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[PMID]:28694260
[Au] Autor:Hu JS; Vogt D; Lindtner S; Sandberg M; Silberberg SN; Rubenstein JLR
[Ad] Endereço:Department of Psychiatry, Neuroscience Program and the Nina Ireland Laboratory of Developmental Neurobiology, University of California San Francisco, San Francisco, CA 94158, USA jia.hu@ucsf.edu john.rubenstein@ucsf.edu.
[Ti] Título: and control subtype and laminar identity of MGE-derived neocortical interneurons.
[So] Source:Development;144(15):2837-2851, 2017 08 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Distinct cortical interneuron (CIN) subtypes have unique circuit functions; dysfunction in specific subtypes is implicated in neuropsychiatric disorders. Somatostatin- and parvalbumin-expressing (SST and PV ) interneurons are the two major subtypes generated by medial ganglionic eminence (MGE) progenitors. Spatial and temporal mechanisms governing their cell-fate specification and differential integration into cortical layers are largely unknown. We provide evidence that and ( and ) transcription factor expression in an arc-shaped progenitor domain within the MGE promotes time-dependent survival of this neuroepithelium and the time-dependent specification of layer V SST CINs. and autonomously repress PV fate in MGE progenitors, in part through directly driving expression. These results have identified, in mouse, a transcriptional pathway that controls SST-PV fate.
[Mh] Termos MeSH primário: Fator II de Transcrição COUP/metabolismo
Fator I de Transcrição COUP/metabolismo
Interneurônios/metabolismo
Neocórtex/citologia
[Mh] Termos MeSH secundário: Animais
Fator I de Transcrição COUP/genética
Fator II de Transcrição COUP/genética
Células Cultivadas
Imunoprecipitação da Cromatina
Feminino
Regulação da Expressão Gênica no Desenvolvimento/genética
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Imuno-Histoquímica
Hibridização In Situ
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Parvalbuminas/genética
Parvalbuminas/metabolismo
Fatores de Transcrição SOXD/genética
Fatores de Transcrição SOXD/metabolismo
Somatostatina/genética
Somatostatina/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 (COUP Transcription Factor I); 0 (COUP Transcription Factor II); 0 (Parvalbumins); 0 (SOXD Transcription Factors); 0 (Sox6 protein, mouse); 51110-01-1 (Somatostatin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170712
[St] Status:MEDLINE
[do] DOI:10.1242/dev.150664


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[PMID]:28506990
[Au] Autor:Parisot J; Flore G; Bertacchi M; Studer M
[Ad] Endereço:Université Côte d'Azur, CNRS, Inserm, iBV, Nice 06100, France.
[Ti] Título:COUP-TFI mitotically regulates production and migration of dentate granule cells and modulates hippocampal Cxcr4 expression.
[So] Source:Development;144(11):2045-2058, 2017 06 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Development of the dentate gyrus (DG), the primary gateway for hippocampal inputs, spans embryonic and postnatal stages, and involves complex morphogenetic events. We have previously identified the nuclear receptor COUP-TFI as a novel transcriptional regulator in the postnatal organization and function of the hippocampus. Here, we dissect its role in DG morphogenesis by inactivating it in either granule cell progenitors or granule neurons. Loss of COUP-TFI function in progenitors leads to decreased granule cell proliferative activity, precocious differentiation and increased apoptosis, resulting in a severe DG growth defect in adult mice. COUP-TFI-deficient cells express high levels of the chemokine receptor Cxcr4 and migrate abnormally, forming heterotopic clusters of differentiated granule cells along their paths. Conversely, high COUP-TFI expression levels downregulate expression, whereas increased expression in wild-type hippocampal cells affects cell migration. Finally, loss of COUP-TFI in postmitotic cells leads to only minor and transient abnormalities, and to normal expression. Together, our results indicate that COUP-TFI is required predominantly in DG progenitors for modulating expression of the receptor during granule cell neurogenesis and migration.
[Mh] Termos MeSH primário: Fator I de Transcrição COUP/metabolismo
Movimento Celular
Giro Denteado/citologia
Giro Denteado/metabolismo
Mitose
Receptores CXCR4/genética
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Contagem de Células
Diferenciação Celular/genética
Movimento Celular/genética
Proliferação Celular/genética
Giro Denteado/embriologia
Deleção de Genes
Regulação da Expressão Gênica no Desenvolvimento
Proteínas de Homeodomínio/metabolismo
Camundongos Knockout
Mitose/genética
Modelos Biológicos
Células-Tronco Neurais/citologia
Células-Tronco Neurais/metabolismo
Neurogênese/genética
Neuroglia/metabolismo
Receptores CXCR4/metabolismo
Fatores de Transcrição/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COUP Transcription Factor I); 0 (Homeodomain Proteins); 0 (Receptors, CXCR4); 0 (Transcription Factors); 0 (empty spiracles homeobox proteins)
[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:170517
[St] Status:MEDLINE
[do] DOI:10.1242/dev.139949


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[PMID]:28114271
[Au] Autor:Fluegen G; Avivar-Valderas A; Wang Y; Padgen MR; Williams JK; Nobre AR; Calvo V; Cheung JF; Bravo-Cordero JJ; Entenberg D; Castracane J; Verkhusha V; Keely PJ; Condeelis J; Aguirre-Ghiso JA
[Ad] Endereço:Department of Medicine and Department of Otolaryngology, Tisch Cancer Institute, Black Family Stem Cell Institute, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, New York 10029, USA.
[Ti] Título:Phenotypic heterogeneity of disseminated tumour cells is preset by primary tumour hypoxic microenvironments.
[So] Source:Nat Cell Biol;19(2):120-132, 2017 Feb.
[Is] ISSN:1476-4679
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Hypoxia is a poor-prognosis microenvironmental hallmark of solid tumours, but it is unclear how it influences the fate of disseminated tumour cells (DTCs) in target organs. Here we report that hypoxic HNSCC and breast primary tumour microenvironments displayed upregulation of key dormancy (NR2F1, DEC2, p27) and hypoxia (GLUT1, HIF1α) genes. Analysis of solitary DTCs in PDX and transgenic mice revealed that post-hypoxic DTCs were frequently NR2F1 /DEC2 /p27 /TGFß2 and dormant. NR2F1 and HIF1α were required for p27 induction in post-hypoxic dormant DTCs, but these DTCs did not display GLUT1 expression. Post-hypoxic DTCs evaded chemotherapy and, unlike ER breast cancer cells, post-hypoxic ER breast cancer cells were more prone to enter NR2F1-dependent dormancy. We propose that primary tumour hypoxic microenvironments give rise to a subpopulation of dormant DTCs that evade therapy. These post-hypoxic dormant DTCs may be the source of disease relapse and poor prognosis associated with hypoxia.
[Mh] Termos MeSH primário: Medula Óssea/metabolismo
Neoplasias da Mama/metabolismo
Microambiente Tumoral
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/patologia
Fator I de Transcrição COUP/metabolismo
Hipóxia Celular
Linhagem Celular Tumoral
Separação Celular/métodos
Seres Humanos
Camundongos
Metástase Neoplásica
Fenótipo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COUP Transcription Factor I); 0 (NR2F1 protein, human)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170124
[St] Status:MEDLINE
[do] DOI:10.1038/ncb3465


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[PMID]:27251161
[Au] Autor:Teratani-Ota Y; Yamamizu K; Piao Y; Sharova L; Amano M; Yu H; Schlessinger D; Ko MS; Sharov AA
[Ad] Endereço:Laboratory of Genetics, National Institute on Aging, National Institutes of Health, Baltimore, MD, 21224, USA.
[Ti] Título:Induction of specific neuron types by overexpression of single transcription factors.
[So] Source:In Vitro Cell Dev Biol Anim;52(9):961-973, 2016 Oct.
[Is] ISSN:1543-706X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Specific neuronal types derived from embryonic stem cells (ESCs) can facilitate mechanistic studies and potentially aid in regenerative medicine. Existing induction methods, however, mostly rely on the effects of the combined action of multiple added growth factors, which generally tend to result in mixed populations of neurons. Here, we report that overexpression of specific transcription factors (TFs) in ESCs can rather guide the differentiation of ESCs towards specific neuron lineages. Analysis of data on gene expression changes 2 d after induction of each of 185 TFs implicated candidate TFs for further ESC differentiation studies. Induction of 23 TFs (out of 49 TFs tested) for 6 d facilitated neural differentiation of ESCs as inferred from increased proportion of cells with neural progenitor marker PSA-NCAM. We identified early activation of the Notch signaling pathway as a common feature of most potent inducers of neural differentiation. The majority of neuron-like cells generated by induction of Ascl1, Smad7, Nr2f1, Dlx2, Dlx4, Nr2f2, Barhl2, and Lhx1 were GABA-positive and expressed other markers of GABAergic neurons. In the same way, we identified Lmx1a and Nr4a2 as inducers for neurons bearing dopaminergic markers and Isl1, Fezf2, and St18 for cholinergic motor neurons. A time-course experiment with induction of Ascl1 showed early upregulation of most neural-specific messenger RNA (mRNA) and microRNAs (miRNAs). Sets of Ascl1-induced mRNAs and miRNAs were enriched in Ascl1 targets. In further studies, enrichment of cells obtained with the induction of Ascl1, Smad7, and Nr2f1 using microbeads resulted in essentially pure population of neuron-like cells with expression profiles similar to neural tissues and expressed markers of GABAergic neurons. In summary, this study indicates that induction of transcription factors is a promising approach to generate cultures that show the transcription profiles characteristic of specific neural cell types.
[Mh] Termos MeSH primário: Neurogênese
Neurônios/citologia
Neurônios/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Fatores de Transcrição Hélice-Alça-Hélice Básicos/metabolismo
Fator I de Transcrição COUP/metabolismo
Reprogramação Celular/genética
Perfilação da Expressão Gênica
Camundongos
Células-Tronco Embrionárias Murinas/citologia
Células-Tronco Embrionárias Murinas/metabolismo
Proteína Smad7/metabolismo
Transcriptoma/genética
Regulação para Cima/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Ascl1 protein, mouse); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (COUP Transcription Factor I); 0 (Nr2f1 protein, mouse); 0 (Smad7 Protein); 0 (Transcription Factors)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170722
[Lr] Data última revisão:
170722
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160603
[St] Status:MEDLINE


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[PMID]:26986877
[Au] Autor:Chen CA; Bosch DG; Cho MT; Rosenfeld JA; Shinawi M; Lewis RA; Mann J; Jayakar P; Payne K; Walsh L; Moss T; Schreiber A; Schoonveld C; Monaghan KG; Elmslie F; Douglas G; Boonstra FN; Millan F; Cremers FP; McKnight D; Richard G; Juusola J; Kendall F; Ramsey K; Anyane-Yeboa K; Malkin E; Chung WK; Niyazov D; Pascual JM; Walkiewicz M; Veluchamy V; Li C; Hisama FM; de Vries BB; Schaaf C
[Ad] Endereço:Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, USA.
[Ti] Título:The expanding clinical phenotype of Bosch-Boonstra-Schaaf optic atrophy syndrome: 20 new cases and possible genotype-phenotype correlations.
[So] Source:Genet Med;18(11):1143-1150, 2016 Nov.
[Is] ISSN:1530-0366
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Bosch-Boonstra-Schaaf optic atrophy syndrome (BBSOAS) is an autosomal-dominant disorder characterized by optic atrophy and intellectual disability caused by loss-of-function mutations in NR2F1. We report 20 new individuals with BBSOAS, exploring the spectrum of clinical phenotypes and assessing potential genotype-phenotype correlations. METHODS: Clinical features of individuals with pathogenic NR2F1 variants were evaluated by review of medical records. The functional relevance of coding nonsynonymous NR2F1 variants was assessed with a luciferase assay measuring the impact on transcriptional activity. The effects of two start codon variants on protein expression were evaluated by western blot analysis. RESULTS: We recruited 20 individuals with novel pathogenic NR2F1 variants (seven missense variants, five translation initiation variants, two frameshifting insertions/deletions, one nonframeshifting insertion/deletion, and five whole-gene deletions). All the missense variants were found to impair transcriptional activity. In addition to visual and cognitive deficits, individuals with BBSOAS manifested hypotonia (75%), seizures (40%), autism spectrum disorder (35%), oromotor dysfunction (60%), thinning of the corpus callosum (53%), and hearing defects (20%). CONCLUSION: BBSOAS encompasses a broad range of clinical phenotypes. Functional studies help determine the severity of novel NR2F1 variants. Some genotype-phenotype correlations seem to exist, with missense mutations in the DNA-binding domain causing the most severe phenotypes.Genet Med 18 11, 1143-1150.
[Mh] Termos MeSH primário: Transtorno do Espectro Autista/genética
Fator I de Transcrição COUP/genética
Estudos de Associação Genética
Atrofia Óptica/genética
[Mh] Termos MeSH secundário: Adolescente
Adulto
Transtorno do Espectro Autista/complicações
Transtorno do Espectro Autista/fisiopatologia
Criança
Pré-Escolar
Feminino
Deleção de Genes
Seres Humanos
Masculino
Mutação de Sentido Incorreto
Atrofia Óptica/complicações
Atrofia Óptica/fisiopatologia
Linhagem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (COUP Transcription Factor I); 0 (NR2F1 protein, human)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170915
[Lr] Data última revisão:
170915
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160318
[St] Status:MEDLINE
[do] DOI:10.1038/gim.2016.18


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[PMID]:25922524
[Au] Autor:Zhou X; Liu F; Tian M; Xu Z; Liang Q; Wang C; Li J; Liu Z; Tang K; He M; Yang Z
[Ad] Endereço:Institutes of Brain Science, State Key Laboratory of Medical Neurobiology, Collaborative Innovation Center for Brain Science, Fudan University, Shanghai 200032, China.
[Ti] Título:Transcription factors COUP-TFI and COUP-TFII are required for the production of granule cells in the mouse olfactory bulb.
[So] Source:Development;142(9):1593-605, 2015 May 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Neural stem cells (NSCs) persist in the adult mammalian subventricular zone (SVZ) of the lateral ventricle. Primary NSCs generate rapidly dividing intermediate progenitor cells, which in turn generate neuroblasts that migrate along the rostral migratory stream (RMS) to the olfactory bulb (OB). Here, we have examined the role of the COUP-TFI and COUP-TFII orphan nuclear receptor transcription factors in mouse OB interneuron development. We observed that COUP-TFI is expressed in a gradient of low rostral to high caudal within the postnatal SVZ neural stem/progenitor cells. COUP-TFI is also expressed in a large number of migrating neuroblasts in the SVZ and RMS, and in mature interneurons in the OB. By contrast, very few COUP-TFII-expressing (+) cells exist in the SVZ-RMS-OB pathway. Conditional inactivation of COUP-TFI resulted in downregulation of tyrosine hydroxylase expression in the OB periglomerular cells and upregulation of COUP-TFII expression in the SVZ, RMS and OB deep granule cell layer. In COUP-TFI/COUP-TFII double conditional mutant SVZ, cell proliferation was increased through the upregulation of the proneural gene Ascl1. Furthermore, COUP-TFI/II-deficient neuroblasts had impaired migration, resulting in ectopic accumulation of calretinin (CR)+ and NeuN+ cells, and an increase in apoptotic cell death in the SVZ. Finally, we found that most Pax6+ and a subset of CR+ granular cells were lost in the OB. Taken together, these results suggest that COUP-TFI/II coordinately regulate the proliferation, migration and survival of a subpopulation of Pax6+ and CR+ granule cells in the OB.
[Mh] Termos MeSH primário: Fator II de Transcrição COUP/metabolismo
Fator I de Transcrição COUP/metabolismo
Diferenciação Celular/fisiologia
Regulação da Expressão Gênica no Desenvolvimento/fisiologia
Interneurônios/fisiologia
Células-Tronco Neurais/fisiologia
Bulbo Olfatório/citologia
[Mh] Termos MeSH secundário: Animais
Bromodesoxiuridina
Movimento Celular/fisiologia
Colágeno
Combinação de Medicamentos
Galactosídeos
Imuno-Histoquímica
Indóis
Interneurônios/metabolismo
Laminina
Camundongos
Microscopia de Fluorescência
Proteoglicanas
Tamoxifeno
Tirosina 3-Mono-Oxigenase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COUP Transcription Factor I); 0 (COUP Transcription Factor II); 0 (Drug Combinations); 0 (Galactosides); 0 (Indoles); 0 (Laminin); 0 (Nr2f2 protein, mouse); 0 (Proteoglycans); 094ZI81Y45 (Tamoxifen); 119978-18-6 (matrigel); 9007-34-5 (Collagen); EC 1.14.16.2 (Tyrosine 3-Monooxygenase); G34N38R2N1 (Bromodeoxyuridine); V595OG374W (5-bromo-4-chloro-3-indolyl beta-galactoside)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:150429
[Lr] Data última revisão:
150429
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150430
[St] Status:MEDLINE
[do] DOI:10.1242/dev.115279


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[PMID]:25877686
[Au] Autor:Hino-Fukuyo N; Kikuchi A; Arai-Ichinoi N; Niihori T; Sato R; Suzuki T; Kudo H; Sato Y; Nakayama T; Kakisaka Y; Kubota Y; Kobayashi T; Funayama R; Nakayama K; Uematsu M; Aoki Y; Haginoya K; Kure S
[Ad] Endereço:Department of Pediatrics, Tohoku University School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai, Miyagi, 980-8574, Japan.
[Ti] Título:Genomic analysis identifies candidate pathogenic variants in 9 of 18 patients with unexplained West syndrome.
[So] Source:Hum Genet;134(6):649-58, 2015 Jun.
[Is] ISSN:1432-1203
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:West syndrome, which is narrowly defined as infantile spasms that occur in clusters and hypsarrhythmia on EEG, is the most common early-onset epileptic encephalopathy (EOEE). Patients with West syndrome may have clear etiologies, including perinatal events, infections, gross chromosomal abnormalities, or cases followed by other EOEEs. However, the genetic etiology of most cases of West syndrome remains unexplained. DNA from 18 patients with unexplained West syndrome was subjected to microarray-based comparative genomic hybridization (array CGH), followed by trio-based whole-exome sequencing in 14 unsolved families. We identified candidate pathogenic variants in 50% of the patients (n = 9/18). The array CGH revealed candidate pathogenic copy number variations in four cases (22%, 4/18), including an Xq28 duplication, a 16p11.2 deletion, a 16p13.1 deletion and a 19p13.2 deletion disrupting CACNA1A. Whole-exome sequencing identified candidate mutations in known epilepsy genes in five cases (36%, 5/14). Three candidate de novo mutations were identified in three cases, with two mutations occurring in two new candidate genes (NR2F1 and CACNA2D1) (21%, 3/14). Hemizygous candidate mutations in ALG13 and BRWD3 were identified in the other two cases (14%, 2/14). Evaluating a panel of 67 known EOEE genes failed to identify significant mutations. Despite the heterogeneity of unexplained West syndrome, the combination of array CGH and whole-exome sequencing is an effective means of evaluating the genetic background in unexplained West syndrome. We provide additional evidence for NR2F1 as a causative gene and for CACNA2D1 and BRWD3 as candidate genes for West syndrome.
[Mh] Termos MeSH primário: Fator I de Transcrição COUP/genética
Canais de Cálcio/genética
Cromossomos Humanos/genética
Mutação
Espasmos Infantis/genética
Fatores de Transcrição/genética
[Mh] Termos MeSH secundário: Feminino
Estudo de Associação Genômica Ampla
Hemizigoto
Seres Humanos
Lactente
Masculino
N-Acetilglucosaminiltransferases/genética
[Pt] Tipo de publicação:CLINICAL TRIAL; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BRWD3 protein, human); 0 (CACNA2D1 protein, human); 0 (COUP Transcription Factor I); 0 (Calcium Channels); 0 (NR2F1 protein, human); 0 (Transcription Factors); EC 2.4.1.- (ALG13 protein, human); EC 2.4.1.- (N-Acetylglucosaminyltransferases)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150417
[St] Status:MEDLINE
[do] DOI:10.1007/s00439-015-1553-6


  8 / 250 MEDLINE  
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[PMID]:25787832
[Au] Autor:Varga C; Tamas G; Barzo P; Olah S; Somogyi P
[Ad] Endereço:Research Group for Cortical Microcircuits of the Hungarian Academy of Science, Department of Physiology, Anatomy and Neuroscience MRC, Brain Networks Dynamics Unit, Department of Pharmacology, University of Oxford, Oxford OX1 3TH, UK Current address: Szentágothai Research Centre, Department of Physi
[Ti] Título:Molecular and Electrophysiological Characterization of GABAergic Interneurons Expressing the Transcription Factor COUP-TFII in the Adult Human Temporal Cortex.
[So] Source:Cereb Cortex;25(11):4430-49, 2015 Nov.
[Is] ISSN:1460-2199
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transcription factors contribute to the differentiation of cortical neurons, orchestrate specific interneuronal circuits, and define synaptic relationships. We have investigated neurons expressing chicken ovalbumin upstream promoter transcription factor II (COUP-TFII), which plays a role in the migration of GABAergic neurons. Whole-cell, patch-clamp recording in vitro combined with colocalization of molecular cell markers in the adult cortex differentiates distinct interneurons. The majority of strongly COUP-TFII-expressing neurons were in layers I-III. Most calretinin (CR) and/or cholecystokinin- (CCK) and/or reelin-positive interneurons were also COUP-TFII-positive. CR-, CCK-, or reelin-positive neurons formed 80%, 20%, or 17% of COUP-TFII-positive interneurons, respectively. About half of COUP-TFII-/CCK-positive interneurons were CR-positive, a quarter of them reelin-positive, but none expressed both. Interneurons positive for COUP-TFII fired irregular, accommodating and adapting trains of action potentials (APs) and innervated mostly small dendritic shafts and rarely spines or somata. Paired recording showed that a calretinin-/COUP-TFII-positive interneuron elicited inhibitory postsynaptic potentials (IPSPs) in a reciprocally connected pyramidal cell. Calbindin, somatostatin, or parvalbumin-immunoreactive interneurons and most pyramidal cells express no immunohistochemically detectable COUP-TFII. In layers V and VI, some pyramidal cells expressed a low level of COUP-TFII in the nucleus. In conclusion, COUP-TFII is expressed in a diverse subset of GABAergic interneurons predominantly innervating small dendritic shafts originating from both interneurons and pyramidal cells.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Fator I de Transcrição COUP/metabolismo
Neurônios GABAérgicos/fisiologia
Lobo Temporal/patologia
Lobo Temporal/fisiologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Neoplasias Encefálicas/patologia
Fator I de Transcrição COUP/genética
Calbindinas/metabolismo
Colecistocinina/metabolismo
Feminino
Neurônios GABAérgicos/ultraestrutura
Seres Humanos
Técnicas In Vitro
Masculino
Meia-Idade
Proteínas do Tecido Nervoso/metabolismo
Parvalbuminas/metabolismo
Técnicas de Patch-Clamp
Coloração pela Prata
Somatostatina/metabolismo
Potenciais Sinápticos/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (COUP Transcription Factor I); 0 (Calbindins); 0 (NR2F1 protein, human); 0 (Nerve Tissue Proteins); 0 (Parvalbumins); 51110-01-1 (Somatostatin); 9011-97-6 (Cholecystokinin)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150320
[St] Status:MEDLINE
[do] DOI:10.1093/cercor/bhv045


  9 / 250 MEDLINE  
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[PMID]:25636082
[Au] Autor:Sosa MS; Parikh F; Maia AG; Estrada Y; Bosch A; Bragado P; Ekpin E; George A; Zheng Y; Lam HM; Morrissey C; Chung CY; Farias EF; Bernstein E; Aguirre-Ghiso JA
[Ad] Endereço:Division of Hematology and Oncology, Department of Medicine, Mount Sinai School of Medicine, New York, New York 10029, USA.
[Ti] Título:NR2F1 controls tumour cell dormancy via SOX9- and RARß-driven quiescence programmes.
[So] Source:Nat Commun;6:6170, 2015 Jan 30.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Metastases can originate from disseminated tumour cells (DTCs), which may be dormant for years before reactivation. Here we find that the orphan nuclear receptor NR2F1 is epigenetically upregulated in experimental head and neck squamous cell carcinoma (HNSCC) dormancy models and in DTCs from prostate cancer patients carrying dormant disease for 7-18 years. NR2F1-dependent dormancy is recapitulated by a co-treatment with the DNA-demethylating agent 5-Aza-C and retinoic acid across various cancer types. NR2F1-induced quiescence is dependent on SOX9, RARß and CDK inhibitors. Intriguingly, NR2F1 induces global chromatin repression and the pluripotency gene NANOG, which contributes to dormancy of DTCs in the bone marrow. When NR2F1 is blocked in vivo, growth arrest or survival of dormant DTCs is interrupted in different organs. We conclude that NR2F1 is a critical node in dormancy induction and maintenance by integrating epigenetic programmes of quiescence and survival in DTCs.
[Mh] Termos MeSH primário: Fator I de Transcrição COUP/metabolismo
Receptores do Ácido Retinoico/metabolismo
Fatores de Transcrição SOX9/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Imunofluorescência
Regulação Neoplásica da Expressão Gênica
Proteínas de Homeodomínio/metabolismo
Seres Humanos
Imuno-Histoquímica
Masculino
Camundongos
Camundongos Nus
Neoplasias da Próstata/metabolismo
Interferência de RNA
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (COUP Transcription Factor I); 0 (Homeodomain Proteins); 0 (Receptors, Retinoic Acid); 0 (SOX9 Transcription Factor)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:161019
[Lr] Data última revisão:
161019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150131
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms7170


  10 / 250 MEDLINE  
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[PMID]:25476200
[Au] Autor:Alfano C; Magrinelli E; Harb K; Hevner RF; Studer M
[Ad] Endereço:1] Univ. Nice Sophia Antipolis, iBV, UMR 7277, 06108 Nice, France [2] Inserm, iBV, U1091, 06108 Nice, France [3] CNRS, iBV, UMR 7277, 06108 Nice, France.
[Ti] Título:Postmitotic control of sensory area specification during neocortical development.
[So] Source:Nat Commun;5:5632, 2014 Dec 05.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The mammalian neocortex is subdivided into cytoarchitectural areas with distinct connectivity, gene expression and neural functions. Areal identity is initially specified by rostrocaudal and mediolateral gene expression gradients in neuroepithelial and radial glial progenitors (the 'protomap'). On further differentiation, distinct sets of gene expression gradients arise in intermediate progenitors and postmitotic neurons, and are necessary to implement areal specification. However, it is still unknown whether postmitotic gene expression gradients can determine areal identity independently of protomap gradients. Here we show, by cell type-restricted genetic loss- and gain-of-function, that high levels of postmitotic COUP-TFI (Nr2f1) expression are necessary and sufficient for the development of sensory (caudal) areal identity. Our data indicate a crucial role for postmitotic patterning genes in areal specification and reveal an unexpected plasticity in this process, which may account for complex and evolutionarily novel structures characteristic of the mammalian neocortex.
[Mh] Termos MeSH primário: Mitose
Neocórtex/crescimento & desenvolvimento
Células Receptoras Sensoriais/citologia
[Mh] Termos MeSH secundário: Animais
Fator I de Transcrição COUP/genética
Fator I de Transcrição COUP/metabolismo
Feminino
Regulação da Expressão Gênica no Desenvolvimento
Masculino
Camundongos
Camundongos Knockout
Neocórtex/citologia
Neocórtex/metabolismo
Células Receptoras Sensoriais/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 (COUP Transcription Factor I); 0 (Nr2f1 protein, mouse)
[Em] Mês de entrada:1510
[Cu] Atualização por classe:141205
[Lr] Data última revisão:
141205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141206
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms6632



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