Base de dados : MEDLINE
Pesquisa : D05.500.562.452.200 [Categoria DeCS]
Referências encontradas : 214 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 22 ir para página                         

  1 / 214 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
[PMID]:28302194
[Au] Autor:Gao ZJ; Jiang Q; Chen Q; Xu KM
[Ad] Endereço:Department of Neurology, Affiliated Children's Hospital of Capital Institute of Pediatrics, Beijing 100020, China. chenqianxhl@163.com.
[Ti] Título:[Clinical and molecular genetic study of nonketotic hyperglycinemia in a Chinese family].
[So] Source:Zhongguo Dang Dai Er Ke Za Zhi;19(3):268-271, 2017 Mar.
[Is] ISSN:1008-8830
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Nonketotic hyperglycinemia (NKH) is a rare, inborn error of metabolism. In this case report, a Chinese male infant was diagnosed with NKH caused by GLDC gene mutation. The clinical characteristics and genetic diagnosis were reported. The infant presented with an onset of early metabolic encephalopathy and Ohtahara syndrome. Both blood and urinary levels of metabolites were in the normal range. Brain MRI images indicated a poor development of corpus callosum, and a burst suppression pattern was found in the EEG. Results of target gene sequencing technology combined with multiplex ligation-dependent probe amplification (MLPA) indicated a heterozygous missense mutation of c.1786 C>T (p.R596X) in maternal exon 15 and a loss of heterozygosity of 4-15 exon gross deletions in paternal GLDC gene. These definite pathogenic mutations confirmed the diagnosis of NKH. The infant's clinical condition was not improved after treatment with adreno-cortico-tropic-hormone, topiramate and dextromethorphan, and he finally died at 4 months of age. Patients with NKH often exhibit complicated clinical phenotypes and are lack of specific symptoms. NKH could be diagnosed by metabolic screening and molecular genetic analysis.
[Mh] Termos MeSH primário: Hiperglicinemia não Cetótica/genética
[Mh] Termos MeSH secundário: Glicina Desidrogenase (Descarboxilante)/genética
Seres Humanos
Hiperglicinemia não Cetótica/diagnóstico
Recém-Nascido
Masculino
Mutação
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating))
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170318
[St] Status:MEDLINE


  2 / 214 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28062918
[Au] Autor:Berezowska S; Galván JA; Langer R; Bubendorf L; Savic S; Gugger M; Schmid RA; Marti TM
[Ad] Endereço:Institute of Pathology, University of Bern, Bern, Switzerland.
[Ti] Título:Glycine decarboxylase and HIF-1α expression are negative prognostic factors in primary resected early-stage non-small cell lung cancer.
[So] Source:Virchows Arch;470(3):323-330, 2017 Mar.
[Is] ISSN:1432-2307
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Glycine decarboxylase (GLDC) was recently described as a critical enzyme of tumor-initiating cells and, thus, a driver of tumorigenesis in lung non-small cell cancer (NSCC). It is important in metabolism under hypoxic conditions. Hypoxia-inducible factor 1-alpha (HIF-1α) is the unique subunit that determines HIF system activity, thereby regulating the adverse effects of hypoxia on cancer outcome. We examined the expression and prognostic significance of GLDC and HIF-1α in primary resected stage I/II NSCC. Immunohistochemistry for GLDC and HIF-1α was validated on two lung NSCC cell lines (A549, NCI-H460) and evaluated on a tissue microarray with 428 lung NSCC: 184 adenocarcinomas, 211 squamous cell carcinomas, and 33 large cell carcinomas (LCC). The results were correlated with clinico-pathological parameters. High levels of GLDC expression were detected in 33/428 cases (7.7%). HIF-1α was expressed in 71 (16.6%) cases and more frequently in squamous cell carcinoma (p < 0.001). Significantly longer survival was seen in younger patients (p = 0.007), patients with non-LCC histology (p = 0.006), lower primary tumor category (p = 0.002), and Union for International Cancer Control (UICC) stage (p = 0.001). Both GLDC and HIF-1α were significantly associated with worse tumor-related survival (p = 0.013, p = 0.021, respectively), although not independent from each other in multivariate models. The combination of low-GLDC/negative HIF-1α expression was significantly prognostic for longer survival (p = 0.002) and emerged as an independent prognostic factor in multivariate analysis (p = 0.007, HR 2.052), next to UICC stage and age. We show that the combination of GLDC and HIF-1α expression is an independent prognostic factor in early-stage NSCC. Our results will assist future development of therapeutic approaches targeting GLDC or exploiting tumor hypoxia.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/análise
Carcinoma Pulmonar de Células não Pequenas/patologia
Glicina Desidrogenase (Descarboxilante)/biossíntese
Subunidade alfa do Fator 1 Induzível por Hipóxia/biossíntese
Neoplasias Pulmonares/patologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Carcinoma Pulmonar de Células não Pequenas/metabolismo
Carcinoma Pulmonar de Células não Pequenas/mortalidade
Intervalo Livre de Doença
Feminino
Glicina Desidrogenase (Descarboxilante)/análise
Seres Humanos
Subunidade alfa do Fator 1 Induzível por Hipóxia/análise
Imuno-Histoquímica
Estimativa de Kaplan-Meier
Neoplasias Pulmonares/metabolismo
Neoplasias Pulmonares/mortalidade
Masculino
Meia-Idade
Prognóstico
Modelos de Riscos Proporcionais
Análise Serial de Tecidos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (HIF1A protein, human); 0 (Hypoxia-Inducible Factor 1, alpha Subunit); EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating))
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170108
[St] Status:MEDLINE
[do] DOI:10.1007/s00428-016-2057-z


  3 / 214 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28056489
[Au] Autor:Autuori MC; Pai YJ; Stuckey DJ; Savery D; Marconi AM; Massa V; Lythgoe MF; Copp AJ; David AL; Greene ND
[Ad] Endereço:Newlife Birth Defects Research Centre and Developmental Biology and Cancer Programme, Great Ormond Street Institute of Child Health, University College London, London, UK.
[Ti] Título:Use of high-frequency ultrasound to study the prenatal development of cranial neural tube defects and hydrocephalus in Gldc-deficient mice.
[So] Source:Prenat Diagn;37(3):273-281, 2017 Mar.
[Is] ISSN:1097-0223
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: We used non-invasive high-frequency ultrasound (HFUS) imaging to investigate embryonic brain development in a mouse model for neural tube defects (NTDs) and non-ketotic hyperglycinemia (NKH). METHOD: Using HFUS, we imaged embryos carrying loss of function alleles of Gldc encoding glycine decarboxylase, a component of the glycine cleavage system in mitochondrial folate metabolism, which is known to be associated with cranial NTDs and NKH in humans. We serially examined the same litter during the second half of embryonic development and quantified cerebral structures. Genotype was confirmed using PCR. Histology was used to confirm ultrasound findings. RESULTS: High-frequency ultrasound allowed in utero detection of two major brain abnormalities in Gldc-deficient mouse embryos, cranial NTDs (exencephaly) and ventriculomegaly (corresponding with the previous finding of post-natal hydrocephalus). Serial ultrasound allowed individual embryos to be analysed at successive gestational time points. From embryonic day 16.5 to 18.5, the lateral ventricle volume reduced in wild-type and heterozygous embryos but increased in homozygous Gldc-deficient embryos. CONCLUSION: Exencephaly and ventriculomegaly were detectable by HFUS in homozygous Gldc-deficient mouse embryos indicating this to be an effective tool to study CNS development. Longitudinal analysis of the same embryo allowed the prenatal onset and progression of ventricle enlargement in Gldc-deficient mice to be determined. © 2017 The Authors. Prenatal Diagnosis published by John Wiley & Sons, Ltd.
[Mh] Termos MeSH primário: Glicina Desidrogenase (Descarboxilante)/genética
Hidrocefalia/diagnóstico
Defeitos do Tubo Neural/diagnóstico
Ultrassonografia Pré-Natal
[Mh] Termos MeSH secundário: Animais
Sistema Nervoso Central/diagnóstico por imagem
Sistema Nervoso Central/embriologia
Embrião de Mamíferos
Feminino
Hidrocefalia/embriologia
Hidrocefalia/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Defeitos do Tubo Neural/embriologia
Defeitos do Tubo Neural/genética
Gravidez
Crânio/diagnóstico por imagem
Crânio/embriologia
Ultrassonografia Pré-Natal/métodos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170106
[St] Status:MEDLINE
[do] DOI:10.1002/pd.5004


  4 / 214 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:27073202
[Au] Autor:Khoshravesh R; Stinson CR; Stata M; Busch FA; Sage RF; Ludwig M; Sage TL
[Ad] Endereço:Department of Ecology and Evolutionary Biology, University of Toronto, 25 Willcocks St., Ontario, ON M5S 3B2, Canada.
[Ti] Título:C3-C4 intermediacy in grasses: organelle enrichment and distribution, glycine decarboxylase expression, and the rise of C2 photosynthesis.
[So] Source:J Exp Bot;67(10):3065-78, 2016 May.
[Is] ISSN:1460-2431
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Photorespiratory glycine shuttling and decarboxylation in bundle sheath (BS) cells exhibited by C2 species is proposed to be the evolutionary bridge to C4 photosynthesis in eudicots. To evaluate this in grasses, we compare anatomy, cellular localization of glycine decarboxylase (GDC), and photosynthetic physiology of a suspected C2 grass, Homolepis aturensis, with these traits in known C2 grasses, Neurachne minor and Steinchisma hians, and C3 S laxum that is sister to S hians We also use publicly available genome and RNA-sequencing data to examine the evolution of GDC subunits and enhance our understanding of the evolution of BS-specific GDC expression in C2 and C4 grasses. Our results confirm the identity of H aturensis as a C2 species; GDC is confined predominantly to the organelle-enriched BS cells in H aturensis and S hians and to mestome sheath cells of N minor Phylogenetic analyses and data obtained from immunodetection of the P-subunit of GDC are consistent with the hypothesis that the BS dominant levels of GDC in C2 and C4 species are due to changes in expression of a single GLDP gene in M and BS cells. All BS mitochondria and peroxisomes and most chloroplasts in H aturensis and S hians are situated centripetally in a pattern identical to C2 eudicots. In S laxum, which has C3-like gas exchange patterns, mitochondria and peroxisomes are positioned centripetally as they are in S hians This subcellular phenotype, also present in eudicots, is posited to initiate a facilitation cascade leading to C2 and C4 photosynthesis.
[Mh] Termos MeSH primário: Glicina Desidrogenase (Descarboxilante)/metabolismo
Fotossíntese/fisiologia
Poaceae/fisiologia
[Mh] Termos MeSH secundário: Evolução Biológica
Genes de Plantas/genética
Genes de Plantas/fisiologia
Glicina Desidrogenase (Descarboxilante)/genética
Filogenia
Folhas de Planta/anatomia & histologia
Folhas de Planta/citologia
Folhas de Planta/fisiologia
Poaceae/citologia
Poaceae/enzimologia
Poaceae/metabolismo
Ribulose-Bifosfato Carboxilase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating)); EC 4.1.1.39 (Ribulose-Bisphosphate Carboxylase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170901
[Lr] Data última revisão:
170901
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160414
[St] Status:MEDLINE
[do] DOI:10.1093/jxb/erw150


  5 / 214 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27038285
[Au] Autor:Schulze S; Westhoff P; Gowik U
[Ad] Endereço:Institute of Plant Molecular and Developmental Biology, Heinrich-Heine-University, Universitaetsstrasse 1, 40225 Duesseldorf, Germany.
[Ti] Título:Glycine decarboxylase in C3, C4 and C3-C4 intermediate species.
[So] Source:Curr Opin Plant Biol;31:29-35, 2016 Jun.
[Is] ISSN:1879-0356
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The glycine decarboxylase complex (GDC) plays a central role in photorespiration. GDC is localized in the mitochondria and together with serine hydroxymethyltransferase it converts two molecules of glycine to one molecule of serine, CO2 and NH3. Overexpression of GDC subunits in the C3 species Arabidopsis thaliana can increase the metabolic flux through the photorespiratory pathway leading to enhanced photosynthetic efficiency and consequently to an enhanced biomass production of the transgenic plants. Changing the spatial expression patterns of GDC subunits was an important step during the evolution of C3-C4 intermediate and likely also C4 plants. Restriction of the GDC activity to the bundle sheath cells led to the establishment of a photorespiratory CO2 pump.
[Mh] Termos MeSH primário: Glicina Desidrogenase (Descarboxilante)/metabolismo
[Mh] Termos MeSH secundário: Arabidopsis/enzimologia
Arabidopsis/genética
Arabidopsis/metabolismo
Proteínas de Arabidopsis/genética
Proteínas de Arabidopsis/metabolismo
Glicina Desidrogenase (Descarboxilante)/genética
Glicina Hidroximetiltransferase/genética
Glicina Hidroximetiltransferase/metabolismo
Fotossíntese/genética
Fotossíntese/fisiologia
Plantas Geneticamente Modificadas/enzimologia
Plantas Geneticamente Modificadas/genética
Plantas Geneticamente Modificadas/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Arabidopsis Proteins); EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating)); EC 2.1.2.1 (Glycine Hydroxymethyltransferase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:170519
[Lr] Data última revisão:
170519
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160403
[St] Status:MEDLINE


  6 / 214 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26947380
[Au] Autor:Chiu CF; Lin JL; Lin JJ; Tseng MH; Lo FS; Chiang MC
[Ad] Endereço:Department of Pediatrics, Chang Gang Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
[Ti] Título:Nonketotic Hyperglycinemia of Infants in Taiwan.
[So] Source:Pediatr Neonatol;57(5):420-426, 2016 Oct.
[Is] ISSN:2212-1692
[Cp] País de publicação:Singapore
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Nonketotic hyperglycinemia (NKH) is a rare, inherited disease, with very poor outcome. It is difficult to confirm the diagnosis due to nonspecific presentations and rapid progression. The incidence was reported in a few countries. We report the clinical and genetic features of typical neonatal NKH with novel splicing mutation, c.1058+3A>C, in the intron 7 of the glycine decarboxylase (GLDC) gene. Furthermore, this study aimed to delineate the estimated incidence and clinical characteristics of NKH in the Taiwanese population. METHODS: Reports of Health Promotion Administration, Ministry of Health and Welfare of Taiwan, during the period from 2000 to 2013; the Human Gene Mutation Database; and literature regarding NKH in Taiwan were reviewed. Demographic information, age of onset, clinical characteristics, genetic analysis, electroencephalography examinations, and outcome of the patients were analyzed. RESULTS: The estimated incidence of NKH in the Taiwanese population was 7.2 cases per 1,000,000 live births. Among the 12 cases reported in Taiwan, more than 90% were of neonatal type. Fifty-five percent of affected patients died within 5 years, and all survivors had severe neurologic outcomes. Only three infants underwent genetic analysis during the study period. Two neonatal NKH infants had mutation in the GLDC gene, and the other one, who had late-onset NKH, had mutation in the glutaredoxin 5 gene. CONCLUSION: Compared with other countries, the estimated incidence of NKH was relatively rare in the Taiwanese population. It is important to characterize all index cases at the genetic level. With more awareness of NKH, increased knowledge of gene mutation, and improvement of diagnostic tools, NKH can be diagnosed more accurately.
[Mh] Termos MeSH primário: Hiperglicinemia não Cetótica/epidemiologia
[Mh] Termos MeSH secundário: Eletroencefalografia
Feminino
Testes Genéticos
Glicina Desidrogenase (Descarboxilante)/genética
Seres Humanos
Hiperglicinemia não Cetótica/diagnóstico
Hiperglicinemia não Cetótica/genética
Incidência
Lactente
Recém-Nascido
Masculino
Mutação
Taiwan/epidemiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating))
[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:160308
[St] Status:MEDLINE


  7 / 214 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26599272
[Au] Autor:Li X; Cui C; Guo Y; Yang G
[Ad] Endereço:Department of Clinical Laboratory Science, Shandong University Affiliated Qianfoshan Hospital, Jinan, China.
[Ti] Título:Glycine Decarboxylase Expression Increased in p53-Mutated B Cell Lymphoma Mice.
[So] Source:Oncol Res Treat;38(11):586-9, 2015.
[Is] ISSN:2296-5262
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: p53 gene mutations are associated with human tumors, and are among the most common genetic abnormalities. To understand the relationship between p53 mutations and glycine decarboxylase (GLDC) expression in B cell lymphoma, we established B cell lymphoma animal models to study GLDC expression in B cell lymphoma mice. MATERIALS AND METHODS: Based on immunohistochemical staining results, BALB/c nude mice were divided into a p53 protein-positive group and a p53 protein-negative group. GLDC mRNA expression was determined by real-time polymerase chain reaction, and GLDC protein expression was determined by Western blot. We designed a GLDC-specific interference fragment siRNA-transfected human B cell lymphoma cell line (Raji) to establish a B cell lymphoma animal model. RESULTS: The results showed both GLDC mRNA and protein expression increased in the B cell lymphoma tissue of the p53 protein-positive group compared with the p53 protein-negative group. The proliferation ability of GLDC siRNA-transfected cells decreased significantly compared with the negative-control siRNA group and the blank control group (p < 0.05), which showed that the GLDC gene can promote cell proliferation in p53-mutated B cell lymphoma. CONCLUSION: These studies support a direct relationship between p53 mutations and GLDC expression in B cell lymphoma. GLDC can induce dramatic changes in glycolysis and glycine/serine metabolism, leading to changes in pyrimidine metabolism and tumor development.
[Mh] Termos MeSH primário: Glicina Desidrogenase (Descarboxilante)/metabolismo
Linfoma de Células B/enzimologia
Linfoma de Células B/genética
Proteína Supressora de Tumor p53/genética
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Regulação Enzimológica da Expressão Gênica
Regulação Neoplásica da Expressão Gênica
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Nus
Mutação/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Tumor Suppressor Protein p53); EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating))
[Em] Mês de entrada:1609
[Cu] Atualização por classe:151125
[Lr] Data última revisão:
151125
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151125
[St] Status:MEDLINE
[do] DOI:10.1159/000441595


  8 / 214 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25855294
[Au] Autor:Kim D; Fiske BP; Birsoy K; Freinkman E; Kami K; Possemato RL; Chudnovsky Y; Pacold ME; Chen WW; Cantor JR; Shelton LM; Gui DY; Kwon M; Ramkissoon SH; Ligon KL; Kang SW; Snuderl M; Vander Heiden MG; Sabatini DM
[Ad] Endereço:1] Whitehead Institute for Biomedical Research, Nine Cambridge Center, Cambridge, Massachusetts 02142, USA [2] Howard Hughes Medical Institute and Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, USA [3] The David H. Koch Institute for Integrative Cancer
[Ti] Título:SHMT2 drives glioma cell survival in ischaemia but imposes a dependence on glycine clearance.
[So] Source:Nature;520(7547):363-7, 2015 Apr 16.
[Is] ISSN:1476-4687
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Cancer cells adapt their metabolic processes to support rapid proliferation, but less is known about how cancer cells alter metabolism to promote cell survival in a poorly vascularized tumour microenvironment. Here we identify a key role for serine and glycine metabolism in the survival of brain cancer cells within the ischaemic zones of gliomas. In human glioblastoma multiforme, mitochondrial serine hydroxymethyltransferase (SHMT2) and glycine decarboxylase (GLDC) are highly expressed in the pseudopalisading cells that surround necrotic foci. We find that SHMT2 activity limits that of pyruvate kinase (PKM2) and reduces oxygen consumption, eliciting a metabolic state that confers a profound survival advantage to cells in poorly vascularized tumour regions. GLDC inhibition impairs cells with high SHMT2 levels as the excess glycine not metabolized by GLDC can be converted to the toxic molecules aminoacetone and methylglyoxal. Thus, SHMT2 is required for cancer cells to adapt to the tumour environment, but also renders these cells sensitive to glycine cleavage system inhibition.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/metabolismo
Neoplasias Encefálicas/patologia
Glioblastoma/metabolismo
Glioblastoma/patologia
Glicina Hidroximetiltransferase/metabolismo
Glicina/metabolismo
Isquemia/metabolismo
[Mh] Termos MeSH secundário: Acetona/análogos & derivados
Acetona/metabolismo
Acetona/toxicidade
Animais
Neoplasias Encefálicas/irrigação sanguínea
Neoplasias Encefálicas/enzimologia
Hipóxia Celular
Linhagem Celular Tumoral
Sobrevivência Celular
Feminino
Glioblastoma/irrigação sanguínea
Glioblastoma/enzimologia
Glicina Desidrogenase (Descarboxilante)/antagonistas & inibidores
Glicina Desidrogenase (Descarboxilante)/metabolismo
Seres Humanos
Isquemia/enzimologia
Isquemia/patologia
Camundongos
Necrose
Consumo de Oxigênio
Aldeído Pirúvico/metabolismo
Aldeído Pirúvico/toxicidade
Piruvato Quinase/metabolismo
Microambiente Tumoral
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
1364PS73AF (Acetone); 722KLD7415 (Pyruvaldehyde); EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating)); EC 2.1.2.1 (Glycine Hydroxymethyltransferase); EC 2.7.1.40 (Pyruvate Kinase); TE7660XO1C (Glycine); ZB4ES38S4R (aminoacetone)
[Em] Mês de entrada:1509
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150410
[St] Status:MEDLINE
[do] DOI:10.1038/nature14363


  9 / 214 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:25736695
[Au] Autor:Pai YJ; Leung KY; Savery D; Hutchin T; Prunty H; Heales S; Brosnan ME; Brosnan JT; Copp AJ; Greene ND
[Ad] Endereço:Birth Defects Research Centre and Developmental Biology &Cancer Programme, Institute of Child Health, University College London, London WC1N 1EH, UK.
[Ti] Título:Glycine decarboxylase deficiency causes neural tube defects and features of non-ketotic hyperglycinemia in mice.
[So] Source:Nat Commun;6:6388, 2015 Mar 04.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glycine decarboxylase (GLDC) acts in the glycine cleavage system to decarboxylate glycine and transfer a one-carbon unit into folate one-carbon metabolism. GLDC mutations cause a rare recessive disease non-ketotic hyperglycinemia (NKH). Mutations have also been identified in patients with neural tube defects (NTDs); however, the relationship between NKH and NTDs is unclear. We show that reduced expression of Gldc in mice suppresses glycine cleavage system activity and causes two distinct disease phenotypes. Mutant embryos develop partially penetrant NTDs while surviving mice exhibit post-natal features of NKH including glycine accumulation, early lethality and hydrocephalus. In addition to elevated glycine, Gldc disruption also results in abnormal tissue folate profiles, with depletion of one-carbon-carrying folates, as well as growth retardation and reduced cellular proliferation. Formate treatment normalizes the folate profile, restores embryonic growth and prevents NTDs, suggesting that Gldc deficiency causes NTDs through limiting supply of one-carbon units from mitochondrial folate metabolism.
[Mh] Termos MeSH primário: Glicina Desidrogenase (Descarboxilante)/deficiência
Hiperglicinemia não Cetótica/enzimologia
Hiperglicinemia não Cetótica/etiologia
Defeitos do Tubo Neural/enzimologia
Defeitos do Tubo Neural/etiologia
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Primers do DNA/genética
Ácido Fólico/metabolismo
Formiatos/farmacologia
Galactosídeos
Cromatografia Gasosa-Espectrometria de Massas
Genótipo
Glicina/metabolismo
Imuno-Histoquímica
Hibridização In Situ
Indóis
Camundongos
Dados de Sequência Molecular
Defeitos do Tubo Neural/prevenção & controle
Reação em Cadeia da Polimerase em Tempo Real
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA Primers); 0 (Formates); 0 (Galactosides); 0 (Indoles); 0YIW783RG1 (formic acid); 935E97BOY8 (Folic Acid); EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating)); TE7660XO1C (Glycine); V595OG374W (5-bromo-4-chloro-3-indolyl beta-galactoside)
[Em] Mês de entrada:1602
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150305
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms7388


  10 / 214 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25227996
[Au] Autor:Wen Z; Zhang M
[Ad] Endereço:Key Laboratory of Biogeography and Bioresource in Arid Land, Xinjiang Institute of Ecology and Geography, Chinese Academy of Sciences, No. 818 South Beijing Road, Ürumqi, 830011, Xinjiang, People's Republic of China, zhibinwen158@gmail.com.
[Ti] Título:Salsola laricifolia, another C3-C 4 intermediate species in tribe Salsoleae s.l. (Chenopodiaceae).
[So] Source:Photosynth Res;123(1):33-43, 2015 Jan.
[Is] ISSN:1573-5079
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:This study identifies Salsola laricifolia as a C3-C4 intermediate in tribe Salsoleae s.l., Chenopodiaceae, and compares S. laricifolia with the previously described C3-C4 intermediates in Salsoleae. Photosynthetic pathway characteristics were studied in four species of this tribe including S. laricifolia, C3 Sympegma regelii, C3-C4 S. arbusculiformis, and C4 S. arbuscula, using the approaches of leaf anatomy and ultrastructure, activities of ribulose 1-5-bisphosphate carboxylase/oxygenase (Rubisco) and PEP carboxylase (PEPC), CO2 compensation point, and immunolocalization of Rubisco, PEPC, and the P-subunit of glycine decarboxylase (GDC). Salsola laricifolia has intermediate features, with near continuous and distinctive Kranz-like cells (KLCs) compared with the C3-Sympegmoid anatomical type and the C3-C4 intermediate S. arbusculiformis, a relatively low CO2 compensation point (30.4 µmol mol(-1)) and mesophyll (M)-to KLC tissue ratio, mitochondria in KLCs primarily occurring along the centripetal wall, and specific localization of P-protein GDC in the KLCs. The C3-type isotope value (-22.4 ‰), the absence of the clear labeling for PEPC in M cells, and the low activity of the PEPC enzyme (61.5 µmol mg(-1 )chlorophyll(-1) h(-1)) support the identification of S. laricifolia as a type I C3-C4 intermediate. Although these C3-C4 intermediate species have different structural features, one with discontinuous KL cells and the other with continuous, they have similar characteristics in physiology and biochemistry.
[Mh] Termos MeSH primário: Carbono/metabolismo
Fotossíntese/fisiologia
Salsola/classificação
Salsola/fisiologia
[Mh] Termos MeSH secundário: Dióxido de Carbono
Isótopos de Carbono
Glicina Desidrogenase (Descarboxilante)/metabolismo
Folhas de Planta
Transporte Proteico
Proteínas Serina-Treonina Quinases/metabolismo
Ribulose-Bifosfato Carboxilase/metabolismo
Especificidade da Espécie
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Carbon Isotopes); 142M471B3J (Carbon Dioxide); 7440-44-0 (Carbon); EC 1.4.4.2 (Glycine Dehydrogenase (Decarboxylating)); EC 2.7.1.- (phosphoenolpyruvate carboxylase kinase); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 4.1.1.39 (Ribulose-Bisphosphate Carboxylase)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140918
[St] Status:MEDLINE
[do] DOI:10.1007/s11120-014-0037-1



página 1 de 22 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde