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Pesquisa : C05.660.207.536.500 [Categoria DeCS]
Referências encontradas : 25 [refinar]
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  1 / 25 MEDLINE  
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[PMID]:28864461
[Au] Autor:Griffin NG; Cronin KD; Walley NM; Hulette CM; Grant GA; Mikati MA; LaBreche HG; Rehder CW; Allen AS; Crino PB; Heinzen EL
[Ad] Endereço:Institute for Genomic Medicine, Columbia University, New York, New York 10032, USA.
[Ti] Título:Somatic uniparental disomy of Chromosome 16p in hemimegalencephaly.
[So] Source:Cold Spring Harb Mol Case Stud;3(5), 2017 Sep.
[Is] ISSN:2373-2873
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hemimegalencephaly (HME) is a heterogeneous cortical malformation characterized by enlargement of one cerebral hemisphere. Somatic variants in mammalian target of rapamycin (mTOR) regulatory genes have been implicated in some HME cases; however, ∼70% have no identified genetic etiology. Here, we screened two HME patients to identify disease-causing somatic variants. DNA from leukocytes, buccal swabs, and surgically resected brain tissue from two HME patients were screened for somatic variants using genome-wide genotyping arrays or sequencing of the protein-coding regions of the genome. Functional studies were performed to evaluate the molecular consequences of candidate disease-causing variants. Both HME patients evaluated were found to have likely disease-causing variants in DNA extracted from brain tissue but not in buccal swab or leukocyte DNA, consistent with a somatic mutational mechanism. In the first case, a previously identified disease-causing somatic single nucleotide in was identified. In the second case, we detected an overrepresentation of the alleles inherited from the mother on Chromosome 16 in brain tissue DNA only, indicative of somatic uniparental disomy (UPD) of the p-arm of Chromosome 16. Using methylation analyses, an imprinted locus on 16p spanning was identified, which results in increased expression of mRNA and protein in the brain tissue of the second case. Enhanced mTOR signaling was observed in tissue specimens from both patients. We speculate that overexpression of maternally expressed led to aberrant hemispheric development in the patient with somatic UPD of Chromosome 16p possibly through modulation of mTOR signaling.
[Mh] Termos MeSH primário: Hemimegalencefalia/genética
[Mh] Termos MeSH secundário: Alelos
Encéfalo/citologia
Pré-Escolar
Cromossomos/genética
Cromossomos Humanos Par 16/genética
DNA/genética
Metilação de DNA/genética
Feminino
Impressão Genômica
Genótipo
Seres Humanos
Lactente
Dissomia Uniparental/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170903
[St] Status:MEDLINE


  2 / 25 MEDLINE  
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[PMID]:28427592
[Au] Autor:Hanai S; Sukigara S; Dai H; Owa T; Horike SI; Otsuki T; Saito T; Nakagawa E; Ikegaya N; Kaido T; Sato N; Takahashi A; Sugai K; Saito Y; Sasaki M; Hoshino M; Goto YI; Koizumi S; Itoh M
[Ad] Endereço:Epilepsy Center, National Center of Neurology and Psychiatry, National Institute of Neuroscience, Kodaira, Japan; Department of Mental Retardation and Birth Defect Research, National Institute of Neuroscience, Kodaira, Japan.
[Ti] Título:Pathologic Active mTOR Mutation in Brain Malformation with Intractable Epilepsy Leads to Cell-Autonomous Migration Delay.
[So] Source:Am J Pathol;187(5):1177-1185, 2017 May.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The activation of phosphatidylinositol 3-kinase-AKTs-mammalian target of rapamycin cell signaling pathway leads to cell overgrowth and abnormal migration and results in various types of cortical malformations, such as hemimegalencephaly (HME), focal cortical dysplasia, and tuberous sclerosis complex. However, the pathomechanism underlying abnormal cell migration remains unknown. With the use of fetal mouse brain, we performed causative gene analysis of the resected brain tissues from a patient with HME and investigated the pathogenesis. We obtained a novel somatic mutation of the MTOR gene, having approximately 11% and 7% mutation frequency in the resected brain tissues. Moreover, we revealed that the MTOR mutation resulted in hyperphosphorylation of its downstream molecules, S6 and 4E-binding protein 1, and delayed cell migration on the radial glial fiber and did not affect other cells. We suspect cell-autonomous migration arrest on the radial glial foot by the active MTOR mutation and offer potential explanations for why this may lead to cortical malformations such as HME.
[Mh] Termos MeSH primário: Epilepsia Resistente a Medicamentos/genética
Hemimegalencefalia/genética
Malformações do Desenvolvimento Cortical do Grupo II/genética
Serina-Treonina Quinases TOR/genética
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Epilepsia Resistente a Medicamentos/cirurgia
Eletroencefalografia
Feminino
Hemimegalencefalia/cirurgia
Seres Humanos
Lactente
Malformações do Desenvolvimento Cortical do Grupo II/cirurgia
Camundongos
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Serina-Treonina Quinases TOR/metabolismo
Transfecção
Regulação para Cima
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170422
[St] Status:MEDLINE


  3 / 25 MEDLINE  
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[PMID]:28195914
[Au] Autor:Roy SG; Tripathi M; Tripathi M; Ramanujam B; Singhal A; Bal C
[Ad] Endereço:From the *Department of Nuclear Medicine and PET/CT, All India Institute of Medical Sciences, New Delhi; and †Department of Neurology, CN Centre, All India Institute of Medical Sciences, New Delhi, India.
[Ti] Título:Ictal PET in Ohtahara Syndrome With Hemimegalencephaly.
[So] Source:Clin Nucl Med;42(5):e263-e264, 2017 May.
[Is] ISSN:1536-0229
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Ohtahara syndrome is one of the causes of infantile epilepsies, which presents with refractory seizures and characteristic EEG changes. It is often associated with structural anomalies in the brain. We report a case of 5-month-old girl with Ohtahara syndrome with hemimegalencephaly who presented with refractory seizures and ictal FDG PET/CT helped in localizing the seizure focus.
[Mh] Termos MeSH primário: Encéfalo/diagnóstico por imagem
Hemimegalencefalia/complicações
Tomografia Computadorizada com Tomografia por Emissão de Pósitrons
Convulsões/diagnóstico por imagem
Espasmos Infantis/complicações
[Mh] Termos MeSH secundário: Eletroencefalografia
Feminino
Seres Humanos
Lactente
Convulsões/etiologia
Espasmos Infantis/diagnóstico por imagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170522
[Lr] Data última revisão:
170522
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170215
[St] Status:MEDLINE
[do] DOI:10.1097/RLU.0000000000001593


  4 / 25 MEDLINE  
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[PMID]:26884417
[Au] Autor:Peterson JL
[Ad] Endereço:Neonatal Department, John Radcliffe Hospital, Oxford OX3 9DU, UK.
[Ti] Título:Hypopigmentation of newborn skin.
[So] Source:BMJ;352:i860, 2016 Feb 16.
[Is] ISSN:1756-1833
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Hemimegalencefalia/diagnóstico
Hipopigmentação/diagnóstico
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Recém-Nascido
Imagem por Ressonância Magnética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1606
[Cu] Atualização por classe:160217
[Lr] Data última revisão:
160217
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:160218
[St] Status:MEDLINE
[do] DOI:10.1136/bmj.i860


  5 / 25 MEDLINE  
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[PMID]:26415548
[Au] Autor:Ono Y; Saito Y; Maegaki Y; Tohyama J; Montassir H; Fujii S; Sugai K; Ohno K
[Ad] Endereço:Division of Child Neurology, Institute of Neurological Sciences, Faculty of Medicine, Tottori University, Yonago, Japan.
[Ti] Título:Three cases of right frontal megalencephaly: Clinical characteristics and long-term outcome.
[So] Source:Brain Dev;38(3):302-9, 2016 Mar.
[Is] ISSN:1872-7131
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIM: To delineate the clinical and neuroimaging characteristics of localized megalencephaly involving the right frontal lobe. METHOD: Data from three patients aged 14-16 years at the last follow-up were retrospectively reviewed. RESULTS: All the patients were normal on neurological examination with no signs of hemiparesis. Enlargement of the right frontal lobe with increased volume of subcortical and deep white matter, as well as thickening of the ipsilateral genu of the corpus callosum was common. The onset of epilepsy was 4-7 years of age, with seizure types of massive myoclonus in two and generalized tonic-clonic in two, which could be eventually controlled by antiepileptics. Interictal electroencephalography showed frontal alpha-like activity in one, and abundant spike-wave complexes resulting in diffuse continuous spike-wave activity during sleep in two patients even after suppression of clinical seizures. Psychomotor development appeared unaffected or slightly delayed before the onset of epilepsy, but became mildly disturbed during follow-up period of 7-11 years. CONCLUSION: Certain patients with right frontal megalencephaly can present with a milder epileptic and intellectual phenotype among those with localized megalencephaly and holohemispheric hemimegalencephaly, whose characteristic as epileptic encephalopathy was assumed from this study.
[Mh] Termos MeSH primário: Lobo Frontal/patologia
Megalencefalia/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Anticonvulsivantes/uso terapêutico
Eletroencefalografia
Epilepsia/tratamento farmacológico
Epilepsia/patologia
Feminino
Lobo Frontal/diagnóstico por imagem
Hemimegalencefalia/diagnóstico
Hemimegalencefalia/diagnóstico por imagem
Hemimegalencefalia/tratamento farmacológico
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Megalencefalia/diagnóstico por imagem
Megalencefalia/tratamento farmacológico
Estudos Retrospectivos
Convulsões/tratamento farmacológico
Convulsões/patologia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anticonvulsants)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150930
[St] Status:MEDLINE


  6 / 25 MEDLINE  
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[PMID]:26481187
[Au] Autor:Oikawa T; Tatewaki Y; Murata T; Kato Y; Mugikura S; Takase K; Takahashi S
[Ad] Endereço:Department of Diagnostic Radiology, Tohoku University Graduate School of Medicine, Japan tomomis1016@gmail.com.
[Ti] Título:Utility of diffusion tensor imaging parameters for diagnosis of hemimegalencephaly.
[So] Source:Neuroradiol J;28(6):628-33, 2015 Dec.
[Is] ISSN:1971-4009
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hemimegalencephaly is a rare hamartomatous entity characterised by enlargement of all or part of the cerebral hemisphere ipsilaterally with cortical dysgenesis, large lateral ventricle and white matter hypertrophy with or without advanced myelination. Although conventional magnetic resonance imaging (MRI) is useful for detecting these diagnostic features, hemimegalencephaly is not always easily distinguished from other entities, especially when hemimegalencephaly shows blurring between the grey and white matter. Diffusion tensor imaging (DTI) is a functional MRI technique commonly used to assess the integrity of white matter. The usefulness of DTI in assessing hemimegalencephaly has not been fully elucidated. In this study, we clarified the characteristics of hemimegalencephaly with regard to DTI and its parameters including fractional anisotropy and apparent diffusion coefficient. METHODS: Three patients with hemimegalencephaly underwent MRI including DTI. We first visually compared fractional anisotropy mapping and conventional MRI. Next, we quantitatively measured the fractional anisotropy and apparent diffusion coefficient values in the subcortical white matter of the hemisphere with hemimegalencephaly and corresponding normal-appearing contralateral regions and analysed the values using the Mann-Whitney U test. RESULTS: On fractional anisotropy mapping, we could clearly distinguish the junction of grey and white matter and observed thicker white matter in the hemisphere with hemimegalencephaly, which was unclear on conventional MRI. The white matter in the hemisphere with hemimegalencephaly showed significantly higher fractional anisotropy (P<0.0001) and lower apparent diffusion coefficient (P=0.0022) values than the normal contralateral side. CONCLUSION: DTI parameters showed salient hemimegalencephaly features and could be useful in its assessment.
[Mh] Termos MeSH primário: Imagem de Tensor de Difusão/métodos
Hemimegalencefalia/diagnóstico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Anisotropia
Mapeamento Encefálico
Feminino
Lateralidade Funcional
Substância Cinzenta/patologia
Seres Humanos
Lactente
Recém-Nascido
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Reprodutibilidade dos Testes
Substância Branca/patologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1602
[Cu] Atualização por classe:161201
[Lr] Data última revisão:
161201
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151021
[St] Status:MEDLINE
[do] DOI:10.1177/1971400915609334


  7 / 25 MEDLINE  
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[PMID]:26231267
[Au] Autor:Cuddapah VA; Thompson M; Blount J; Li R; Guleria S; Goyal M
[Ad] Endereço:University of Alabama at Birmingham, Birmingham, Alabama.
[Ti] Título:Hemispherectomy for Hemimegalencephaly Due to Tuberous Sclerosis and a Review of the Literature.
[So] Source:Pediatr Neurol;53(5):452-5, 2015 Nov.
[Is] ISSN:1873-5150
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Hemimegalencephaly with tuberous sclerosis complex is an uncommon association, usually associated with intractable seizures that begin in the neonatal period or early infancy. Typically, the seizures are managed with medications until the patient is older when surgical treatment is considered safe. PATIENT DESCRIPTION: We describe a 7-week-old infant with tuberous sclerosis (TSC1 mutation) and hemimegalencephaly who underwent a functional hemispherectomy for status epilepticus. No clinical seizures have occurred since surgery nearly 5 years ago and subsequent weaning of antiepileptic drugs 3 years ago. This is one of the youngest patients with tuberous sclerosis complex treated with a hemispherectomy and one of seven patients described in the literature. CONCLUSIONS: Our patient, along with previously reported cases, suggests that a hemispherectomy is a viable option in the very young. With evolution of this surgical process since its inception nearly 6 decades ago, it may now be performed safely in early infancy, engendering the possibility of seizure freedom in most and thus optimizing neurodevelopmental outcome.
[Mh] Termos MeSH primário: Hemimegalencefalia/etiologia
Hemimegalencefalia/cirurgia
Hemisferectomia/métodos
Esclerose Tuberosa/complicações
Esclerose Tuberosa/cirurgia
[Mh] Termos MeSH secundário: Encéfalo/diagnóstico por imagem
Encéfalo/patologia
Encéfalo/cirurgia
Hemimegalencefalia/genética
Hemimegalencefalia/patologia
Seres Humanos
Lactente
Imagem por Ressonância Magnética
Masculino
Tomografia por Emissão de Pósitrons
Estado Epiléptico/etiologia
Estado Epiléptico/genética
Estado Epiléptico/patologia
Estado Epiléptico/cirurgia
Resultado do Tratamento
Esclerose Tuberosa/genética
Esclerose Tuberosa/patologia
Proteínas Supressoras de Tumor/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; REVIEW
[Nm] Nome de substância:
0 (Tumor Suppressor Proteins); 0 (tuberous sclerosis complex 1 protein)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161125
[Lr] Data última revisão:
161125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150802
[St] Status:MEDLINE


  8 / 25 MEDLINE  
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[PMID]:26078402
[Au] Autor:Kishima H; Nakamura H; Oshino S; Tanaka H; Yoshimine T
[Ad] Endereço:From the Departments of Neurosurgery (H.K., H.N., S.O., T.Y.) and Radiology (H.T.), Osaka University Graduate School of Medicine, Epilepsy Center, Osaka University Hospital, Japan. hkishima@nsurg.med.osaka-u.ac.jp.
[Ti] Título:Adult hemimegalencephaly associated with multiple cerebral aneurysms.
[So] Source:Neurology;84(24):2460-1, 2015 Jun 16.
[Is] ISSN:1526-632X
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Hemimegalencefalia/complicações
Hemimegalencefalia/patologia
Aneurisma Intracraniano/complicações
Aneurisma Intracraniano/patologia
[Mh] Termos MeSH secundário: Encéfalo/irrigação sanguínea
Encéfalo/patologia
Artéria Carótida Interna/patologia
Angiografia Cerebral
Feminino
Seres Humanos
Imagem por Ressonância Magnética
Meia-Idade
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Em] Mês de entrada:1508
[Cu] Atualização por classe:150616
[Lr] Data última revisão:
150616
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150617
[St] Status:MEDLINE
[do] DOI:10.1212/WNL.0000000000001685


  9 / 25 MEDLINE  
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[PMID]:26013804
[Au] Autor:Crino PB
[Ad] Endereço:Shriners Hospitals Paediatric Research Centre, Department of Neurology, Temple University School of Medicine, Philadelphia, USA peter.crino@temple.edu.
[Ti] Título:The enlarging spectrum of focal cortical dysplasias.
[So] Source:Brain;138(Pt 6):1446-8, 2015 Jun.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Encéfalo/anormalidades
Hemimegalencefalia/genética
Malformações do Desenvolvimento Cortical/genética
Megalencefalia/genética
Fosfatidilinositol 3-Quinases/genética
Proteínas Proto-Oncogênicas c-akt/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:160601
[Lr] Data última revisão:
160601
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150528
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awv098


  10 / 25 MEDLINE  
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[PMID]:25722288
[Au] Autor:Jansen LA; Mirzaa GM; Ishak GE; O'Roak BJ; Hiatt JB; Roden WH; Gunter SA; Christian SL; Collins S; Adams C; Rivière JB; St-Onge J; Ojemann JG; Shendure J; Hevner RF; Dobyns WB
[Ad] Endereço:1 University of Virginia, Neurology, Charlottesville, VA, USA 2 Seattle Children's Research Institute, Centre for Integrative Brain Research, Seattle, WA, USA laura.jansen@virginia.edu.
[Ti] Título:PI3K/AKT pathway mutations cause a spectrum of brain malformations from megalencephaly to focal cortical dysplasia.
[So] Source:Brain;138(Pt 6):1613-28, 2015 Jun.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Malformations of cortical development containing dysplastic neuronal and glial elements, including hemimegalencephaly and focal cortical dysplasia, are common causes of intractable paediatric epilepsy. In this study we performed multiplex targeted sequencing of 10 genes in the PI3K/AKT pathway on brain tissue from 33 children who underwent surgical resection of dysplastic cortex for the treatment of intractable epilepsy. Sequencing results were correlated with clinical, imaging, pathological and immunohistological phenotypes. We identified mosaic activating mutations in PIK3CA and AKT3 in this cohort, including cancer-associated hotspot PIK3CA mutations in dysplastic megalencephaly, hemimegalencephaly, and focal cortical dysplasia type IIa. In addition, a germline PTEN mutation was identified in a male with hemimegalencephaly but no peripheral manifestations of the PTEN hamartoma tumour syndrome. A spectrum of clinical, imaging and pathological abnormalities was found in this cohort. While patients with more severe brain imaging abnormalities and systemic manifestations were more likely to have detected mutations, routine histopathological studies did not predict mutation status. In addition, elevated levels of phosphorylated S6 ribosomal protein were identified in both neurons and astrocytes of all hemimegalencephaly and focal cortical dysplasia type II specimens, regardless of the presence or absence of detected PI3K/AKT pathway mutations. In contrast, expression patterns of the T308 and S473 phosphorylated forms of AKT and in vitro AKT kinase activities discriminated between mutation-positive dysplasia cortex, mutation-negative dysplasia cortex, and non-dysplasia epilepsy cortex. Our findings identify PI3K/AKT pathway mutations as an important cause of epileptogenic brain malformations and establish megalencephaly, hemimegalencephaly, and focal cortical dysplasia as part of a single pathogenic spectrum.
[Mh] Termos MeSH primário: Encéfalo/anormalidades
Hemimegalencefalia/genética
Malformações do Desenvolvimento Cortical/genética
Megalencefalia/genética
Fosfatidilinositol 3-Quinases/genética
Proteínas Proto-Oncogênicas c-akt/genética
Transdução de Sinais/genética
[Mh] Termos MeSH secundário: Adolescente
Encéfalo/metabolismo
Criança
Pré-Escolar
Classe I de Fosfatidilinositol 3-Quinases
Feminino
Predisposição Genética para Doença/genética
Hemimegalencefalia/metabolismo
Hemimegalencefalia/patologia
Seres Humanos
Lactente
Recém-Nascido
Imagem por Ressonância Magnética
Masculino
Malformações do Desenvolvimento Cortical/metabolismo
Malformações do Desenvolvimento Cortical/patologia
Megalencefalia/metabolismo
Megalencefalia/patologia
Mutação
Neuroimagem
PTEN Fosfo-Hidrolase/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Proteínas Quinases S6 Ribossômicas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (Class I Phosphatidylinositol 3-Kinases); EC 2.7.1.137 (PIK3CA protein, human); EC 2.7.11.1 (AKT3 protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 2.7.11.1 (Ribosomal Protein S6 Kinases); EC 3.1.3.67 (PTEN Phosphohydrolase); EC 3.1.3.67 (PTEN protein, human)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:150228
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awv045



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