADAM22 complex, revealing a 2:2 heterotetrameric assembly. The hydrophobic pocket of the C-Terminal epitempin-repeat (EPTP) domain of LGI1 binds to the metalloprotease-like domain of ADAM22. The N-Terminal leucine-rich repeat and EPTP domains of LGI1 mediate the intermolecular LGI1-LGI1 interaction. A pathogenic R474Q mutation of LGI1, which does not exceptionally affect either the secretion or the ADAM22 binding, is located in the LGI1-LGI1 interface and disrupts the higher-order assembly of the LGI1-ADAM22 complex in vitro and in a mouse model for familial epilepsy. These studies support the notion that the LGI1-ADAM22 complex functions as the trans-synaptic machinery for precise synaptic transmission.

DOI： 10.1038/s41467-018-03947-w

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その他リンク： http://www.nature.com/articles/s41467-018-03947-w

記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Journal of Neuroimmunology  

The clinical features of cerebellar ataxia associated with anti-metabotropic glutamate receptor 1 (mGluR1) autoantibodies, a rare autoimmune-mediated cerebellar ataxia, remain to be elucidated. Here, we describe a patient with non-paraneoplastic cerebellar ataxia associated with anti-mGluR1 autoantibodies, who was followed up over 5 years. She presented with relapses and remissions of subacute progressive cerebellar ataxia that were responsive to immunotherapy. Although serum anti-mGluR1 autoantibodies were continuously detected and cerebellar atrophy gradually progressed, repeated intravenous immunoglobulin therapy and oral immunosuppressants ensured cerebellar ataxia remained at almost the same level during the observation period.

DOI： 10.1016/j.jneuroim.2018.04.001

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記述言語：英語   出版者・発行元：Current Opinion in Neurobiology  

Autoimmune encephalitis presenting with amnesia, seizures, and psychosis is highly topical in basic and clinical neuroscience. Recent studies have identified numerous associated autoantibodies, targeting cell-surface synaptic proteins including neurotransmitter receptors (e.g. NMDA receptors (NMDARs)) and a secreted protein, LGI1. In vitro and in vivo analyses of the influence of the autoantibodies have begun to clarify their causal roles. Of particular interest is the generation of recombinant monoclonal antibodies from patients’ B cells with anti-NMDAR encephalitis. Patient monoclonal antibodies could be useful to reveal their direct, detailed pathogenicity. Such identification and characterization of autoantibodies could create new categories of neurological diseases and promote the understanding of patho-physiologic roles of target proteins in human brain function.

DOI： 10.1016/j.conb.2017.07.012

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記述言語：英語   出版者・発行元：Neuroscience Research  

Physiological functioning of the brain requires fine-tuned synaptic transmission, and its dysfunction causes various brain disorders such as autism, dementia, and epilepsy. It is therefore extremely important to identify and characterize key regulators of synaptic function. In particular, disease-related synaptic proteins, such as autism-related neurexin–neuroligin and psychiatric disorder-related NMDA receptor, have attracted considerable attention. Recent basic and clinical research has highlighted critical roles of a ligand–receptor complex, LGI1–ADAM22, in synaptic transmission and brain function, as mutations in the LGI1 gene cause autosomal dominant lateral temporal lobe epilepsy and autoantibodies to LGI1 cause limbic encephalitis which is characterized by memory loss and seizures. Here, we will review our current knowledge about LGI1 and ADAM22, and discuss their patho-physiological roles in synaptic transmission and synaptic disorders.

DOI： 10.1016/j.neures.2016.09.011

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Journal of Neuroscience  

Postsynaptic density (PSD)-95, the most abundant postsynaptic scaffolding protein, plays a pivotal role in synapse development and function. Continuous palmitoylation cycles on PSD-95 are essential for its synaptic clustering and regulation ofAMPAreceptor function. However, molecular mechanisms for palmitate cycling on PSD-95 remain incompletely understood, as PSD-95 depalmitoylating enzymes remain unknown. Here, we isolated 38 mouse or rat serine hydrolases and found that a subset specifically depalmitoylated PSD-95 in heterologous cells. These enzymes showed distinct substrate specificity. α/β-Hydrolase domain-containing protein 17 members (ABHD17A, 17B, and 17C), showing the strongest depalmitoylating activity to PSD-95, showed different localization from other candidates in rat hippocampal neurons, and were distributed to recycling endosomes, the dendritic plasma membrane, and the synaptic fraction. Expression of ABHD17 in neurons selectively reduced PSD-95 palmitoylation and synaptic clustering of PSD-95 and AMPA receptors. Furthermore, taking advantage of the acyl-PEGyl exchange gel shift (APEGS) method, we quantitatively monitored the palmitoylation stoichiometry and the depalmitoylation kinetics of representative synaptic proteins, PSD-95, GluA1, GluN2A, mGluR5, Gαq, and HRas. Unexpectedly, palmitate on all of them did not turn over in neurons. Uniquely, most of the PSD-95 population underwent rapid palmitoylation cycles, and palmitate cycling on PSD-95 decelerated accompanied by its increased stoichiometry as synapses developed, probably contributing to postsynaptic receptor consolidation. Finally, inhibition of ABHD17 expression dramatically delayed the kinetics of PSD-95 depalmitoylation. This study suggests that local palmitoylation machinery composed of synaptic DHHC palmitoylating enzymes and ABHD17 finely controls the amount of synaptic PSD-95 and synaptic function.

DOI： 10.1523/JNEUROSCI.0419-16.2016

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Current Topics in Membranes  

Palmitoylation is an evolutionally conserved lipid modification of proteins. Dynamic and reversible palmitoylation controls a wide range of molecular and cellular properties of proteins including the protein trafficking, protein function, protein stability, and specialized membrane domain organization. However, technical difficulties in (1) detection of palmitoylated substrate proteins and (2) purification and enzymology of palmitoylating enzymes have prevented the progress in palmitoylation research, compared with that in phosphorylation research. The recent development of proteomic and chemical biology techniques has unexpectedly expanded the known complement of palmitoylated proteins in various species and tissues/cells, and revealed the unique occurrence of palmitoylated proteins in membrane-bound organelles and specific membrane compartments. Furthermore, identification and characterization of DHHC (Asp-His-His-Cys) palmitoylating enzyme–substrate pairs have contributed to elucidating the regulatory mechanisms and pathophysiological significance of protein palmitoylation. Here, we review the recent progress in protein palmitoylation at the molecular, cellular, and in vivo level and discuss how locally regulated palmitoylation machinery works for dynamic nanoscale organization of membrane domains.

DOI： 10.1016/bs.ctm.2015.10.003

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Portland Press Ltd.  

<jats:p>Precise regulation of protein assembly at specialized membrane domains is essential for diverse cellular functions including synaptic transmission. However, it is incompletely understood how protein clustering at the plasma membrane is initiated, maintained and controlled. Protein palmitoylation, a common post-translational modification, regulates protein targeting to the plasma membrane. Such modified proteins are enriched in these specialized membrane domains. In this review, we focus on palmitoylation of PSD-95, which is a major postsynaptic scaffolding protein and makes discrete postsynaptic nanodomains in a palmitoylation-dependent manner and discuss a determinant role of local palmitoylation cycles in creating highly localized hotspots at the membrane where specific proteins concentrate to organize functional domains.</jats:p>

DOI： 10.1042/bst20140238

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Nature Medicine  

Epilepsy is one of the most common and intractable brain disorders. Mutations in the human gene LGI1, encoding a neuronal secreted protein, cause autosomal dominant lateral temporal lobe epilepsy (ADLTE). However, the pathogenic mechanisms of LGI1 mutations remain unclear. We classified 22 reported LGI1 missense mutations as either secretion defective or secretion competent, and we generated and analyzed two mouse models of ADLTE encoding mutant proteins representative of the two groups. The secretion-defective LGI1 E383A protein was recognized by the ER quality-control machinery and prematurely degraded, whereas the secretable LGI1 S473L protein abnormally dimerized and was selectively defective in binding to one of its receptors, ADAM22. Both mutations caused a loss of function, compromising intracellular trafficking or ligand activity of LGI1 and converging on reduced synaptic LGI1-ADAM22 interaction. A chemical corrector, 4-phenylbutyrate (4PBA), restored LGI1 E383A folding and binding to ADAM22 and ameliorated the increased seizure susceptibility of the LGI1 E383A model mice. This study establishes LGI1-related epilepsy as a conformational disease and suggests new therapeutic options for human epilepsy.

DOI： 10.1038/nm.3759

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Journal of Neuroscience  

Autoimmune forms of encephalitis have been associated with autoantibodies against synaptic cell surface antigens such as NMDA- and AMPA-type glutamate receptors, GABAB receptor, and LGI1. However, it remains unclear how many synaptic autoantigens are yet to be defined. Using immunoproteomics, we identified autoantibodies against theGABAA receptor inhumansera from two patients diagnosed with encephalitis who presented with cognitive impairment and multifocal brain MRI abnormalities. Both patients had antibodies directed against the extracellular epitope of the β3 subunit of the GABAA receptor. The β3-subunit-containing GABAA receptor was a major target of the patients' serum antibodies in rat hippocampal neurons because the serum reactivity to the neuronal surface was greatly decreased by 80% when theβ3 subunit was knocked down. Our developed multiplex ELISA testing showed that both patients had similar levels of GABAA receptor antibodies, one patient also had a low level of LGI1 antibodies, and the other also had CASPR2 antibodies. Application of the patients' serum at the time ofsymptompresentation of encephalitis to rat hippocampal neuron cultures specifically decreased both synaptic and surface GABAA receptors. Furthermore, treatment of neurons with the patients' serum selectively reduced miniature IPSC amplitude and frequency without affecting miniature EPSCs. These results strongly suggest that the patients' GABAA receptor antibodies play a central role in the patients' symptoms. Therefore, this study establishes anti-GABAA receptor encephalitis and expands the pathogenic roles of GABAA receptor autoantibodies. © 2014 the authors.

DOI： 10.1523/JNEUROSCI.4415-13.2014

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Journal of Neuroscience  

More than 30 mutations in LGI1, a secreted neuronal protein, have been reported with autosomal dominant lateral temporal lobe epilepsy (ADLTE). Although LGI1 haploinsufficiency is thought to cause ADLTE, the underlying molecular mechanism that results in abnormal brain excitability remains mysterious. Here, we focused on a mode of action of LGI1 autoantibodies associated with limbic encephalitis (LE), which is one of acquired epileptic disorders characterized by subacute onset of amnesia and seizures.Wecomprehensively screened human sera from patients with immune-mediated neurological disorders for LGI1 autoantibodies, which also uncovered novel autoantibodies against six cell surface antigens including DCC, DPP10, and ADAM23. Our developed ELISA arrays revealed a specific role for LGI1 antibodies in LE and concomitant involvement of multiple antibodies, including LGI1 antibodies in neuromyotonia, a peripheral nerve disorder. LGI1 antibodies associated with LE specifically inhibited the ligand-receptor interaction between LGI1 and ADAM22/23 by targeting the EPTP repeat domain of LGI1 and reversibly reduced synaptic AMPA receptor clusters in rat hippocampal neurons. Furthermore, we found that disruption of LGI1-ADAM22 interaction by soluble extracellular domain ofADAM22was sufficient to reduce synapticAMPAreceptors in rat hippocampal neurons and that levels ofAMPAreceptor were greatly reduced in the hippocampal dentate gyrus in the epileptic LGI1 knock-out mouse. Therefore, either genetic or acquired loss of the LGI1-ADAM22 interaction reduces theAMPAreceptor function, causing epileptic disorders. These results suggest that by finely regulating the synapticAMPAreceptors, the LGI1-ADAM22 interaction maintains physiological brain excitability throughout life. © 2013 the authors.

DOI： 10.1523/JNEUROSCI.3506-13.2013

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記述言語：英語   掲載種別：論文集(書籍)内論文   出版者・発行元：International Review of Cell and Molecular Biology  

α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPARs) mediate the majority of fast excitatory synaptic transmission in the brain. AMPARs dynamically cycle in and out of the postsynaptic membrane in an activity-dependent manner. Because the number and functional properties of AMPARs at the postsynapse determine the efficacy of synaptic transmission, molecular mechanisms underlying AMPAR trafficking and gating are considered to have a central role in synaptic plasticity, a basic mechanism for learning and memory. In this chapter, we review the current knowledge about the regulatory mechanisms for AMPAR trafficking and channel gating by protein-protein interactions and posttranslational modifications. Especially, we focus on the recently established mode of action of the AMPAR auxiliary subunit, stargazin/TARPs, and PSD-95 scaffold. Furthermore, we introduce novel players in AMPAR regulation, PSD-95 palmitoylating enzymes and epilepsy-related ligand, LGI1. © 2012 Elsevier Inc.

DOI： 10.1016/B978-0-12-394308-8.00001-7

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記述言語：英語   掲載種別：研究論文（学術雑誌）  

DOI： 10.1039/c0cc03015e

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Small  

Achieving control over the structures of artifi cial protein and peptide assemblies is a worthwhile goal because it would provide a powerful approach for the construction of nanomaterials.[1-4] Artifi cial self-assembled proteins obtained using protein engineering techniques could then be obtained by designing quaternary structures that include modifi ed protein-protein interfaces,[5-9] fusion proteins,[10-13] chemical conjugations,[14,15] and self-assembly of short peptides. [16,17] The resulting protein assembly structures in the form of tubes,[6,10] cages,[5,7,9,11] rings [18] and 2D layers [12,14,15] could serve as nanoreactors and nanotemplates. In particular, tube structures offer great promise as building blocks of nanomaterials designed for applications such as molecular sensing, drug delivery, imaging, catalysis, and the synthesis of new materials. [2,4,10,13,19-23] Although several studies showed that tubular protein assemblies have been adopted as protein-based platforms for catalytic reactions promoted by enzymes or fl uorescent molecules displayed on the surfaces,[2,4,10,13,19-23] it is diffi cult to control the reactivity of these systems by fixation of functional molecules at appropriate sites. Thus, it has remained challenging to obtain tube structures with high stability and well-defi ned nanoscale lengths for properly aligning synthetic molecules on the surfaces of the nanotubes.Copyright © 2010 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.

DOI： 10.1002/smll.201000772

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Proceedings of the National Academy of Sciences  

<jats:p>
Epilepsy is a devastating and poorly understood disease. Mutations in a secreted neuronal protein, leucine-rich glioma inactivated 1 (LGI1), were reported in patients with an inherited form of human epilepsy, autosomal dominant partial epilepsy with auditory features (ADPEAF). Here, we report an essential role of LGI1 as an antiepileptogenic ligand. We find that loss of LGI1 in mice (LGI1
<jats:sup>−/−</jats:sup>
) causes lethal epilepsy, which is specifically rescued by the neuronal expression of LGI1 transgene, but not LGI3. Moreover, heterozygous mice for the LGI1 mutation (LGI1
<jats:sup>+/−</jats:sup>
) show lowered seizure thresholds. Extracellularly secreted LGI1 links two epilepsy-related receptors, ADAM22 and ADAM23, in the brain and organizes a transsynaptic protein complex that includes presynaptic potassium channels and postsynaptic AMPA receptor scaffolds. A lack of LGI1 disrupts this synaptic protein connection and selectively reduces AMPA receptor–mediated synaptic transmission in the hippocampus. Thus, LGI1 may serve as a major determinant of brain excitation, and the LGI1 gene-targeted mouse provides a good model for human epilepsy.
</jats:p>

DOI： 10.1073/pnas.0914537107

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Small  

The use of heteroprotein assemblies for providing a bionanocup to construct catalysts, sensors, and materials with novel properties, is discussed. It is used as a catalytic reaction space that consists of a heteroprotein assembly, which is a trimer of gene product 27 and gene product 5, isolated from bacteriophase T4. The bionanocup can be used for the accommodation of metal-porphyrin complexes by covalent linkage with cysteinyl thiols and its activity as an oxidation catalyst. Inductively coupled plasma (ICP) atomic-emission measurement and biocinchonianate (BCA) assay were used to observe the number of atoms in the reactor. The electron density map of derivatives shows a clear density between the male-amide moiety of FePP-MI and N7C. The proportions of Fe atoms to protein in the bionanocup were determined using the Vista-PRO (VARIAN) and bicinchonianate (BCA) methods.

DOI： 10.1002/smll.200700855

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Chemical Communications  

We have succeeded in improving the stability of Fe(Schiff-base)•heme oxygenase (HO) hybrids by ligand design based on the crystal structure of Fe(N,N′-bis(salicylidene)-3.4-diaminobenzene propionic acid)•HO. © The Royal Society of Chemistry.

DOI： 10.1039/b713468a

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Journal of Inorganic Biochemistry  

Preparation of metal/protein hybrids is growing into important topics in the field of bioinorganic chemistry. X-ray crystal structure analyses of them provide direct information on unique interactions of metal cations or metal cofactors to understand and design enzymatic functions. In this mini review, the authors focus on the recent studies on the metal/protein hybrids concerning crystal structure analyses since 2002 and our related works. The precise structural determination promise us to deeply understand coordination chemistry in protein scaffold and shows intriguing suggestions on rational design and application use for biocatalysts, metal drugs and so on. © 2007 Elsevier Inc. All rights reserved.

DOI： 10.1016/j.jinorgbio.2007.06.025

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出版者・発行元：Coordination Chemistry Reviews  

Design of artificial metalloproteins is one of the most important subjects in the field of bioinorganic chemistry. In order to prepare them, vacant space of proteins has been utilized because it gives us unique chemical environment to construct catalysts and materials. This article reviews on preparation methods and properties of metal/protein composites. The discussion includes our recent results and development in the screening of composites, crystal structures, molecular design of bio-inspired systems concerning catalysts, electrochemistry, and materials. © 2007 Elsevier B.V. All rights reserved.

DOI： 10.1016/j.ccr.2007.04.007

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Journal of Organometallic Chemistry  

Construction of artificial metalloenzymes is one of the most attractive targets in the field of inorganic and catalytic chemistry, since they show remarkable chemoselectivity and reactivity in aqueous media. For the purpose, covalent modification of protein and cofactors have usually been utilized to attach a metal complex(es) to a protein scaffold. This article focuses on non-covalent insertion of metal complexes into protein environments. The discussion includes the screening of stable metal complex/protein composites, crystal structures, molecular design for regulating enantioselectivity of the target catalytic reactions. Our recent results show that the non-covalent conjugation will provide us a new way in semi-synthesis of artificial metalloenzymes. © 2006 Elsevier B.V. All rights reserved.

DOI： 10.1016/j.jorganchem.2006.08.043

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記述言語：英語   掲載種別：研究論文（学術雑誌）   出版者・発行元：Proceedings of the National Academy of Sciences  

<jats:p>
Protein-to-protein electron transfer (ET) is a critical process in biological chemistry for which fundamental understanding is expected to provide a wealth of applications in biotechnology. Investigations of protein–protein ET systems in reductive activation of artificial cofactors introduced into proteins remains particularly challenging because of the complexity of interactions between the cofactor and the system contributing to ET. In this work, we construct an artificial protein–protein ET system, using heme oxygenase (HO), which is known to catalyze the conversion of heme to biliverdin. HO uses electrons provided from NADPH/cytochrome P450 reductase (CPR) through protein–protein complex formation during the enzymatic reaction. We report that a Fe
<jats:sup>III</jats:sup>
(Schiff-base), in the place of the active-site heme prosthetic group of HO, can be reduced by NADPH/CPR. The crystal structure of the Fe(10-CH
<jats:sub>2</jats:sub>
CH
<jats:sub>2</jats:sub>
COOH-Schiff-base)·HO composite indicates the presence of a hydrogen bond between the propionic acid carboxyl group and Arg-177 of HO. Furthermore, the ET rate from NADPH/CPR to the composite is 3.5-fold faster than that of Fe(Schiff-base)·HO, although the redox potential of Fe(10-CH
<jats:sub>2</jats:sub>
CH
<jats:sub>2</jats:sub>
COOH-Schiff-base)·HO (−79 mV vs. NHE) is lower than that of Fe(Schiff-base)·HO (+15 mV vs. NHE), where NHE is normal hydrogen electrode. This work describes a synthetic metal complex activated by means of a protein–protein ET system, which has not previously been reported. Moreover, the result suggests the importance of the hydrogen bond for the ET reaction of HO. Our Fe(Schiff-base)·HO composite model system may provide insights with regard to design of ET biosystems for sensors, catalysts, and electronics devices.
</jats:p>

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掲載種別：記事・総説・解説・論説等（商業誌、新聞、ウェブメディア）  

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記述言語：日本語   出版者・発行元：オーム社  

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会議種別：口頭発表（招待・特別）  

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