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Pesquisa : G04.152.912.750.500 [Categoria DeCS]
Referências encontradas : 65 [refinar]
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[PMID]:27770832
[Au] Autor:Bjorke B; Shoja-Taheri F; Kim M; Robinson GE; Fontelonga T; Kim KT; Song MR; Mastick GS
[Ad] Endereço:Department of Biology, University of Nevada, Reno, NV, 89557, USA.
[Ti] Título:Contralateral migration of oculomotor neurons is regulated by Slit/Robo signaling.
[So] Source:Neural Dev;11(1):18, 2016 10 22.
[Is] ISSN:1749-8104
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Oculomotor neurons develop initially like typical motor neurons, projecting axons out of the ventral midbrain to their ipsilateral targets, the extraocular muscles. However, in all vertebrates, after the oculomotor nerve (nIII) has reached the extraocular muscle primordia, the cell bodies that innervate the superior rectus migrate to join the contralateral nucleus. This motor neuron migration represents a unique strategy to form a contralateral motor projection. Whether migration is guided by diffusible cues remains unknown. METHODS: We examined the role of Slit chemorepellent signals in contralateral oculomotor migration by analyzing mutant mouse embryos. RESULTS: We found that the ventral midbrain expresses high levels of both Slit1 and 2, and that oculomotor neurons express the repellent Slit receptors Robo1 and Robo2. Therefore, Slit signals are in a position to influence the migration of oculomotor neurons. In Slit 1/2 or Robo1/2 double mutant embryos, motor neuron cell bodies migrated into the ventral midbrain on E10.5, three days prior to normal migration. These early migrating neurons had leading projections into and across the floor plate. In contrast to the double mutants, embryos which were mutant for single Slit or Robo genes did not have premature migration or outgrowth on E10.5, demonstrating a cooperative requirement of Slit1 and 2, as well as Robo1 and 2. To test how Slit/Robo midline repulsion is modulated, we found that the normal migration did not require the receptors Robo3 and CXCR4, or the chemoattractant, Netrin 1. The signal to initiate contralateral migration is likely autonomous to the midbrain because oculomotor neurons migrate in embryos that lack either nerve outgrowth or extraocular muscles, or in cultured midbrains that lacked peripheral tissue. CONCLUSION: Overall, our results demonstrate that a migratory subset of motor neurons respond to floor plate-derived Slit repulsion to properly control the timing of contralateral migration.
[Mh] Termos MeSH primário: Orientação de Axônios
Movimento Celular
Peptídeos e Proteínas de Sinalização Intercelular/fisiologia
Neurônios Motores/fisiologia
Proteínas do Tecido Nervoso/fisiologia
Nervo Oculomotor/crescimento & desenvolvimento
Receptores Imunológicos/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Membrana/fisiologia
Mesencéfalo/fisiologia
Camundongos
Fatores de Crescimento Neural/fisiologia
Netrina-1
Receptores CXCR4/fisiologia
Transdução de Sinais
Proteínas Supressoras de Tumor/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (CXCR4 protein, mouse); 0 (Intercellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Nerve Growth Factors); 0 (Nerve Tissue Proteins); 0 (Ntn1 protein, mouse); 0 (Receptors, CXCR4); 0 (Receptors, Immunologic); 0 (Robo2 protein, mouse); 0 (Robo3 protein, mouse); 0 (Slit homolog 2 protein); 0 (Slit1 protein, mouse); 0 (Tumor Suppressor Proteins); 0 (roundabout protein); 158651-98-0 (Netrin-1)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171204
[Lr] Data última revisão:
171204
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE


  2 / 65 MEDLINE  
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[PMID]:29025592
[Au] Autor:Sundaresan V; Lin VT; Liang F; Kaye FJ; Kawabata-Iwakawa R; Shiraishi K; Kohno T; Yokota J; Zhou L
[Ad] Endereço:Department of Molecular Genetics and Microbiology, University of Florida, Gainesville, FL, USA; UF Health Cancer Center, University of Florida, Gainesville, FL, USA.
[Ti] Título:Significantly mutated genes and regulatory pathways in SCLC-a meta-analysis.
[So] Source:Cancer Genet;216-217:20-28, 2017 Oct.
[Is] ISSN:2210-7762
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Small cell lung cancer (SCLC) accounts for approximately 15% of all lung cancers and demands effective targeted therapeutic strategies. In this meta-analysis study, we aim to identify significantly mutated genes and regulatory pathways to help us better understand the progression of SCLC and to identify potential biomarkers. Besides ranking genes based on their mutation frequencies, we sought to identify statistically significant mutations in SCLC with the MutSigCV software. Our analysis identified several genes with relatively low mutation frequency, including PTEN, as highly significant (p < 0.001), suggesting these genes may play an important role in the progression of SCLC. Our results also indicated mutations in genes involved in the axon guidance pathways likely play an important role in SCLC progression. In addition, we observed that the mutation rate was significantly higher in samples with RB1 gene mutated when compared to samples with wild type RB1, suggesting that RB1 status has significant impact on the mutation profile and disease progression in SCLC.
[Mh] Termos MeSH primário: Neoplasias Pulmonares/genética
Mutação/genética
Transdução de Sinais/genética
Carcinoma de Pequenas Células do Pulmão/genética
[Mh] Termos MeSH secundário: Orientação de Axônios/genética
Análise por Conglomerados
Bases de Dados Genéticas
Seres Humanos
Taxa de Mutação
Proteína do Retinoblastoma/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; META-ANALYSIS
[Nm] Nome de substância:
0 (Retinoblastoma Protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


  3 / 65 MEDLINE  
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[PMID]:28904001
[Au] Autor:Kaczmarek LK; Zhang Y
[Ad] Endereço:Departments of Pharmacology and of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, Connecticut.
[Ti] Título:Kv3 Channels: Enablers of Rapid Firing, Neurotransmitter Release, and Neuronal Endurance.
[So] Source:Physiol Rev;97(4):1431-1468, 2017 Oct 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The intrinsic electrical characteristics of different types of neurons are shaped by the K channels they express. From among the more than 70 different K channel genes expressed in neurons, Kv3 family voltage-dependent K channels are uniquely associated with the ability of certain neurons to fire action potentials and to release neurotransmitter at high rates of up to 1,000 Hz. In general, the four Kv3 channels Kv3.1-Kv3.4 share the property of activating and deactivating rapidly at potentials more positive than other channels. Each Kv3 channel gene can generate multiple protein isoforms, which contribute to the high-frequency firing of neurons such as auditory brain stem neurons, fast-spiking GABAergic interneurons, and Purkinje cells of the cerebellum, and to regulation of neurotransmitter release at the terminals of many neurons. The different Kv3 channels have unique expression patterns and biophysical properties and are regulated in different ways by protein kinases. In this review, we cover the function, localization, and modulation of Kv3 channels and describe how levels and properties of the channels are altered by changes in ongoing neuronal activity. We also cover how the protein-protein interaction of these channels with other proteins affects neuronal functions, and how mutations or abnormal regulation of Kv3 channels are associated with neurological disorders such as ataxias, epilepsies, schizophrenia, and Alzheimer's disease.
[Mh] Termos MeSH primário: Neurônios/metabolismo
Neurotransmissores/metabolismo
Canais de Potássio Shaw/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Orientação de Axônios
Seres Humanos
Dados de Sequência Molecular
Doenças do Sistema Nervoso/metabolismo
Fosfotransferases/metabolismo
Canais de Potássio Shaw/antagonistas & inibidores
Transdução de Sinais
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Neurotransmitter Agents); 0 (Shaw Potassium Channels); EC 2.7.- (Phosphotransferases)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170915
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00002.2017


  4 / 65 MEDLINE  
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[PMID]:28859089
[Au] Autor:Gujar MR; Stricker AM; Lundquist EA
[Ad] Endereço:Department of Molecular Biosciences, Program in Molecular, Cellular, and Developmental Biology, The University of Kansas, Lawrence, KS, United States of America.
[Ti] Título:Flavin monooxygenases regulate Caenorhabditis elegans axon guidance and growth cone protrusion with UNC-6/Netrin signaling and Rac GTPases.
[So] Source:PLoS Genet;13(8):e1006998, 2017 Aug.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The guidance cue UNC-6/Netrin regulates both attractive and repulsive axon guidance. Our previous work showed that in C. elegans, the attractive UNC-6/Netrin receptor UNC-40/DCC stimulates growth cone protrusion, and that the repulsive receptor, an UNC-5:UNC-40 heterodimer, inhibits growth cone protrusion. We have also shown that inhibition of growth cone protrusion downstream of the UNC-5:UNC-40 repulsive receptor involves Rac GTPases, the Rac GTP exchange factor UNC-73/Trio, and the cytoskeletal regulator UNC-33/CRMP, which mediates Semaphorin-induced growth cone collapse in other systems. The multidomain flavoprotein monooxygenase (FMO) MICAL (Molecule Interacting with CasL) also mediates growth cone collapse in response to Semaphorin by directly oxidizing F-actin, resulting in depolymerization. The C. elegans genome does not encode a multidomain MICAL-like molecule, but does encode five flavin monooxygenases (FMO-1, -2, -3, -4, and 5) and another molecule, EHBP-1, similar to the non-FMO portion of MICAL. Here we show that FMO-1, FMO-4, FMO-5, and EHBP-1 may play a role in UNC-6/Netrin directed repulsive guidance mediated through UNC-40 and UNC-5 receptors. Mutations in fmo-1, fmo-4, fmo-5, and ehbp-1 showed VD/DD axon guidance and branching defects, and variably enhanced unc-40 and unc-5 VD/DD axon guidance defects. Developing growth cones in vivo of fmo-1, fmo-4, fmo-5, and ehbp-1 mutants displayed excessive filopodial protrusion, and transgenic expression of FMO-5 inhibited growth cone protrusion. Mutations suppressed growth cone inhibition caused by activated UNC-40 and UNC-5 signaling, and activated Rac GTPase CED-10 and MIG-2, suggesting that these molecules are required downstream of UNC-6/Netrin receptors and Rac GTPases. From these studies we conclude that FMO-1, FMO-4, FMO-5, and EHBP-1 represent new players downstream of UNC-6/Netrin receptors and Rac GTPases that inhibit growth cone filopodial protrusion in repulsive axon guidance.
[Mh] Termos MeSH primário: Orientação de Axônios/genética
Proteínas de Caenorhabditis elegans/genética
Caenorhabditis elegans/genética
Oxigenases de Função Mista/genética
Proteínas do Tecido Nervoso/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Caenorhabditis elegans/crescimento & desenvolvimento
Dinitrocresóis/metabolismo
Mutação
Netrinas
Pseudópodes/genética
Pseudópodes/metabolismo
Transdução de Sinais
Proteínas rac de Ligação ao GTP/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Dinitrocresols); 0 (Nerve Tissue Proteins); 0 (Netrins); 0 (UNC-6 protein, C elegans); 1604ZJR09T (4,6-dinitro-o-cresol); EC 1.- (Mixed Function Oxygenases); EC 3.6.5.2 (rac GTP-Binding Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006998


  5 / 65 MEDLINE  
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[PMID]:28859078
[Au] Autor:Justice ED; Barnum SJ; Kidd T
[Ad] Endereço:Department of Biology/ms 314, University of Nevada, Reno, Nevada, United States of America.
[Ti] Título:The WAGR syndrome gene PRRG4 is a functional homologue of the commissureless axon guidance gene.
[So] Source:PLoS Genet;13(8):e1006865, 2017 Aug.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:WAGR syndrome is characterized by Wilm's tumor, aniridia, genitourinary abnormalities and intellectual disabilities. WAGR is caused by a chromosomal deletion that includes the PAX6, WT1 and PRRG4 genes. PRRG4 is proposed to contribute to the autistic symptoms of WAGR syndrome, but the molecular function of PRRG4 genes remains unknown. The Drosophila commissureless (comm) gene encodes a short transmembrane protein characterized by PY motifs, features that are shared by the PRRG4 protein. Comm intercepts the Robo axon guidance receptor in the ER/Golgi and targets Robo for degradation, allowing commissural axons to cross the CNS midline. Expression of human Robo1 in the fly CNS increases midline crossing and this was enhanced by co-expression of PRRG4, but not CYYR, Shisa or the yeast Rcr genes. In cell culture experiments, PRRG4 could re-localize hRobo1 from the cell surface, suggesting that PRRG4 is a functional homologue of Comm. Comm is required for axon guidance and synapse formation in the fly, so PRRG4 could contribute to the autistic symptoms of WAGR by disturbing either of these processes in the developing human brain.
[Mh] Termos MeSH primário: Transtorno Autístico/genética
Proteínas de Drosophila/genética
Proteínas de Membrana/genética
Proteínas do Tecido Nervoso/genética
Receptores Imunológicos/genética
Síndrome WAGR/genética
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Transtorno Autístico/fisiopatologia
Orientação de Axônios/genética
Axônios/metabolismo
Sistema Nervoso Central/metabolismo
Sistema Nervoso Central/patologia
Deleção Cromossômica
Drosophila melanogaster/genética
Regulação da Expressão Gênica no Desenvolvimento
Seres Humanos
Medula Espinal/crescimento & desenvolvimento
Medula Espinal/fisiopatologia
Sinapses/genética
Síndrome WAGR/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CYYR1 protein, human); 0 (Drosophila Proteins); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (Receptors, Immunologic); 0 (TMG4 protein, human); 0 (commissureless protein, Drosophila); 0 (roundabout protein)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170901
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006865


  6 / 65 MEDLINE  
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[PMID]:28846083
[Au] Autor:Rapti G; Li C; Shan A; Lu Y; Shaham S
[Ad] Endereço:Laboratory of Developmental Genetics, The Rockefeller University, New York, New York, USA.
[Ti] Título:Glia initiate brain assembly through noncanonical Chimaerin-Furin axon guidance in C. elegans.
[So] Source:Nat Neurosci;20(10):1350-1360, 2017 Oct.
[Is] ISSN:1546-1726
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Brain assembly is hypothesized to begin when pioneer axons extend over non-neuronal cells, forming tracts guiding follower axons. Yet pioneer-neuron identities, their guidance substrates, and their interactions are not well understood. Here, using time-lapse embryonic imaging, genetics, protein-interaction, and functional studies, we uncover the early events of C. elegans brain assembly. We demonstrate that C. elegans glia are key for assembly initiation, guiding pioneer and follower axons using distinct signals. Pioneer sublateral neurons, with unique growth properties, anatomy, and innervation, cooperate with glia to mediate follower-axon guidance. We further identify a Chimaerin (CHIN-1)- Furin (KPC-1) double-mutant that severely disrupts assembly. CHIN-1 and KPC-1 function noncanonically, in glia and pioneer neurons, for guidance-cue trafficking. We exploit this bottleneck to define roles for glial Netrin and Semaphorin in pioneer- and follower-axon guidance, respectively, and for glial and pioneer-neuron Flamingo (CELSR) in follower-axon navigation. Taken together, our studies reveal previously undescribed glial roles in pioneer-axon guidance, suggesting conserved principles of brain assembly.
[Mh] Termos MeSH primário: Orientação de Axônios/fisiologia
Encéfalo/crescimento & desenvolvimento
Proteínas de Caenorhabditis elegans/fisiologia
Caenorhabditis elegans/fisiologia
Proteínas Ativadoras de GTPase/fisiologia
Neuroglia/fisiologia
Pró-Proteína Convertases/fisiologia
[Mh] Termos MeSH secundário: Animais
Animais Geneticamente Modificados
Encéfalo/ultraestrutura
Proteínas de Caenorhabditis elegans/genética
Proteínas Ativadoras de GTPase/genética
Mutação
Proteínas do Tecido Nervoso/fisiologia
Netrinas
Neuroglia/ultraestrutura
Neurônios/fisiologia
Pró-Proteína Convertases/genética
Semaforinas/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (CHIN-1 protein, C elegans); 0 (Caenorhabditis elegans Proteins); 0 (GTPase-Activating Proteins); 0 (Nerve Tissue Proteins); 0 (Netrins); 0 (Semaphorins); 0 (UNC-6 protein, C elegans); EC 3.4.21.- (KPC-1 protein, C elegans); EC 3.4.21.- (Proprotein Convertases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170829
[St] Status:MEDLINE
[do] DOI:10.1038/nn.4630


  7 / 65 MEDLINE  
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[PMID]:28784295
[Au] Autor:Suter TACS; DeLoughery ZJ; Jaworski A
[Ad] Endereço:Department of Neuroscience, Brown University, Providence, RI 02912, United States.
[Ti] Título:Meninges-derived cues control axon guidance.
[So] Source:Dev Biol;430(1):1-10, 2017 10 01.
[Is] ISSN:1095-564X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The axons of developing neurons travel long distances along stereotyped pathways under the direction of extracellular cues sensed by the axonal growth cone. Guidance cues are either secreted proteins that diffuse freely or bind the extracellular matrix, or membrane-anchored proteins. Different populations of axons express distinct sets of receptors for guidance cues, which results in differential responses to specific ligands. The full repertoire of axon guidance cues and receptors and the identity of the tissues producing these cues remain to be elucidated. The meninges are connective tissue layers enveloping the vertebrate brain and spinal cord that serve to protect the central nervous system (CNS). The meninges also instruct nervous system development by regulating the generation and migration of neural progenitors, but it has not been determined whether they help guide axons to their targets. Here, we investigate a possible role for the meninges in neuronal wiring. Using mouse neural tissue explants, we show that developing spinal cord meninges produce secreted attractive and repulsive cues that can guide multiple types of axons in vitro. We find that motor and sensory neurons, which project axons across the CNS-peripheral nervous system (PNS) boundary, are attracted by meninges. Conversely, axons of both ipsi- and contralaterally projecting dorsal spinal cord interneurons are repelled by meninges. The responses of these axonal populations to the meninges are consistent with their trajectories relative to meninges in vivo, suggesting that meningeal guidance factors contribute to nervous system wiring and control which axons are able to traverse the CNS-PNS boundary.
[Mh] Termos MeSH primário: Orientação de Axônios
Sinais (Psicologia)
Meninges/metabolismo
[Mh] Termos MeSH secundário: Animais
Axônios/metabolismo
Interneurônios/metabolismo
Camundongos Transgênicos
Neurônios Motores/metabolismo
Medula Espinal/crescimento & desenvolvimento
Medula Espinal/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170809
[St] Status:MEDLINE


  8 / 65 MEDLINE  
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[PMID]:28692932
[Au] Autor:Lei H; Yan Z; Sun X; Zhang Y; Wang J; Ma C; Xu Q; Wang R; Jarvis ED; Sun Z
[Ad] Endereço:Department of Neurobiology, Beijing Institute for Brain Disorders, Beijing Center of Neural Regeneration and Repair, Key Laboratory for Neurodegenerative Diseases of the Ministry of Education, Capital Medical University, Beijing 100069, China. Electronic address: leihm@ccmu.edu.cn.
[Ti] Título:Axon guidance pathways served as common targets for human speech/language evolution and related disorders.
[So] Source:Brain Lang;174:1-8, 2017 Nov.
[Is] ISSN:1090-2155
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Human and several nonhuman species share the rare ability of modifying acoustic and/or syntactic features of sounds produced, i.e. vocal learning, which is the important neurobiological and behavioral substrate of human speech/language. This convergent trait was suggested to be associated with significant genomic convergence and best manifested at the ROBO-SLIT axon guidance pathway. Here we verified the significance of such genomic convergence and assessed its functional relevance to human speech/language using human genetic variation data. In normal human populations, we found the affected amino acid sites were well fixed and accompanied with significantly more associated protein-coding SNPs in the same genes than the rest genes. Diseased individuals with speech/language disorders have significant more low frequency protein coding SNPs but they preferentially occurred outside the affected genes. Such patients' SNPs were enriched in several functional categories including two axon guidance pathways (mediated by netrin and semaphorin) that interact with ROBO-SLITs. Four of the six patients have homozygous missense SNPs on PRAME gene family, one youngest gene family in human lineage, which possibly acts upon retinoic acid receptor signaling, similarly as FOXP2, to modulate axon guidance. Taken together, we suggest the axon guidance pathways (e.g. ROBO-SLIT, PRAME gene family) served as common targets for human speech/language evolution and related disorders.
[Mh] Termos MeSH primário: Orientação de Axônios/genética
Orientação de Axônios/fisiologia
Axônios/metabolismo
Evolução Molecular
Transtornos da Linguagem/genética
Linguagem
Mutação de Sentido Incorreto/genética
Fala/fisiologia
[Mh] Termos MeSH secundário: Criança
Pré-Escolar
Fatores de Transcrição Forkhead/metabolismo
Seres Humanos
Transtornos da Linguagem/metabolismo
Aprendizagem/fisiologia
Masculino
Fatores de Crescimento Neural/metabolismo
Netrina-1
Polimorfismo de Nucleotídeo Único/genética
Receptores do Ácido Retinoico/metabolismo
Semaforinas/metabolismo
Proteínas Supressoras de Tumor/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (FOXP2 protein, human); 0 (Forkhead Transcription Factors); 0 (Nerve Growth Factors); 0 (Receptors, Retinoic Acid); 0 (Semaphorins); 0 (Tumor Suppressor Proteins); 158651-98-0 (Netrin-1)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE


  9 / 65 MEDLINE  
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[PMID]:28689759
[Au] Autor:Yoon J; Kim SB; Ahmed G; Shay JW; Terman JR
[Ad] Endereço:Departments of Neuroscience and Pharmacology, Harold C. Simmons Comprehensive Cancer Center, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
[Ti] Título:Amplification of F-Actin Disassembly and Cellular Repulsion by Growth Factor Signaling.
[So] Source:Dev Cell;42(2):117-129.e8, 2017 Jul 24.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Extracellular cues that regulate cellular shape, motility, and navigation are generally classified as growth promoting (i.e., growth factors/chemoattractants and attractive guidance cues) or growth preventing (i.e., repellents and inhibitors). Yet, these designations are often based on complex assays and undefined signaling pathways and thus may misrepresent direct roles of specific cues. Here, we find that a recognized growth-promoting signaling pathway amplifies the F-actin disassembly and repulsive effects of a growth-preventing pathway. Focusing on Semaphorin/Plexin repulsion, we identified an interaction between the F-actin-disassembly enzyme Mical and the Abl tyrosine kinase. Biochemical assays revealed Abl phosphorylates Mical to directly amplify Mical Redox-mediated F-actin disassembly. Genetic assays revealed that Abl allows growth factors and Semaphorin/Plexin repellents to combinatorially increase Mical-mediated F-actin disassembly, cellular remodeling, and repulsive axon guidance. Similar roles for Mical in growth factor/Abl-related cancer cell behaviors further revealed contexts in which characterized positive effectors of growth/guidance stimulate such negative cellular effects as F-actin disassembly/repulsion.
[Mh] Termos MeSH primário: Actinas/metabolismo
Peptídeos e Proteínas de Sinalização Intercelular/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Orientação de Axônios/efeitos dos fármacos
Biocatálise/efeitos dos fármacos
Fenômenos Biomecânicos
Moléculas de Adesão Celular/metabolismo
Proliferação Celular/efeitos dos fármacos
Drosophila melanogaster/embriologia
Drosophila melanogaster/metabolismo
Seres Humanos
Mesilato de Imatinib/farmacologia
Camundongos Nus
Oxigenases de Função Mista/química
Oxigenases de Função Mista/metabolismo
Modelos Biológicos
Neoplasias/patologia
Proteínas do Tecido Nervoso/metabolismo
Oxirredução
Fosforilação/efeitos dos fármacos
Ligação Proteica/efeitos dos fármacos
Domínios Proteicos
Proteínas Proto-Oncogênicas c-abl/antagonistas & inibidores
Proteínas Proto-Oncogênicas c-abl/metabolismo
Semaforinas/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Cell Adhesion Molecules); 0 (Intercellular Signaling Peptides and Proteins); 0 (Nerve Tissue Proteins); 0 (Semaphorins); 0 (plexin); 8A1O1M485B (Imatinib Mesylate); EC 1.- (Mixed Function Oxygenases); EC 2.7.10.2 (Proto-Oncogene Proteins c-abl)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170711
[St] Status:MEDLINE


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[PMID]:28676566
[Au] Autor:Rajman M; Schratt G
[Ad] Endereço:Biochemisch-Pharmakologisches Centrum, Institut für Physiologische Chemie, Philipps-Universität Marburg, Marburg 35043, Germany.
[Ti] Título:MicroRNAs in neural development: from master regulators to fine-tuners.
[So] Source:Development;144(13):2310-2322, 2017 07 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The proper formation and function of neuronal networks is required for cognition and behavior. Indeed, pathophysiological states that disrupt neuronal networks can lead to neurodevelopmental disorders such as autism, schizophrenia or intellectual disability. It is well-established that transcriptional programs play major roles in neural circuit development. However, in recent years, post-transcriptional control of gene expression has emerged as an additional, and probably equally important, regulatory layer. In particular, it has been shown that microRNAs (miRNAs), an abundant class of small regulatory RNAs, can regulate neuronal circuit development, maturation and function by controlling, for example, local mRNA translation. It is also becoming clear that miRNAs are frequently dysregulated in neurodevelopmental disorders, suggesting a role for miRNAs in the etiology and/or maintenance of neurological disease states. Here, we provide an overview of the most prominent regulatory miRNAs that control neural development, highlighting how they act as 'master regulators' or 'fine-tuners' of gene expression, depending on context, to influence processes such as cell fate determination, cell migration, neuronal polarization and synapse formation.
[Mh] Termos MeSH primário: MicroRNAs/metabolismo
Neurogênese/genética
[Mh] Termos MeSH secundário: Animais
Orientação de Axônios/genética
Linhagem da Célula/genética
Movimento Celular/genética
Seres Humanos
MicroRNAs/genética
Sinapses/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (MicroRNAs)
[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:170706
[St] Status:MEDLINE
[do] DOI:10.1242/dev.144337



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