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[PMID]:27986918
[Au] Autor:Guo J; Hezaveh S; Tatur J; Zeng AP; Jandt U
[Ad] Endereço:Institute of Bioprocess and Biosystems Engineering, Technische Universität Hamburg, 21073 Hamburg, Germany.
[Ti] Título:Reengineering of the human pyruvate dehydrogenase complex: from disintegration to highly active agglomerates.
[So] Source:Biochem J;474(5):865-875, 2017 Feb 20.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The pyruvate dehydrogenase complex (PDC) plays a central role in cellular metabolism and regulation. As a metabolite-channeling multi-enzyme complex it acts as a complete nanomachine due to its unique geometry and by coupling a cascade of catalytic reactions using 'swinging arms'. Mammalian and specifically human PDC (hPDC) is assembled from multiple copies of E1 and E3 bound to a large E2/E3BP 60-meric core. A less restrictive and smaller catalytic core, which is still active, is highly desired for both fundamental research on channeling mechanisms and also to create a basis for further modification and engineering of new enzyme cascades. Here, we present the first experimental results of the successful disintegration of the E2/E3BP core while retaining its activity. This was achieved by C-terminal α-helixes double truncations (eight residues from E2 and seven residues from E3BP). Disintegration of the hPDC core via double truncations led to the formation of highly active (approximately 70% of wildtype) apparently unordered clusters or agglomerates and inactive non-agglomerated species (hexamer/trimer). After additional deletion of N-terminal 'swinging arms', the aforementioned C-terminal truncations also caused the formation of agglomerates of minimized E2/E3BP complexes. It is likely that these 'swinging arm' regions are not solely responsible for the formation of the large agglomerates.
[Mh] Termos MeSH primário: Acetilcoenzima A/química
Di-Hidrolipoamida Desidrogenase/química
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/química
Piruvato Desidrogenase (Lipoamida)/química
Complexo Piruvato Desidrogenase/química
Ácido Pirúvico/química
[Mh] Termos MeSH secundário: Acetilcoenzima A/metabolismo
Sequência de Aminoácidos
Animais
Domínio Catalítico
Clonagem Molecular
Di-Hidrolipoamida Desidrogenase/genética
Di-Hidrolipoamida Desidrogenase/metabolismo
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/genética
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/metabolismo
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Seres Humanos
Cinética
Mutação
Engenharia de Proteínas
Multimerização Proteica
Estrutura Secundária de Proteína
Piruvato Desidrogenase (Lipoamida)/genética
Piruvato Desidrogenase (Lipoamida)/metabolismo
Complexo Piruvato Desidrogenase/genética
Complexo Piruvato Desidrogenase/metabolismo
Ácido Pirúvico/metabolismo
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Relação Estrutura-Atividade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Pyruvate Dehydrogenase Complex); 0 (Recombinant Proteins); 72-89-9 (Acetyl Coenzyme A); 8558G7RUTR (Pyruvic Acid); EC 1.2.4.1 (Pyruvate Dehydrogenase (Lipoamide)); EC 1.8.1.4 (Dihydrolipoamide Dehydrogenase); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170614
[Lr] Data última revisão:
170614
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161218
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160916


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[PMID]:26996208
[Au] Autor:Arsenijevic A; Milovanovic M; Milovanovic J; Stojanovic B; Zdravkovic N; Leung PS; Liu FT; Gershwin ME; Lukic ML
[Ad] Endereço:Center for Molecular Medicine and Stem Cell Research, Faculty of Medical Sciences, University of Kragujevac, Serbia.
[Ti] Título:Deletion of Galectin-3 Enhances Xenobiotic Induced Murine Primary Biliary Cholangitis by Facilitating Apoptosis of BECs and Release of Autoantigens.
[So] Source:Sci Rep;6:23348, 2016 Mar 21.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Galectin-3 (Gal-3) is a carbohydrate binding lectin, with multiple roles in inflammatory diseases and autoimmunity including its antiapoptotic effect on epithelial cells. In particular, increased expression of Gal-3 in epithelial cells is protective from apoptosis. Based on the thesis that apoptosis of biliary epithelial cells (BECs) is critical to the pathogenesis of Primary Biliary Cholangitis (PBC), we have analyzed the role of Gal-3 in the murine model of autoimmune cholangitis. We took advantage of Gal-3 knockout mice and immunized them with a mimotope of the major mitochondrial autoantigen of PBC, 2-octynoic acid (2-OA) coupled to BSA (2OA-BSA) and evaluated the natural history of subsequent disease, compared to control wild-type mice, by measuring levels of antibodies to PDC-E2, immunohistology of liver, and expression of Gal-3. We report herein that deletion of Gal-3 significantly exacerbates autoimmune cholangitis in these mice. This is manifested by increased periportal infiltrations, bile duct damage, granulomas and fibrosis. Interestingly, the BECs of Gal-3 knockout mice had a higher response to apoptotic stimuli and there were more pro-inflammatory lymphocytes and dendritic cells (DCs) in the livers of Gal-3 knockout mice. In conclusion, Gal-3 plays a protective role in the pathways that lead to the inflammatory destruction of biliary epithelial cells.
[Mh] Termos MeSH primário: Apoptose
Colangite Esclerosante/imunologia
Células Epiteliais/imunologia
Galectina 3/imunologia
[Mh] Termos MeSH secundário: Animais
Autoantígenos/imunologia
Linfócitos T CD8-Positivos/imunologia
Colangite Esclerosante/patologia
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/imunologia
Modelos Animais de Doenças
Células Epiteliais/metabolismo
Ácidos Graxos Monoinsaturados/administração & dosagem
Ácidos Graxos Monoinsaturados/imunologia
Feminino
Galectina 3/genética
Interleucina-13/sangue
Interleucina-17/sangue
Fígado/imunologia
Fígado/metabolismo
Fígado/patologia
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Proteínas Mitocondriais/imunologia
Células Th1/imunologia
Células Th17/imunologia
Xenobióticos/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (Fatty Acids, Monounsaturated); 0 (Galectin 3); 0 (Interleukin-13); 0 (Interleukin-17); 0 (Mitochondrial Proteins); 0 (Xenobiotics); 5663-96-7 (2-octynoic acid); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase); EC 2.3.1.12 (Dlat protein, mouse)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160322
[St] Status:MEDLINE
[do] DOI:10.1038/srep23348


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[PMID]:26755880
[Au] Autor:Wang J; Yang G; Dubrovsky AM; Choi J; Leung PS
[Ad] Endereço:Jinjun Wang, Guoxiang Yang, Alana Mari Dubrovsky, Jinjung Choi, Patrick SC Leung, Division of Rheumatology, Allergy and Clinical Immunology, University of California at Davis, School of Medicine, Davis, CA 95616, United States.
[Ti] Título:Xenobiotics and loss of tolerance in primary biliary cholangitis.
[So] Source:World J Gastroenterol;22(1):338-48, 2016 Jan 07.
[Is] ISSN:2219-2840
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Data from genome wide association studies and geoepidemiological studies established that a combination of genetic predisposition and environmental stimulation is required for the loss of tolerance in primary biliary cholangitis (PBC). The serologic hallmark of PBC are the presence of high titer anti-mitochondrial autoantibodies (AMA) that recognize the lipoyl domain of the mitochondrial pyruvate dehydrogenase E2 (PDC-E2) subunit. Extensive efforts have been directed to investigate the molecular basis of AMA. Recently, experimental data has pointed to the thesis that the breaking of tolerance to PDC-E2 is a pivotal event in the initial etiology of PBC, including environmental xenobiotics including those commonly found in cosmetics and food additives, suggesting that chemical modification of the PDC-E2 epitope may render its vulnerable to become a neo-antigen and trigger an immune response in genetically susceptible hosts. Here, we will discuss the natural history, genetics and immunobiology of PBC and structural constraints of PDC-E2 in AMA recognition which makes it vulnerable to chemical modification.
[Mh] Termos MeSH primário: Colangite/etiologia
Xenobióticos/efeitos adversos
[Mh] Termos MeSH secundário: Acetaminofen/efeitos adversos
Animais
Autoanticorpos/metabolismo
Autoantígenos/imunologia
Doença Hepática Induzida por Substâncias e Drogas/etiologia
Colangite/imunologia
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/imunologia
Modelos Animais de Doenças
Seres Humanos
Tolerância Imunológica
Camundongos
Mitocôndrias/imunologia
Proteínas Mitocondriais/imunologia
Mimetismo Molecular
Ácido Tióctico/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Autoantigens); 0 (Mitochondrial Proteins); 0 (Xenobiotics); 362O9ITL9D (Acetaminophen); 73Y7P0K73Y (Thioctic Acid); EC 2.3.1.12 (DLAT protein, human); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160113
[St] Status:MEDLINE
[do] DOI:10.3748/wjg.v22.i1.338


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[PMID]:26753982
[Au] Autor:Chen R; Xiao M; Gao H; Chen Y; Li Y; Liu Y; Zhang N
[Ad] Endereço:Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy; Research Center of Basic Medical Sciences; School of Medical Laboratory, Tianjin Medical University, Tianjin, 300070, China. chenruibing@tijmu.edu.
[Ti] Título:Identification of a novel mitochondrial interacting protein of C1QBP using subcellular fractionation coupled with CoIP-MS.
[So] Source:Anal Bioanal Chem;408(6):1557-64, 2016 Feb.
[Is] ISSN:1618-2650
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The study of protein-protein interactions is an essential process to understand the biological functions of proteins and the underlying mechanisms. Co-immunoprecipitation coupled with mass spectrometry (CoIP-MS) is one of the most extensively used high-throughput techniques to discover novel protein-protein interactions. However, the traditional CoIP process uses whole cell lysate, disrupts cellular organization, and leads to potential false positives by inducing artificial protein-protein interactions. Here, we have developed a strategy by combining subcellular fractionation with CoIP-MS to study the interacting proteins of the complement component 1, q subcomponent binding protein (C1QBP) in the mitochondria. Using this method, a novel C1QBP interacting protein, dihydrolipoyllysine-residue acetyltransferase component of pyruvate dehydrogenase complex, mitochondrial (DLAT) was identified and validated. Furthermore, the activity of the pyruvate dehydrogenase (PDH) was found to be affected by the expression level of C1QBP. These results provide novel insights regarding the mitochondrial function of C1QBP in the regulation of cellular energy metabolism. This method could also be used to analyze the subcellular protein-protein interactions for other proteins of interest.
[Mh] Termos MeSH primário: Autoantígenos/metabolismo
Proteínas de Transporte/metabolismo
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/metabolismo
Imunoprecipitação/métodos
Proteínas Mitocondriais/análise
Espectrometria de Massas em Tandem/métodos
[Mh] Termos MeSH secundário: Autoantígenos/análise
Proteínas de Transporte/análise
Proteínas de Transporte/genética
Fracionamento Químico/métodos
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/análise
Células HEK293
Seres Humanos
Mitocôndrias/química
Mitocôndrias/metabolismo
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/isolamento & purificação
Proteínas Mitocondriais/metabolismo
Mapeamento de Interação de Proteínas/métodos
Complexo Piruvato Desidrogenase/metabolismo
Reprodutibilidade dos Testes
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (C1QBP protein, human); 0 (Carrier Proteins); 0 (Mitochondrial Proteins); 0 (Pyruvate Dehydrogenase Complex); EC 2.3.1.12 (DLAT protein, human); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160113
[St] Status:MEDLINE
[do] DOI:10.1007/s00216-015-9228-7


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[PMID]:26593289
[Au] Autor:Marzorati S; Invernizzi P; Lleo A
[Ad] Endereço:Liver Unit and Center for Autoimmune Liver Diseases, Humanitas Clinical and Research Center, Via A. Manzoni 113, Rozzano, Milan 20089, Italy; Department of Electronics, Information and Bioengineering, Politecnico di Milano, via Ponzio 34/5, Milan 20133, Italy.
[Ti] Título:Making Sense of Autoantibodies in Cholestatic Liver Diseases.
[So] Source:Clin Liver Dis;20(1):33-46, 2016 Feb.
[Is] ISSN:1557-8224
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Primary biliary cirrhosis (PBC) and primary sclerosing cholangitis (PSC) are the most common chronic cholestatic liver diseases (CLD) in adults and are associated with immune mechanisms. PBC is considered a model autoimmune disease, and more than 90% of patients present very specific autoantibodies against mitochondrial antigens. Whether PSC should be considered an autoimmune or merely immune-mediated disease is still under debate. This review addresses the clinical relevance of autoantibodies in CLD and their pathogenic mechanisms and illustrates the technology available for appropriate autoantibody detection.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Doenças Autoimunes/imunologia
Colangite Esclerosante/imunologia
Cirrose Hepática Biliar/imunologia
[Mh] Termos MeSH secundário: Anticorpos Antinucleares/sangue
Autoantígenos/imunologia
Doenças Autoimunes/diagnóstico
Colangite Esclerosante/diagnóstico
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/imunologia
Ensaio de Imunoadsorção Enzimática
Técnica Indireta de Fluorescência para Anticorpo
Seres Humanos
Cirrose Hepática Biliar/diagnóstico
Proteínas Mitocondriais/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Antibodies, Antinuclear); 0 (Autoantibodies); 0 (Autoantigens); 0 (Mitochondrial Proteins); EC 2.3.1.12 (DLAT protein, human); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151123
[Lr] Data última revisão:
151123
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151124
[St] Status:MEDLINE


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[PMID]:26405201
[Au] Autor:Matsuda S; Adachi J; Ihara M; Tanuma N; Shima H; Kakizuka A; Ikura M; Ikura T; Matsuda T
[Ad] Endereço:Research Center for Environmental Quality Management, Kyoto University, Shiga 520-0811, Japan.
[Ti] Título:Nuclear pyruvate kinase M2 complex serves as a transcriptional coactivator of arylhydrocarbon receptor.
[So] Source:Nucleic Acids Res;44(2):636-47, 2016 Jan 29.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Pyruvate kinase M2 (PKM2) and pyruvate dehydrogenase complex (PDC) regulate production of acetyl-CoA, which functions as an acetyl donor in diverse enzymatic reactions, including histone acetylation. However, the mechanism by which the acetyl-CoA required for histone acetylation is ensured in a gene context-dependent manner is not clear. Here we show that PKM2, the E2 subunit of PDC and histone acetyltransferase p300 constitute a complex on chromatin with arylhydrocarbon receptor (AhR), a transcription factor associated with xenobiotic metabolism. All of these factors are recruited to the enhancer of AhR-target genes, in an AhR-dependent manner. PKM2 contributes to enhancement of transcription of cytochrome P450 1A1 (CYP1A1), an AhR-target gene, acetylation at lysine 9 of histone H3 at the CYP1A1 enhancer. Site-directed mutagenesis of PKM2 indicates that this enhancement of histone acetylation requires the pyruvate kinase activity of the enzyme. Furthermore, we reveal that PDC activity is present in nuclei. Based on these findings, we propose a local acetyl-CoA production system in which PKM2 and PDC locally supply acetyl-CoA to p300 from abundant PEP for histone acetylation at the gene enhancer, and our data suggest that PKM2 sensitizes AhR-mediated detoxification in actively proliferating cells such as cancer and fetal cells.
[Mh] Termos MeSH primário: Proteínas de Transporte/metabolismo
Proteínas de Membrana/metabolismo
Receptores de Hidrocarboneto Arílico/metabolismo
Hormônios Tireóideos/metabolismo
[Mh] Termos MeSH secundário: Acetilação
Autoantígenos/genética
Autoantígenos/metabolismo
Proteínas de Transporte/genética
Cromatina/metabolismo
Citocromo P-450 CYP1A1/genética
Citocromo P-450 CYP1A1/metabolismo
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/genética
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/metabolismo
Elementos Facilitadores Genéticos
Células HeLa
Histonas/metabolismo
Seres Humanos
Proteínas de Membrana/genética
Proteínas Mitocondriais/genética
Proteínas Mitocondriais/metabolismo
Receptores de Hidrocarboneto Arílico/genética
Hormônios Tireóideos/genética
Ativação Transcricional
Fatores de Transcrição de p300-CBP/genética
Fatores de Transcrição de p300-CBP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Autoantigens); 0 (Carrier Proteins); 0 (Chromatin); 0 (Histones); 0 (Membrane Proteins); 0 (Mitochondrial Proteins); 0 (Receptors, Aryl Hydrocarbon); 0 (Thyroid Hormones); 0 (thyroid hormone-binding proteins); EC 1.14.14.1 (CYP1A1 protein, human); EC 1.14.14.1 (Cytochrome P-450 CYP1A1); EC 2.3.1.12 (DLAT protein, human); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase); EC 2.3.1.48 (p300-CBP Transcription Factors); EC 2.3.1.48 (p300-CBP-associated factor)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:160204
[Lr] Data última revisão:
160204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150926
[St] Status:MEDLINE
[do] DOI:10.1093/nar/gkv967


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[PMID]:26553462
[Au] Autor:Schutte KM; Fisher DJ; Burdick MD; Mehrad B; Mathers AJ; Mann BJ; Nakamoto RK; Hughes MA
[Ad] Endereço:Department of Medicine, Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia, USA.
[Ti] Título:Escherichia coli Pyruvate Dehydrogenase Complex Is an Important Component of CXCL10-Mediated Antimicrobial Activity.
[So] Source:Infect Immun;84(1):320-8, 2015 Nov 09.
[Is] ISSN:1098-5522
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Chemokines are best recognized for their role within the innate immune system as chemotactic cytokines, signaling and recruiting host immune cells to sites of infection. Certain chemokines, such as CXCL10, have been found to play an additional role in innate immunity, mediating CXCR3-independent killing of a diverse array of pathogenic microorganisms. While this is still not clearly understood, elucidating the mechanisms underlying chemokine-mediated antimicrobial activity may facilitate the development of novel therapeutic strategies effective against antibiotic-resistant Gram-negative pathogens. Here, we show that CXCL10 exerts antibacterial effects on clinical and laboratory strains of Escherichia coli and report that disruption of pyruvate dehydrogenase complex (PDHc), which converts pyruvate to acetyl coenzyme A, enables E. coli to resist these antimicrobial effects. Through generation and screening of a transposon mutant library, we identified two mutants with increased resistance to CXCL10, both with unique disruptions of the gene encoding the E1 subunit of PDHc, aceE. Resistance to CXCL10 also occurred following deletion of either aceF or lpdA, genes that encode the remaining two subunits of PDHc. Although PDHc resides within the bacterial cytosol, electron microscopy revealed localization of immunogold-labeled CXCL10 to the bacterial cell surface in both the E. coli parent and aceE deletion mutant strains. Taken together, our findings suggest that while CXCL10 interacts with an as-yet-unidentified component on the cell surface, PDHc is an important mediator of killing by CXCL10. To our knowledge, this is the first description of PDHc as a key bacterial component involved in the antibacterial effect of a chemokine.
[Mh] Termos MeSH primário: Antibacterianos/metabolismo
Proteínas da Membrana Bacteriana Externa/metabolismo
Quimiocina CXCL10/metabolismo
Imunidade Inata/imunologia
Piruvato Desidrogenase (Lipoamida)/metabolismo
[Mh] Termos MeSH secundário: Sítios de Ligação
Di-Hidrolipoamida Desidrogenase/genética
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/genética
Farmacorresistência Bacteriana Múltipla/genética
Escherichia coli
Técnicas de Inativação de Genes
Seres Humanos
Ligação Proteica
Piruvato Desidrogenase (Lipoamida)/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Bacterial Outer Membrane Proteins); 0 (Chemokine CXCL10); EC 1.2.4.1 (Pyruvate Dehydrogenase (Lipoamide)); EC 1.8.1.4 (Dihydrolipoamide Dehydrogenase); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151111
[St] Status:MEDLINE
[do] DOI:10.1128/IAI.00552-15


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[PMID]:26259963
[Au] Autor:Sasaki M; Hsu M; Yeh MM; Nakanuma Y
[Ad] Endereço:Department of Human Pathology, Kanazawa University Graduate School of Medicine, Kanazawa, 920-8640, Japan. m8sasaki@med.kanazawa-u.ac.jp.
[Ti] Título:In recurrent primary biliary cirrhosis after liver transplantation, biliary epithelial cells show increased expression of mitochondrial proteins.
[So] Source:Virchows Arch;467(4):417-25, 2015 Oct.
[Is] ISSN:1432-2307
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:In biliary epithelial lesions in primary biliary cirrhosis (PBC), mitochondrial proteins associated with deregulated autophagy are abnormally expressed. We examined whether this could be used as a diagnostic marker for end-stage PBC and recurrent PBC after liver transplantation. We examined the expression of the mitochondrial protein pyruvate dehydrogenase complex-E2 component and cytochrome c oxidase, subunit I (CCO), the autophagy-related marker microtubule-associated protein-light chain 3 (LC3), and p62/sequestosome-1 and the senescence markers p16(Ink4a) and p21(WAF1/Cip1) in small bile ducts and bile ductules in explanted livers from patients with PBC (n = 20) in comparison with liver tissue from control patients (n = 21) and post-transplant samples including recurrent PBC and cellular rejection (n = 28). Intense granular expression of mitochondrial proteins was significantly more frequent in small bile ducts in explanted livers with PBC than in control livers (p < 0.05). Post-transplant samples comprised of three groups: group A (positive for mitochondrial proteins, n = 7), group B (positive for either autophagy-related or senescence markers but negative for mitochondrial proteins, n = 7), and group C (all negative, n = 14). All but one case of group A were clinically and histologically diagnosed as recurrent PBC. In contrast, all cases of group B were diagnosed as cellular rejection. This study suggests that the expression of mitochondrial proteins in small bile ducts may be a useful diagnostic marker for end-stage PBC and recurrent PBC after liver transplantation.
[Mh] Termos MeSH primário: Ductos Biliares/metabolismo
Cirrose Hepática Biliar/diagnóstico
Transplante de Fígado/efeitos adversos
Proteínas Mitocondriais/análise
[Mh] Termos MeSH secundário: Alanina Transaminase/sangue
Autofagia
Biomarcadores/análise
Inibidor p16 de Quinase Dependente de Ciclina
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/análise
Complexo IV da Cadeia de Transporte de Elétrons/análise
Células Epiteliais/metabolismo
Seres Humanos
Cirrose Hepática Biliar/metabolismo
Proteínas de Neoplasias/análise
Proteínas de Ligação a RNA/análise
Recidiva
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cyclin-Dependent Kinase Inhibitor p16); 0 (Mitochondrial Proteins); 0 (Neoplasm Proteins); 0 (P16 protein, human); 0 (P62 protein, human); 0 (RNA-Binding Proteins); EC 1.9.3.1 (Electron Transport Complex IV); EC 1.9.3.1 (cytochrome c oxidase subunit I, human); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase); EC 2.6.1.2 (Alanine Transaminase)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150812
[St] Status:MEDLINE
[do] DOI:10.1007/s00428-015-1819-3


  9 / 372 MEDLINE  
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[PMID]:25820084
[Au] Autor:Rentier C; Pacini G; Nuti F; Peroni E; Rovero P; Papini AM
[Ad] Endereço:French-Italian Interdepartmental Laboratory of Peptide and Protein Chemistry & Biology - PeptLab; Laboratoire de Chimie Biologique EA4505, University of Cergy-Pontoise, 5 mail Gay-Lussac, Neuville-sur-Oise, 95000, Cergy-Pontoise, France; Department of Chemistry "Ugo Schiff", University of Florence, Via della Lastruccia 3/13, I-50019, Sesto Fiorentino, Italy.
[Ti] Título:Synthesis of diastereomerically pure Lys(Nε-lipoyl) building blocks and their use in Fmoc/tBu solid phase synthesis of lipoyl-containing peptides for diagnosis of primary biliary cirrhosis.
[So] Source:J Pept Sci;21(5):408-14, 2015 May.
[Is] ISSN:1099-1387
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Primary Biliary Cirrhosis is an immune-mediated disease in which one of the epitopes recognized by antimitochondrial autoantibodies is a lipoylated fragment of the PDC-E2 protein. Accordingly, the synthesis of lipoylated peptides as diagnostic tools is a relevant target. Up to now, the proper tools for the introduction of lipoylation on building blocks to be used in Fmoc/tBu solid phase peptide synthesis (SPPS) are lacking, and the role of chirality in lipoylation remains poorly studied. In this paper, we present the synthesis of lipoylated lysine derivatives as pure diastereomeric building blocks suitable for Fmoc/tBu SPPS and their introduction in relevant peptide sequences to possibly serve as synthetic probes for the development of novel diagnostic tools for this disease. The optimization of the synthesis of lipoylated building blocks derived from racemic, (R)-, and (S)-α-lipoic acid is described. Synthesis of peptide probes incorporating lipoylation is described. An insight regarding the cleavage of lipoylated peptides is given, as well as a method to oxidize or reduce the 1,2-dithiolane ring of the lipoyl moiety directly on the peptide without any subsequent purification.
[Mh] Termos MeSH primário: Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/química
Lisina/química
Peptídeos/síntese química
[Mh] Termos MeSH secundário: Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/imunologia
Epitopos/química
Epitopos/imunologia
Seres Humanos
Lipoilação
Cirrose Hepática Biliar/diagnóstico
Estrutura Molecular
Peptídeos/química
Peptídeos/imunologia
Técnicas de Síntese em Fase Sólida
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Epitopes); 0 (Peptides); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150429
[Lr] Data última revisão:
150429
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150331
[St] Status:MEDLINE
[do] DOI:10.1002/psc.2761


  10 / 372 MEDLINE  
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[PMID]:25547679
[Au] Autor:Alvarez-Calderon F; Gregory MA; Pham-Danis C; DeRyckere D; Stevens BM; Zaberezhnyy V; Hill AA; Gemta L; Kumar A; Kumar V; Wempe MF; Pollyea DA; Jordan CT; Serkova NJ; Graham DK; DeGregori J
[Ad] Endereço:Integrated Department of Immunology, University of Colorado Anschutz Medical Campus, Aurora, Colorado. Medical Scientist Training Program, University of Colorado Anschutz Medical Campus, Aurora, Colorado. School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
[Ti] Título:Tyrosine kinase inhibition in leukemia induces an altered metabolic state sensitive to mitochondrial perturbations.
[So] Source:Clin Cancer Res;21(6):1360-72, 2015 Mar 15.
[Is] ISSN:1078-0432
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Although tyrosine kinase inhibitors (TKI) can be effective therapies for leukemia, they fail to fully eliminate leukemic cells and achieve durable remissions for many patients with advanced BCR-ABL(+) leukemias or acute myelogenous leukemia (AML). Through a large-scale synthetic lethal RNAi screen, we identified pyruvate dehydrogenase, the limiting enzyme for pyruvate entry into the mitochondrial tricarboxylic acid cycle, as critical for the survival of chronic myelogenous leukemia (CML) cells upon BCR-ABL inhibition. Here, we examined the role of mitochondrial metabolism in the survival of Ph(+) leukemia and AML upon TK inhibition. EXPERIMENTAL DESIGN: Ph(+) cancer cell lines, AML cell lines, leukemia xenografts, cord blood, and patient samples were examined. RESULTS: We showed that the mitochondrial ATP-synthase inhibitor oligomycin-A greatly sensitized leukemia cells to TKI in vitro. Surprisingly, oligomycin-A sensitized leukemia cells to BCR-ABL inhibition at concentrations of 100- to 1,000-fold below those required for inhibition of respiration. Oligomycin-A treatment rapidly led to mitochondrial membrane depolarization and reduced ATP levels, and promoted superoxide production and leukemia cell apoptosis when combined with TKI. Importantly, oligomycin-A enhanced elimination of BCR-ABL(+) leukemia cells by TKI in a mouse model and in primary blast crisis CML samples. Moreover, oligomycin-A also greatly potentiated the elimination of FLT3-dependent AML cells when combined with an FLT3 TKI, both in vitro and in vivo. CONCLUSIONS: TKI therapy in leukemia cells creates a novel metabolic state that is highly sensitive to particular mitochondrial perturbations. Targeting mitochondrial metabolism as an adjuvant therapy could therefore improve therapeutic responses to TKI for patients with BCR-ABL(+) and FLT3(ITD) leukemias.
[Mh] Termos MeSH primário: Leucemia Mielogênica Crônica BCR-ABL Positiva/tratamento farmacológico
ATPases Mitocondriais Próton-Translocadoras/antagonistas & inibidores
Oligomicinas/farmacologia
Inibidores de Proteínas Quinases/farmacologia
Tirosina Quinase 3 Semelhante a fms/genética
[Mh] Termos MeSH secundário: Animais
Protocolos de Quimioterapia Combinada Antineoplásica/farmacologia
Apoptose/efeitos dos fármacos
Linhagem Celular Tumoral
Di-Hidrolipoil-Lisina-Resíduo Acetiltransferase/genética
Modelos Animais de Doenças
Feminino
Proteínas de Fusão bcr-abl/metabolismo
Seres Humanos
Mesilato de Imatinib/farmacologia
Cetona Oxirredutases/metabolismo
Leucemia Mielogênica Crônica BCR-ABL Positiva/genética
Leucemia Mielogênica Crônica BCR-ABL Positiva/patologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos NOD
Camundongos Knockout
Mitocôndrias/metabolismo
Proteínas Mitocondriais/genética
Proteínas Tirosina Quinases/antagonistas & inibidores
Interferência de RNA
RNA Interferente Pequeno
Superóxidos/metabolismo
Tirosina Quinase 3 Semelhante a fms/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mitochondrial Proteins); 0 (Oligomycins); 0 (Protein Kinase Inhibitors); 0 (RNA, Small Interfering); 05HQS4AI99 (oligomycin A); 11062-77-4 (Superoxides); 8A1O1M485B (Imatinib Mesylate); EC 1.2.- (Ketone Oxidoreductases); EC 1.2.1.51 (pyruvate dehydrogenase (NADP+)); EC 2.3.1.12 (Dihydrolipoyllysine-Residue Acetyltransferase); EC 2.3.1.12 (Dlat protein, mouse); EC 2.7.10.1 (Flt3 protein, mouse); EC 2.7.10.1 (Protein-Tyrosine Kinases); EC 2.7.10.1 (fms-Like Tyrosine Kinase 3); EC 2.7.10.2 (Fusion Proteins, bcr-abl); EC 3.6.3.- (Mitochondrial Proton-Translocating ATPases)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141231
[St] Status:MEDLINE
[do] DOI:10.1158/1078-0432.CCR-14-2146



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