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[PMID]:29175332
[Au] Autor:Kozlov G; Wong K; Wang W; Skubák P; Muñoz-Escobar J; Liu Y; Siddiqui N; Pannu NS; Gehring K
[Ad] Endereço:Department of Biochemistry, Groupe de recherche axé sur la structure des protéines, McGill University, Montreal, QC H3G 0B1, Canada.
[Ti] Título:Ankyrin repeats as a dimerization module.
[So] Source:Biochem Biophys Res Commun;495(1):1002-1007, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Legionella pneumophila is a pathogen, causing severe pneumonia in humans called Legionnaires' disease. AnkC (LegA12) is a poorly characterized 495-residue effector protein conserved in multiple Legionella species. Here, we report the crystal structure of a C-terminally truncated AnkC (2-384) at 3.2 Å resolution. The structure shows seven ankyrin repeats (ARs) with unique structural features. AnkC forms a dimer along the outer surface of loops between ARs. The dimer exists both in the crystal form and in solution, as shown by analytical ultracentrifugation. This is the first example of ARs as a dimerization module as opposed to solely a protein interaction domain. In addition, a novel α-helix insert between AR3-AR4 is positioned across the surface opposite the ankyrin groove. Sequence conservation suggests that the ankyrin groove of AnkC is a functional site that interacts with binding targets. This ankyrin domain structure is an important step towards a functional characterization of AnkC.
[Mh] Termos MeSH primário: Repetição de Anquirina
Anquirinas/química
Anquirinas/ultraestrutura
Modelos Químicos
Modelos Moleculares
Multimerização Proteica
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Sítios de Ligação
Simulação por Computador
Sequência Conservada
Legionella pneumophila/metabolismo
Dados de Sequência Molecular
Ligação Proteica
Conformação Proteica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ankyrins)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


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[PMID]:28700589
[Au] Autor:Mastroeni D; Sekar S; Nolz J; Delvaux E; Lunnon K; Mill J; Liang WS; Coleman PD
[Ad] Endereço:Biodesign, ASU-Banner Biodesign Neurodegenerative Disease Research Center, and School of Life Sciences, Arizona State University, Tempe, AZ, United States of America.
[Ti] Título:ANK1 is up-regulated in laser captured microglia in Alzheimer's brain; the importance of addressing cellular heterogeneity.
[So] Source:PLoS One;12(7):e0177814, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Recent epigenetic association studies have identified a new gene, ANK1, in the pathogenesis of Alzheimer's disease (AD). Although strong associations were observed, brain homogenates were used to generate the data, introducing complications because of the range of cell types analyzed. In order to address the issue of cellular heterogeneity in homogenate samples we isolated microglial, astrocytes and neurons by laser capture microdissection from CA1 of hippocampus in the same individuals with a clinical and pathological diagnosis of AD and matched control cases. Using this unique RNAseq data set, we show that in the hippocampus, ANK1 is significantly (p<0.0001) up-regulated 4-fold in AD microglia, but not in neurons or astrocytes from the same individuals. These data provide evidence that microglia are the source of ANK1 differential expression previously identified in homogenate samples in AD.
[Mh] Termos MeSH primário: Doença de Alzheimer/metabolismo
Anquirinas/genética
Microglia/metabolismo
Regulação para Cima
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Doença de Alzheimer/patologia
Anquirinas/metabolismo
Estudos de Casos e Controles
Feminino
Hipocampo/citologia
Hipocampo/metabolismo
Seres Humanos
Masculino
Neurônios/metabolismo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANK1 protein, human); 0 (Ankyrins); 0 (RNA, Messenger)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170713
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0177814


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[PMID]:28694211
[Au] Autor:He Y; Jia S; Dewan RK; Liao N
[Ad] Endereço:Department of Pediatrics, The First Affiliated Hospital of Guangxi Medical University, N0.6, Shuangyong Road, Qingxiu District, Nanning, Guangxi Province 530021, PR China.
[Ti] Título:Novel mutations in patients with hereditary red blood cell membrane disorders using next-generation sequencing.
[So] Source:Gene;627:556-562, 2017 Sep 05.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:To diagnose and investigate the genotype-phenotype relationship in intractable hereditary red blood cell (RBC) membrane cases, we have utilized next-generation sequencing (NGS) to develop a high-throughput, highly sensitive assay. Three unrelated families including 15 individuals were analysed with a panel interrogating 600 genes related to haematopathy disorders. Where possible, inheritance patterns of pathogenic mutations were determined by sequencing the relatives. We identified 2 novel mutations in ANK1 (Y216X and E142X) responsible for hereditary spherocytosis (HS) that were stop-gain single nucleotide variants (SNVs). Furthermore, a novel SPTA1 mutation (H54P) was identified; it is a nonsynonymous SNV and is associated with hereditary elliptocytosis (HE). In addition, patients who also carried erythropoiesis gene mutations showed more severe disease phenotype. The NGS panel provides a fast and accurate method for molecular diagnosis in patients with intractable hereditary RBC membrane disorders. An approach integrating medical history, clinical and molecular testing, and pedigree analysis is beneficial for these patients and families.
[Mh] Termos MeSH primário: Anquirinas/genética
Eliptocitose Hereditária/genética
Mutação de Sentido Incorreto
Espectrina/genética
Esferocitose Hereditária/genética
[Mh] Termos MeSH secundário: Adulto
Criança
Eritropoese
Feminino
Seres Humanos
Lactente
Masculino
Linhagem
Fenótipo
Polimorfismo de Nucleotídeo Único
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANK1 protein, human); 0 (Ankyrins); 12634-43-4 (Spectrin)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE


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[PMID]:28487373
[Au] Autor:Desmond PF; Labuza A; Muriel J; Markwardt ML; Mancini AE; Rizzo MA; Bloch RJ
[Ad] Endereço:From the Department of Physiology and.
[Ti] Título:Interactions between small ankyrin 1 and sarcolipin coordinately regulate activity of the sarco(endo)plasmic reticulum Ca -ATPase (SERCA1).
[So] Source:J Biol Chem;292(26):10961-10972, 2017 Jun 30.
[Is] ISSN:1083-351X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:SERCA1, the sarco(endo)plasmic reticulum Ca -ATPase of skeletal muscle, is essential for muscle relaxation and maintenance of low resting Ca levels in the myoplasm. We recently reported that small ankyrin 1 (sAnk1) interacts with the sarco(endo)plasmic reticulum Ca -ATPase in skeletal muscle (SERCA1) to inhibit its activity. We also showed that this interaction is mediated at least in part through sAnk1's transmembrane domain in a manner similar to that of sarcolipin (SLN). Earlier studies have shown that SLN and phospholamban, the other well studied small SERCA-regulatory proteins, oligomerize either alone or together. As sAnk1 is coexpressed with SLN in muscle, we sought to determine whether these two proteins interact with one another when coexpressed exogenously in COS7 cells. Coimmunoprecipitation (coIP) and anisotropy-based FRET (AFRET) assays confirmed this interaction. Our results indicated that sAnk1 and SLN can associate in the sarcoplasmic reticulum membrane and after exogenous expression in COS7 cells but that their association did not require endogenous SERCA2. Significantly, SLN promoted the interaction between sAnk1 and SERCA1 when the three proteins were coexpressed, and both coIP and AFRET experiments suggested the formation of a complex consisting of all three proteins. Ca -ATPase assays showed that sAnk1 ablated SLN's inhibition of SERCA1 activity. These results suggest that sAnk1 interacts with SLN both directly and in complex with SERCA1 and reduces SLN's inhibitory effect on SERCA1 activity.
[Mh] Termos MeSH primário: Anquirinas/metabolismo
Proteínas Musculares/metabolismo
Proteolipídeos/metabolismo
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
Retículo Sarcoplasmático/metabolismo
[Mh] Termos MeSH secundário: Animais
Anquirinas/genética
Células COS
Cercopithecus aethiops
Células HEK293
Seres Humanos
Proteínas Musculares/genética
Proteolipídeos/genética
Retículo Sarcoplasmático/genética
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANK1 protein, human); 0 (Ankyrins); 0 (Muscle Proteins); 0 (Proteolipids); 145018-73-1 (sarcolipin); EC 3.6.3.8 (ATP2A1 protein, human); EC 3.6.3.8 (Sarcoplasmic Reticulum Calcium-Transporting ATPases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170715
[Lr] Data última revisão:
170715
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170511
[St] Status:MEDLINE
[do] DOI:10.1074/jbc.M117.783613


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[PMID]:28424069
[Au] Autor:Wisitponchai T; Shoombuatong W; Lee VS; Kitidee K; Tayapiwatana C
[Ad] Endereço:Division of Clinical Immunology, Department of Medical Technology, Faculty of Associated Medical Sciences, Chiang Mai University, Chiang Mai, 50200, Thailand.
[Ti] Título:AnkPlex: algorithmic structure for refinement of near-native ankyrin-protein docking.
[So] Source:BMC Bioinformatics;18(1):220, 2017 Apr 19.
[Is] ISSN:1471-2105
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Computational analysis of protein-protein interaction provided the crucial information to increase the binding affinity without a change in basic conformation. Several docking programs were used to predict the near-native poses of the protein-protein complex in 10 top-rankings. The universal criteria for discriminating the near-native pose are not available since there are several classes of recognition protein. Currently, the explicit criteria for identifying the near-native pose of ankyrin-protein complexes (APKs) have not been reported yet. RESULTS: In this study, we established an ensemble computational model for discriminating the near-native docking pose of APKs named "AnkPlex". A dataset of APKs was generated from seven X-ray APKs, which consisted of 3 internal domains, using the reliable docking tool ZDOCK. The dataset was composed of 669 and 44,334 near-native and non-near-native poses, respectively, and it was used to generate eleven informative features. Subsequently, a re-scoring rank was generated by AnkPlex using a combination of a decision tree algorithm and logistic regression. AnkPlex achieved superior efficiency with ≥1 near-native complexes in the 10 top-rankings for nine X-ray complexes compared to ZDOCK, which only obtained six X-ray complexes. In addition, feature analysis demonstrated that the van der Waals feature was the dominant near-native pose out of the potential ankyrin-protein docking poses. CONCLUSION: The AnkPlex model achieved a success at predicting near-native docking poses and led to the discovery of informative characteristics that could further improve our understanding of the ankyrin-protein complex. Our computational study could be useful for predicting the near-native poses of binding proteins and desired targets, especially for ankyrin-protein complexes. The AnkPlex web server is freely accessible at http://ankplex.ams.cmu.ac.th .
[Mh] Termos MeSH primário: Algoritmos
Anquirinas/metabolismo
Modelos Químicos
Proteínas/metabolismo
[Mh] Termos MeSH secundário: Biologia Computacional
Ligação Proteica
Conformação Proteica
Proteínas/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ankyrins); 0 (Proteins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170512
[Lr] Data última revisão:
170512
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.1186/s12859-017-1628-6


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[PMID]:28196901
[Au] Autor:Swayne LA; Murphy NP; Asuri S; Chen L; Xu X; McIntosh S; Wang C; Lancione PJ; Roberts JD; Kerr C; Sanatani S; Sherwin E; Kline CF; Zhang M; Mohler PJ; Arbour LT
[Ad] Endereço:From the Division of Medical Sciences, University of Victoria, BC, Canada (L.A.S., L.C., X.X., L.T.A.); University of British Columbia Island Medical Program, Victoria, BC, Canada (L.A.S., L.T.A.); Department of Medical Genetics (S.A., S.M., L.T.A.), Division of Cardiology (C.K.), and Division of Ca
[Ti] Título:Novel Variant in the Membrane-Binding Domain Is Associated With Ankyrin-B Syndrome and Structural Heart Disease in a First Nations Population With a High Rate of Long QT Syndrome.
[So] Source:Circ Cardiovasc Genet;10(1), 2017 Jan.
[Is] ISSN:1942-3268
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Long QT syndrome confers susceptibility to ventricular arrhythmia, predisposing to syncope, seizures, and sudden death. While rare globally, long QT syndrome is ≈15× more common in First Nations of Northern British Columbia largely because of a known mutation in . However, 2 large multigenerational families were affected, but negative for the known mutation. METHODS AND RESULTS: Long QT syndrome panel testing was carried out in the index case of each family, and clinical information was collected. Cascade genotyping was performed. Biochemical and myocyte-based assays were performed to evaluate the identified gene variant for loss-of-function activity. Index cases in these 2 families harbored a novel c.1937C>T variant (p.S646F). An additional 16 carriers were identified, including 2 with structural heart disease: one with cardiomyopathy resulting in sudden death and the other with congenital heart disease. For all carriers of this variant, the average QTc was 475 ms (±40). Although ankyrin-B p.S646F is appropriately folded and expressed in bacteria, the mutant polypeptide displays reduced expression in cultured H9c2 cells and aberrant localization in primary cardiomyocytes. Furthermore, myocytes expressing ankyrin-B p.S646F lack normal membrane targeting of the ankyrin-binding partner, the Na/Ca exchanger. Thus, ankyrin-B p.S646F is a loss-of-function variant. CONCLUSIONS: We identify the first disease-causing variant localized to the membrane-binding domain resulting in reduced ankyrin-B expression and abnormal localization. Further study is warranted on the potential association of this variant with structural heart disease given the role of in targeting and stabilization of key structural and signaling molecules in cardiac cells.
[Mh] Termos MeSH primário: Anquirinas/genética
Arritmias Cardíacas/genética
Variação Genética
Índios Norte-Americanos/genética
Síndrome do QT Longo/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Animais
Anquirinas/química
Anquirinas/metabolismo
Arritmias Cardíacas/diagnóstico
Arritmias Cardíacas/etnologia
Arritmias Cardíacas/metabolismo
Colúmbia Britânica/epidemiologia
Linhagem Celular
Criança
Pré-Escolar
Eletrocardiografia
Feminino
Predisposição Genética para Doença
Seres Humanos
Síndrome do QT Longo/diagnóstico
Síndrome do QT Longo/etnologia
Síndrome do QT Longo/metabolismo
Masculino
Camundongos Knockout
Meia-Idade
Miócitos Cardíacos/metabolismo
Fenótipo
Ligação Proteica
Domínios e Motivos de Interação entre Proteínas
Estabilidade Proteica
Ratos
Trocador de Sódio e Cálcio/metabolismo
Relação Estrutura-Atividade
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ANK2 protein, human); 0 (Ankyrins); 0 (Sodium-Calcium Exchanger)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170216
[St] Status:MEDLINE


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[PMID]:28160493
[Au] Autor:Müller GDAES; de Lima D; Zacchi FL; Piazza RS; Lüchmann KH; Mattos JJ; Schlenk D; Bainy ACD
[Ad] Endereço:Biochemistry Department, Federal University of Santa Catarina, Florianópolis, Santa Catarina, Brazil.
[Ti] Título:Analysis of transcriptional responses of normalizing genes on Crassostrea brasiliana under different experimental conditions.
[So] Source:Environ Toxicol Chem;36(8):2190-2198, 2017 Aug.
[Is] ISSN:1552-8618
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Bivalves show remarkable plasticity to environmental changes and have been proposed as sentinel organisms in biomonitoring. Studies related to transcriptional analysis using quantitative real-time polymerase chain reaction (qRT-PCR) in these organisms have notably increased, imposing a need to identify and validate adequate reference genes for an accurate and reliable analysis. In the present study, 9 reference genes were selected from transcriptome data of Crassostrea brasiliana to identify their suitability as qRT-PCR normalizer genes. The transcriptional patterns were analyzed in gills of oysters under 3 different conditions: different temperatures (18, 24, or 32 °C) and phenanthrene (100 µg L ) combined exposure; different salinities (10, 25, or 35‰) and phenanthrene combined exposure; and 10% of diesel fuel water-accommodated fraction (diesel-WAF) exposure. Reference gene stability was calculated using 5 algorithms (geNorm, NormFinder, BestKeeper, ΔCt, RefFinder). Transcripts of ankyrin-like (ANK), glyceraldehyde 3-phosphate dehydrogenase-like (GAPDH), and α-tubulin-like (TUBA) genes showed minor changes in different temperature/phenanthrene treatment. Transcripts of ANK, ß-actin-like, and ß-tubulin-like genes showed better stability at salinity/phenanthrene treatment, and ANK, TUBA, and 28S ribosomal protein-like genes showed the most stable transcription pattern in oysters exposed to diesel-WAF exposure. The present study constitutes the first systematic analysis of reference gene selection for qRT-PCR normalization in C. brasiliana. These genes could be employed in studies using qRT-PCR analysis under similar experimental conditions. Environ Toxicol Chem 2017;36:2190-2198. © 2017 SETAC.
[Mh] Termos MeSH primário: Crassostrea
Monitoramento Ambiental/métodos
Transcriptoma/genética
Poluentes Químicos da Água/toxicidade
[Mh] Termos MeSH secundário: Animais
Anquirinas/genética
Crassostrea/efeitos dos fármacos
Crassostrea/genética
Gasolina/toxicidade
Perfilação da Expressão Gênica
Brânquias/efeitos dos fármacos
Brânquias/metabolismo
Gliceraldeído-3-Fosfato Desidrogenases/genética
Fenantrenos/toxicidade
Reação em Cadeia da Polimerase em Tempo Real
Padrões de Referência
Salinidade
Temperatura Ambiente
Transcriptoma/efeitos dos fármacos
Tubulina (Proteína)/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ankyrins); 0 (Gasoline); 0 (Phenanthrenes); 0 (Tubulin); 0 (Water Pollutants, Chemical); 448J8E5BST (phenanthrene); EC 1.2.1.- (Glyceraldehyde-3-Phosphate Dehydrogenases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171107
[Lr] Data última revisão:
171107
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170205
[St] Status:MEDLINE
[do] DOI:10.1002/etc.3755


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[PMID]:28148727
[Au] Autor:Saifetiarova J; Taylor AM; Bhat MA
[Ad] Endereço:Department of Cellular and Integrative Physiology, Center for Biomedical Neuroscience, School of Medicine, University of Texas Health Science Center, San Antonio, Texas 78229-3900.
[Ti] Título:Early and Late Loss of the Cytoskeletal Scaffolding Protein, Ankyrin G Reveals Its Role in Maturation and Maintenance of Nodes of Ranvier in Myelinated Axons.
[So] Source:J Neurosci;37(10):2524-2538, 2017 Mar 08.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The mechanisms that govern node of Ranvier organization, stability, and long-term maintenance remain to be fully elucidated. One of the molecular components of the node is the cytoskeletal scaffolding protein, ankyrin G (AnkG), which interacts with multiple members of the nodal complex. The role of AnkG in nodal organization and maintenance is still not clearly defined as to whether AnkG functions as an initial nodal organizer or whether it functions as a nodal stabilizer after the nodal complex has been assembled. Using a mouse model system, we report here that perinatal and juvenile neuronal ablation of AnkG has differential consequences on nodal stability. Early loss of AnkG creates immature nodes with abnormal morphology, which undergo accelerated destabilization within a month, resulting in rapid voltage-gated sodium (Na ) channel and ßIV spectrin loss with reduced effects on neurofascin 186. On the other hand, late ablation of AnkG from established nodal complexes leads to slow but progressive nodal destabilization over 10 months, primarily affecting ßIV spectrin, followed by Na channels, with modest impact on neurofascin 186. We also show that ankyrin R and ßI spectrin are not sufficient to prevent nodal disorganization after AnkG ablation. Additionally, nodal disorganization in both early and late AnkG mutants is accompanied by axonal pathology and neurological dysfunction. Together, our results suggest that AnkG plays an indispensable role in the maturation and long-term stabilization of the newly assembled nodal complex, and that loss of AnkG after nodal stabilization does not lead to rapid nodal disassembly but to loss of specific nodal components in a time-dependent manner. Nodes of Ranvier are the myelin-free gaps along myelinated axons that allow fast communication between neurons and their target cells by propagating action potentials in a saltatory manner. The cytoskeletal scaffolding protein ankyrin G (AnkG) has been thought to play an important role in node formation; however, its precise role in nodal assembly, stability, and maintenance is still not clear. By using spatiotemporal ablation of AnkG, we report its differential role in nodal maturation and stabilization. We show that early AnkG-deficient nodes fail to mature and undergo rapid destabilization. In contrast, nodes that assemble with AnkG are much more stable and undergo gradual disintegration with sequential loss of nodal components in the absence of AnkG.
[Mh] Termos MeSH primário: Anquirinas/metabolismo
Axônios/fisiologia
Proteínas do Citoesqueleto/metabolismo
Citoesqueleto/fisiologia
Condução Nervosa/fisiologia
Nós Neurofibrosos/fisiologia
[Mh] Termos MeSH secundário: Animais
Axônios/ultraestrutura
Crescimento Celular
Células Cultivadas
Citoesqueleto/ultraestrutura
Feminino
Masculino
Camundongos
Camundongos Knockout
Camundongos Transgênicos
Fibras Nervosas Mielinizadas/fisiologia
Fibras Nervosas Mielinizadas/ultraestrutura
Nós Neurofibrosos/ultraestrutura
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ank3 protein, mouse); 0 (Ankyrins); 0 (Cytoskeletal Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170909
[Lr] Data última revisão:
170909
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170203
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.2661-16.2017


  9 / 1530 MEDLINE  
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[PMID]:28111017
[Au] Autor:Wong K; Perpich JD; Kozlov G; Cygler M; Abu Kwaik Y; Gehring K
[Ad] Endereço:Department of Biochemistry and Groupe de recherche axé sur la structure des protéines, McGill University, Montreal, QC H3G 0B1, Canada.
[Ti] Título:Structural Mimicry by a Bacterial F Box Effector Hijacks the Host Ubiquitin-Proteasome System.
[So] Source:Structure;25(2):376-383, 2017 Feb 07.
[Is] ISSN:1878-4186
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ankyrin B (AnkB/LegAU13) is a translocated F box effector essential for the intracellular replication of the pathogen Legionella pneumophila. AnkB co-opts a host ubiquitin ligase to decorate the pathogen-containing vacuole with K -linked polyubiquitinated proteins and degrade host proteins as a source of energy. Here, we report that AnkB commandeers the host ubiquitin-proteasome system through mimicry of two eukaryotic protein domains. Using X-ray crystallography, we determined the 3D structure of AnkB in complex with Skp1, a component of the human SCF ubiquitination ligase. The structure confirms that AnkB contains an N-terminal F box similar to Skp2 and a C-terminal substrate-binding domain similar to eukaryotic ankyrin repeats. We identified crucial amino acids in the substrate-binding domain of AnkB and showed them to be essential for the function of AnkB in L. pneumophila intracellular proliferation. The study reveals how Legionella uses molecular mimicry to manipulate the host ubiquitination pathway and proliferate intracellularly.
[Mh] Termos MeSH primário: Anquirinas/química
Interações Hospedeiro-Patógeno
Legionella pneumophila/genética
Proteínas Periplásmicas/química
Proteínas Quinases Associadas a Fase S/química
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Anquirinas/genética
Anquirinas/metabolismo
Sítios de Ligação
Linhagem Celular
Clonagem Molecular
Cristalografia por Raios X
Escherichia coli/genética
Escherichia coli/metabolismo
Expressão Gênica
Seres Humanos
Cinética
Legionella pneumophila/crescimento & desenvolvimento
Legionella pneumophila/patogenicidade
Macrófagos/microbiologia
Modelos Moleculares
Mimetismo Molecular
Proteínas Periplásmicas/genética
Proteínas Periplásmicas/metabolismo
Complexo de Endopeptidases do Proteassoma/metabolismo
Ligação Proteica
Conformação Proteica em alfa-Hélice
Conformação Proteica em Folha beta
Domínios e Motivos de Interação entre Proteínas
Proteínas Recombinantes/química
Proteínas Recombinantes/genética
Proteínas Recombinantes/metabolismo
Proteínas Quinases Associadas a Fase S/genética
Proteínas Quinases Associadas a Fase S/metabolismo
Alinhamento de Sequência
Homologia de Sequência de Aminoácidos
Especificidade por Substrato
Ubiquitina/química
Ubiquitina/genética
Ubiquitina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ankyrins); 0 (Periplasmic Proteins); 0 (Recombinant Proteins); 0 (S-Phase Kinase-Associated Proteins); 0 (SKP1 protein, human); 0 (Ubiquitin); EC 3.4.25.1 (Proteasome Endopeptidase Complex)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE


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[PMID]:28087624
[Au] Autor:Chen F; Chisholm AD; Jin Y
[Ad] Endereço:Neurobiology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093, USA.
[Ti] Título:Tissue-specific regulation of alternative polyadenylation represses expression of a neuronal ankyrin isoform in epidermal development.
[So] Source:Development;144(4):698-707, 2017 02 15.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Differential mRNA polyadenylation plays an important role in shaping the neuronal transcriptome. In , several ankyrin isoforms are produced from the locus through alternative polyadenylation. Here, we identify a key role for an intronic polyadenylation site (PAS) in temporal- and tissue-specific regulation of UNC-44/ankyrin isoforms. Removing an intronic PAS results in ectopic expression of the neuronal ankyrin isoform in non-neural tissues. This mis-expression underlies epidermal developmental defects in mutants of the conserved tumor suppressor death-associated protein kinase We have previously reported that the use of this intronic PAS depends on the nuclear polyadenylation factor SYDN-1, which inhibits the RNA polymerase II CTD phosphatase SSUP-72. Consistent with this, loss of blocks ectopic expression of neuronal ankyrin and suppresses epidermal morphology defects of These effects of are mediated by autonomously in the epidermis. We also show that a peptidyl-prolyl isomerase PINN-1 antagonizes SYDN-1 in the spatiotemporal control of neuronal ankyrin isoform. Moreover, the nuclear localization of PINN-1 is altered in mutants. Our data reveal that tissue and stage-specific expression of ankyrin isoforms relies on differential activity of positive and negative regulators of alternative polyadenylation.
[Mh] Termos MeSH primário: Anquirinas/metabolismo
Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/embriologia
Epiderme/embriologia
Regulação da Expressão Gênica no Desenvolvimento
Neurônios/metabolismo
[Mh] Termos MeSH secundário: Animais
Anquirinas/genética
Núcleo Celular/metabolismo
Proteínas Quinases Associadas com Morte Celular/metabolismo
Perfilação da Expressão Gênica
Proteínas de Fluorescência Verde/metabolismo
Íntrons
Mutação
Fenótipo
Poliadenilação
Isoformas de Proteínas
RNA Mensageiro/metabolismo
Distribuição Tecidual
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ankyrins); 0 (Caenorhabditis elegans Proteins); 0 (Protein Isoforms); 0 (RNA, Messenger); 147336-22-9 (Green Fluorescent Proteins); EC 2.7.11.1 (Death-Associated Protein Kinases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170115
[St] Status:MEDLINE
[do] DOI:10.1242/dev.146001



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