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Pesquisa : D08.811.913.477.700.500 [Categoria DeCS]
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[PMID]:28423621
[Au] Autor:Gao W; Li ZH; Chen S; Chan JY; Yin M; Zhang MJ; Wong TS
[Ad] Endereço:Department of Surgery, The University of Hong Kong, Hong Kong SAR.
[Ti] Título:Epstein-Barr virus encoded microRNA BART7 regulates radiation sensitivity of nasopharyngeal carcinoma.
[So] Source:Oncotarget;8(12):20297-20308, 2017 Mar 21.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epstein-Barr virus (EBV)-associated nasopharyngeal carcinoma (NPC) is very sensitive to radiotherapy. To date, the underlying mechanism remains poorly understood. Here, we demonstrated that expression of EBV-encoded microRNA BART7 (ebv-miR-BART7) increases responsiveness of NPC to radiation treatment by targeting GFPT1/TGFß1 signaling. GFPT1 is the the key rate-limiting enzyme of the hexosamine signaling pathway and governs TGFß1 production. TGFß1, a pleotropic cytokine with the potency to trigger self-renewal and damage-repair machinery in somatic cells. TGFß1 can protect zebrafish embryo from the lethal effects of radiation treatment. In silico analysis showed that ebv-miR-BART7 could target GFPT1 transcript. Correlation analysis on primary NPC tissues suggested that ebv-miR-BART7 and GFPT1 have negative expression correlation. Expression of GFPT1 and TGFß1 were inducible by radiation in NPC cell with ebv-miR-BART7 expression. Further, suppressing endogenous GFPT1 expression inhibited TGFß1 which subsequently increased the responsiveness of NPC to radiation treatment. Taken together, our results demonstrated that ebv-miR-BART7 controls TGFß1 production by targeting GFPT1. Detection of ebv-miR-BART7 may provide useful indicator for monitoring NPC progression and predict therapeutic outcomes.
[Mh] Termos MeSH primário: Carcinoma/virologia
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/metabolismo
MicroRNAs/metabolismo
Neoplasias Nasofaríngeas/virologia
Tolerância a Radiação/genética
Fator de Crescimento Transformador beta1/biossíntese
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Animais
Western Blotting
Carcinoma/metabolismo
Criança
Infecções por Vírus Epstein-Barr/complicações
Infecções por Vírus Epstein-Barr/genética
Feminino
Herpesvirus Humano 4/genética
Seres Humanos
Imuno-Histoquímica
Masculino
MicroRNAs/genética
Meia-Idade
Neoplasias Nasofaríngeas/metabolismo
Análise de Sequência com Séries de Oligonucleotídeos
RNA Viral/genética
RNA Viral/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Adulto Jovem
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MicroRNAs); 0 (RNA, Viral); 0 (TGFB1 protein, human); 0 (Transforming Growth Factor beta1); EC 2.6.1.16 (GFPT1 protein, human); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing))
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170421
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15526


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[PMID]:28186970
[Au] Autor:Li L; Shao M; Peng P; Yang C; Song S; Duan F; Jia D; Zhang M; Zhao J; Zhao R; Wu W; Wang L; Li C; Wu H; Zhang J; Wu X; Ruan Y; Gu J
[Ad] Endereço:Key Laboratory of Glycoconjugate Research Ministry of Public Health, School of Basic Medical Sciences, Fudan University, Shanghai, P.R.China.
[Ti] Título:High expression of GFAT1 predicts unfavorable prognosis in patients with hepatocellular carcinoma.
[So] Source:Oncotarget;8(12):19205-19217, 2017 Mar 21.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. As a branch of glucose metabolism, hexosamine biosynthesis pathway (HBP) has been reported to play a critical role in the insulin resistance and progression of cancer. Glutamine:fructose-6-phosphate amidotransferase (GFAT) is the rate-limiting enzyme of the HBP; nevertheless, the prognostic value of GFAT1 in HCC remains elusive. In this study, we found that high expression of GFAT1 was significantly associated with serum alpha-fetoprotein (AFP), serum alanine aminotransferase (ALT), tumor size, tumor encapsulation, T stage and TNM stage. High GFAT1 expression was identified as an independent prognostic factor which predicted poor overall survival (OS) and recurrence-free survival (RFS) in HCC patients. Incorporation of GFAT1 expression could improve the prognostic accuracy of traditional TNM stage system. Integration of GFAT1 expression with other independent prognosticators generated a predictive nomogram, which showed better prognostic efficiency for OS and RFS in HCC patients. In vitro studies also revealed that GFAT1 promoted the proliferation, cell cycle progression, migration and invasion of HCC cells. In conclusion, GFAT1 is a potential prognostic biomarker for overall survival and recurrence-free survival of HCC patients after surgery.
[Mh] Termos MeSH primário: Biomarcadores Tumorais/metabolismo
Carcinoma Hepatocelular/enzimologia
Proliferação Celular
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/metabolismo
Neoplasias Hepáticas/enzimologia
Neoplasias Hepáticas/patologia
[Mh] Termos MeSH secundário: Apoptose
Biomarcadores Tumorais/genética
Carcinoma Hepatocelular/genética
Feminino
Seguimentos
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/genética
Seres Humanos
Neoplasias Hepáticas/genética
Masculino
Meia-Idade
Estadiamento de Neoplasias
Prognóstico
Taxa de Sobrevida
Células Tumorais Cultivadas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing))
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170211
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.15164


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[PMID]:28008135
[Au] Autor:Zibrova D; Vandermoere F; Göransson O; Peggie M; Mariño KV; Knierim A; Spengler K; Weigert C; Viollet B; Morrice NA; Sakamoto K; Heller R
[Ad] Endereço:Institute of Molecular Cell Biology, Center for Molecular Biomedicine, Jena University Hospital, Hans-Knöll-Straße 2, 07745 Jena, Germany.
[Ti] Título:GFAT1 phosphorylation by AMPK promotes VEGF-induced angiogenesis.
[So] Source:Biochem J;474(6):983-1001, 2017 Mar 07.
[Is] ISSN:1470-8728
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Activation of AMP-activated protein kinase (AMPK) in endothelial cells regulates energy homeostasis, stress protection and angiogenesis, but the underlying mechanisms are incompletely understood. Using a label-free phosphoproteomic analysis, we identified glutamine:fructose-6-phosphate amidotransferase 1 (GFAT1) as an AMPK substrate. GFAT1 is the rate-limiting enzyme in the hexosamine biosynthesis pathway (HBP) and as such controls the modification of proteins by -linked ß- -acetylglucosamine ( -GlcNAc). In the present study, we tested the hypothesis that AMPK controls -GlcNAc levels and function of endothelial cells via GFAT1 phosphorylation using biochemical, pharmacological, genetic and angiogenesis approaches. Activation of AMPK in primary human endothelial cells by 5-aminoimidazole-4-carboxamide riboside (AICAR) or by vascular endothelial growth factor (VEGF) led to GFAT1 phosphorylation at serine 243. This effect was not seen when AMPK was down-regulated by siRNA. Upon AMPK activation, diminished GFAT activity and reduced -GlcNAc levels were observed in endothelial cells containing wild-type (WT)-GFAT1 but not in cells expressing non-phosphorylatable S243A-GFAT1. Pharmacological inhibition or siRNA-mediated down-regulation of GFAT1 potentiated VEGF-induced sprouting, indicating that GFAT1 acts as a negative regulator of angiogenesis. In cells expressing S243A-GFAT1, VEGF-induced sprouting was reduced, suggesting that VEGF relieves the inhibitory action of GFAT1/HBP on angiogenesis via AMPK-mediated GFAT1 phosphorylation. Activation of GFAT1/HBP by high glucose led to impairment of vascular sprouting, whereas GFAT1 inhibition improved sprouting even if glucose level was high. Our findings provide novel mechanistic insights into the role of HBP in angiogenesis. They suggest that targeting AMPK in endothelium might help to ameliorate hyperglycaemia-induced vascular dysfunction associated with metabolic disorders.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Acetilglucosamina/metabolismo
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/metabolismo
Neovascularização Fisiológica/efeitos dos fármacos
Processamento de Proteína Pós-Traducional
Fator A de Crescimento do Endotélio Vascular/farmacologia
[Mh] Termos MeSH secundário: Proteínas Quinases Ativadas por AMP/antagonistas & inibidores
Proteínas Quinases Ativadas por AMP/genética
Alanina/química
Alanina/metabolismo
Substituição de Aminoácidos
Aminoimidazol Carboxamida/análogos & derivados
Aminoimidazol Carboxamida/farmacologia
Animais
Fibroblastos/citologia
Fibroblastos/efeitos dos fármacos
Fibroblastos/metabolismo
Glucose/farmacologia
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/antagonistas & inibidores
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/genética
Hexosaminas/biossíntese
Células Endoteliais da Veia Umbilical Humana/citologia
Células Endoteliais da Veia Umbilical Humana/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana/metabolismo
Seres Humanos
Camundongos
Fosfoproteínas/genética
Fosfoproteínas/metabolismo
Fosforilação/efeitos dos fármacos
Cultura Primária de Células
RNA Interferente Pequeno/genética
RNA Interferente Pequeno/metabolismo
Ribonucleotídeos/farmacologia
Serina/química
Serina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Hexosamines); 0 (Phosphoproteins); 0 (RNA, Small Interfering); 0 (Ribonucleotides); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 360-97-4 (Aminoimidazole Carboxamide); 452VLY9402 (Serine); EC 2.6.1.16 (GFPT1 protein, human); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing)); EC 2.7.11.31 (AMP-Activated Protein Kinases); F0X88YW0YK (AICA ribonucleotide); IY9XDZ35W2 (Glucose); OF5P57N2ZX (Alanine); V956696549 (Acetylglucosamine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161224
[St] Status:MEDLINE
[do] DOI:10.1042/BCJ20160980


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[PMID]:27941137
[Au] Autor:Brady S; Healy EG; Gang Q; Parton M; Quinlivan R; Jacob S; Curtis E; Al-Sarraj S; Sewry CA; Hanna MG; Houlden H; Beeson D; Holton JL
[Ad] Endereço:From the Department of Neurology, Southmead Hospital, Bristol, UK (SB); Department of Neuropathology, Royal Victoria Hospital, N. Ireland, Belfast, Northern Ireland (EGH); UCL Institute of Neurology, Queen Square, London, UK (QG, HH, JLH); MRC Centre for Neuromuscular Diseases, University College Ho
[Ti] Título:Tubular Aggregates and Cylindrical Spirals Have Distinct Immunohistochemical Signatures.
[So] Source:J Neuropathol Exp Neurol;75(12):1171-1178, 2016 Dec.
[Is] ISSN:1554-6578
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tubular aggregates and cylindrical spirals are 2 distinct ultrastructural abnormalities observed in muscle biopsies that have similar histochemical staining characteristics on light microscopy. Both are found in a wide range of disorders. Recently, a number of genetic mutations have been reported in conditions with tubular aggregates in skeletal muscle. It is widely accepted that tubular aggregates arise from the sarcoplasmic reticulum, but the origin of cylindrical spirals has been less clearly defined. We describe the histopathological features of myopathies with tubular aggregates, including a detailed immunohistochemical analysis of congenital myasthenic syndromes with tubular aggregates due to mutations in GFPT1 and DPAGT1, and myopathies with cylindrical spirals. Our findings support the notion that cylindrical spirals, like tubular aggregates, derive primarily from the sarcoplasmic reticulum; however, immunohistochemistry indicates that different molecular components of the sarcoplasmic reticulum may be involved and can be used to distinguish between these different inclusions. The immunohistochemical differences may also help to guide genetic testing.
[Mh] Termos MeSH primário: Fibras Musculares Esqueléticas/patologia
Miopatias Congênitas Estruturais/genética
Miopatias Congênitas Estruturais/patologia
[Mh] Termos MeSH secundário: Adolescente
Adulto
Feminino
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/genética
Seres Humanos
Masculino
Meia-Idade
Músculo Esquelético/patologia
Doenças Musculares/genética
Doenças Musculares/patologia
N-Acetilglucosaminiltransferases/genética
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.1.- (N-Acetylglucosaminyltransferases); EC 2.4.1.153 (dolichyl-phosphate alpha-N-acetylglucosaminyltransferase); EC 2.6.1.16 (GFPT1 protein, human); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing))
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161213
[St] Status:MEDLINE


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[PMID]:27324977
[Au] Autor:Pawlak D; Schielmann M; Wojciechowski M; Andruszkiewicz R
[Ad] Endereço:Department of Pharmaceutical Technology and Biochemistry, Gdansk University of Technology, Gdansk, Poland.
[Ti] Título:Synthesis and biological activity of novel ester derivatives of N(3)-(4-metoxyfumaroyl)-(S)-2,3-diaminopropanoic acid containing amide and keto function as inhibitors of glucosamine-6-phosphate synthase.
[So] Source:Bioorg Med Chem Lett;26(15):3586-9, 2016 08 01.
[Is] ISSN:1464-3405
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:A short series of novel ester derivatives of N(3)-4-metoxyfumaroyl-(S)-2,3-diaminopropanoic acid (FMDP) containing amide or keto functions have been designed and synthesized. Their antifungal activity and inhibitory properties toward fungal glucosamine-6-phosphate synthase has also been evaluated. The obtained compounds 11-13 and 15-17 demonstrated good antifungal activity against Candida albicans. Compounds 11-13 displayed also potent inhibitory activity against fungal glucosamine-6-phosphate synthase, comparable to that of FMDP.
[Mh] Termos MeSH primário: Amidas/farmacologia
Antifúngicos/farmacologia
Candida albicans/efeitos dos fármacos
Ésteres/farmacologia
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/antagonistas & inibidores
Cetonas/farmacologia
beta-Alanina/análogos & derivados
beta-Alanina/farmacologia
[Mh] Termos MeSH secundário: Amidas/química
Antifúngicos/síntese química
Antifúngicos/química
Candida albicans/enzimologia
Relação Dose-Resposta a Droga
Ésteres/síntese química
Ésteres/química
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/metabolismo
Cetonas/química
Testes de Sensibilidade Microbiana
Estrutura Molecular
Relação Estrutura-Atividade
beta-Alanina/síntese química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amides); 0 (Antifungal Agents); 0 (Esters); 0 (Ketones); 11P2JDE17B (beta-Alanine); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing))
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171122
[Lr] Data última revisão:
171122
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160622
[St] Status:MEDLINE


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[PMID]:27017337
[Au] Autor:Bennett AM; Shippy DC; Eakley N; Okwumabua O; Fadl AA
[Ad] Endereço:Department of Animal Sciences, University of Wisconsin-Madison, 1675 Observatory Drive, Madison, WI, 53706, USA.
[Ti] Título:Functional characterization of glucosamine-6-phosphate synthase (GlmS) in Salmonella enterica serovar Enteritidis.
[So] Source:Arch Microbiol;198(6):541-9, 2016 Aug.
[Is] ISSN:1432-072X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Salmonella is a threat to public health due to consumption of contaminated food. Screening of a transposon library identified a unique mutant that was growth and host cell binding deficient. The objective of this study was to determine the functional role of glucosamine-6-phosphate synthase (GlmS) in the biology and pathogenesis of Salmonella. To examine this, we created a glmS mutant (ΔglmS) of Salmonella and examined the effect on cell envelope integrity, growth, metabolism, and pathogenesis. Our data indicated ΔglmS was defective in growth unless media were supplemented with D-glucosamine (D-GlcN). Examination of the bacterial cell envelope revealed that ΔglmS was highly sensitive to detergents, hydrophobic antibiotics, and bile salts compared to the wild type (WT). A release assay indicated that ΔglmS secreted higher amounts of ß-lactamase than the WT in culture supernatant fractions. Furthermore, ΔglmS was attenuated in cell culture models of Salmonella infection. Taken together, this study determined an important role for GlmS in the pathogenesis and biology of Salmonella.
[Mh] Termos MeSH primário: Proteínas de Bactérias/genética
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/genética
Salmonella enteritidis/genética
Salmonella enteritidis/patogenicidade
beta-Lactamases/secreção
[Mh] Termos MeSH secundário: Antibacterianos/farmacologia
Membrana Celular/fisiologia
Detergentes/farmacologia
Farmacorresistência Bacteriana Múltipla/genética
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/metabolismo
Seres Humanos
Infecções por Salmonella/microbiologia
Salmonella enteritidis/enzimologia
Salmonella enteritidis/metabolismo
Virulência/genética
beta-Lactamases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Bacterial Proteins); 0 (Detergents); 0 (component S, glutamate mutase protein, Bacteria); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing)); EC 3.5.2.6 (beta-Lactamases)
[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:160328
[St] Status:MEDLINE
[do] DOI:10.1007/s00203-016-1212-x


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[PMID]:26833073
[Au] Autor:Laczkowski KZ; Biernasiuk A; Baranowska-Laczkowska A; Misiura K; Malm A; Plech T; Paneth A
[Ad] Endereço:Department of Chemical Technology and Pharmaceuticals, Faculty of Pharmacy, Collegium Medicum, Nicolaus Copernicus University, Jurasza 2, 85-089 Bydgoszcz, Poland. krzysztof.laczkowski@cm.umk.pl.
[Ti] Título:Synthesis, Antibacterial Activity, Interaction with Nucleobase and Molecular Docking Studies of 4-Formylbenzoic Acid Based Thiazoles.
[So] Source:Med Chem;12(6):553-62, 2016.
[Is] ISSN:1875-6638
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Synthesis, characterization and investigation of antibacterial activity of ten novel Schiff base derivatives of 4-formylbenzoic acid is presented. Their structures were determined using 1H and 13CNMR, EI(+)-MS and elemental analyses. Additionally, DFT calculations of interaction energies in complexes of the novel drugs and DNA bases are carried out. OBJECTIVE: Design and synthesis of thiazole derivatives with benzoic acid scaffold to obtain compounds with an improved antibacterial activity. METHOD: The examined compounds were screened in vitro for antibacterial activity using the broth microdilution method. Geometrical parameters of the investigated complexes were optimized within the Density Functional Theory (DFT) approximation using the B3LYP functional and the 6-311G** basis set. The docking simulations were performed using the FlexX docking module. RESULTS: Among the derivatives, compound 4b showed very strong bacterial activity against staphylococci, MIC 1.95-3.91 µg/ml, micrococci, MIC 0.98 µg/ml, and Bacillus spp., MIC 7.81-15.62 µg/ml. The compounds 4c, 4d, 4e and 4j also showed high bioactivity against staphylococci, MIC 3.91-31.25 µg/ml, and micrococci, MIC 0.98-15.62 µg/ml. Interaction energy values for investigated guanine complexes are about 2 kcal/mol lower than for the corresponding cytosine complexes. Molecular docking studies of all compounds on the active sites of bacterial enzymes indicated gyrase B as possible target. CONCLUSION: To conclude, an efficient and economic method for the synthesis of thiazoles containing benzoic acid moiety has been developed. The results of antibacterial screenings reveal that some obtained compounds show high to very strong antibacterial activity. The DFT calculations showed that interaction of the obtained drugs with guanine is stronger than with cytosine. Molecular docking studies of all compounds on the active sites of bacterial enzymes indicated gyrase B as possible target.
[Mh] Termos MeSH primário: Antibacterianos/farmacologia
Benzoatos/farmacologia
Tiazóis/farmacologia
[Mh] Termos MeSH secundário: 3-Oxoacil-(Proteína de Transporte de Acila) Sintase/antagonistas & inibidores
3-Oxoacil-(Proteína de Transporte de Acila) Sintase/química
Adenina/química
Antibacterianos/síntese química
Antibacterianos/química
Benzoatos/síntese química
Benzoatos/química
Citosina/química
DNA Topoisomerase IV/antagonistas & inibidores
DNA Topoisomerase IV/química
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/antagonistas & inibidores
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/química
Bactérias Gram-Negativas/efeitos dos fármacos
Bactérias Gram-Positivas/efeitos dos fármacos
Guanina/química
Simulação de Acoplamento Molecular
Peptídeo Sintases/antagonistas & inibidores
Peptídeo Sintases/química
Teoria Quântica
Estereoisomerismo
Relação Estrutura-Atividade
Termodinâmica
Tiazóis/síntese química
Tiazóis/química
Timina/química
Inibidores da Topoisomerase II/síntese química
Inibidores da Topoisomerase II/química
Inibidores da Topoisomerase II/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Benzoates); 0 (Thiazoles); 0 (Topoisomerase II Inhibitors); 5Z93L87A1R (Guanine); 8J337D1HZY (Cytosine); EC 2.3.1.180 (3-ketoacyl-acyl carrier protein synthase III); EC 2.3.1.41 (3-Oxoacyl-(Acyl-Carrier-Protein) Synthase); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing)); EC 5.99.1.- (DNA Topoisomerase IV); EC 6.3.2.- (Peptide Synthases); EC 6.3.2.9 (UDP-N-acetylmuramoylalanine-D-glutamate ligase); JAC85A2161 (Adenine); QR26YLT7LT (Thymine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170704
[Lr] Data última revisão:
170704
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160203
[St] Status:MEDLINE


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[PMID]:26721333
[Au] Autor:Willems AP; van Engelen BG; Lefeber DJ
[Ad] Endereço:Department of Neurology, Donders Institute for Brain, Cognition and Behavior, Radboud University Medical Centre, Box 9101, 6500 HB Nijmegen, The Netherlands; Department of Laboratory Medicine, Translational Metabolic Laboratory, Radboudumc Institute for Molecular Life Sciences, Radboud University Medical Center, 6525 GA Nijmegen, The Netherlands.
[Ti] Título:Genetic defects in the hexosamine and sialic acid biosynthesis pathway.
[So] Source:Biochim Biophys Acta;1860(8):1640-54, 2016 Aug.
[Is] ISSN:0006-3002
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Congenital disorders of glycosylation are caused by defects in the glycosylation of proteins and lipids. Classically, gene defects with multisystem disease have been identified in the ubiquitously expressed glycosyltransferases required for protein N-glycosylation. An increasing number of defects are being described in sugar supply pathways for protein glycosylation with tissue-restricted clinical symptoms. SCOPE OF REVIEW: In this review, we address the hexosamine and sialic acid biosynthesis pathways in sugar metabolism. GFPT1, PGM3 and GNE are essential for synthesis of nucleotide sugars uridine diphosphate N-acetylglucosamine (UDP-GlcNAc) and cytidine-5'-monophospho-N-acetylneuraminic acid (CMP-sialic acid) as precursors for various glycosylation pathways. Defects in these enzymes result in contrasting clinical phenotypes of congenital myasthenia, immunodeficiency or adult-onset myopathy, respectively. We therefore discuss the biochemical mechanisms of known genetic defects in the hexosamine and CMP-sialic acid synthesis pathway in relation to the clinical phenotypes. MAJOR CONCLUSIONS: Both UDP-GlcNAc and CMP-sialic acid are important precursors for diverse protein glycosylation reactions and for conversion into other nucleotide-sugars. Defects in the synthesis of these nucleotide sugars might affect a wide range of protein glycosylation reactions. Involvement of multiple glycosylation pathways might contribute to disease phenotype, but the currently available biochemical information on sugar metabolism is insufficient to understand why defects in these pathways present with tissue-specific phenotypes. GENERAL SIGNIFICANCE: Future research on the interplay between sugar metabolism and different glycosylation pathways in a tissue- and cell-specific manner will contribute to elucidation of disease mechanisms and will create new opportunities for therapeutic intervention. This article is part of a Special Issue entitled "Glycans in personalised medicine" Guest Editor: Professor Gordan Lauc.
[Mh] Termos MeSH primário: Erros Inatos do Metabolismo dos Carboidratos
Glicoproteínas
Hexosaminas
Ácido N-Acetilneuramínico
[Mh] Termos MeSH secundário: Adulto
Erros Inatos do Metabolismo dos Carboidratos/genética
Erros Inatos do Metabolismo dos Carboidratos/metabolismo
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/genética
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/metabolismo
Glicoproteínas/genética
Glicoproteínas/metabolismo
Glicosilação
Hexosaminas/genética
Hexosaminas/metabolismo
Seres Humanos
Ácido N-Acetilneuramínico/genética
Ácido N-Acetilneuramínico/metabolismo
Fosfoglucomutase/genética
Fosfoglucomutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Glycoproteins); 0 (Hexosamines); EC 2.6.1.16 (GFPT1 protein, human); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing)); EC 5.4.2.2 (PGM3 protein, human); EC 5.4.2.2 (Phosphoglucomutase); GZP2782OP0 (N-Acetylneuraminic Acid)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160102
[St] Status:MEDLINE


  9 / 387 MEDLINE  
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[PMID]:26715276
[Au] Autor:Dong T; Kang X; Liu Z; Zhao S; Ma W; Xuan Q; Liu H; Wang Z; Zhang Q
[Ad] Endereço:Department of Internal Medicine, The Third Affiliated Hospital of Harbin Medical University, Haping Road 150 of Nangang District, Harbin, Heilongjiang Province, 150081, China.
[Ti] Título:Altered glycometabolism affects both clinical features and prognosis of triple-negative and neoadjuvant chemotherapy-treated breast cancer.
[So] Source:Tumour Biol;37(6):8159-68, 2016 Jun.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glycometabolism is a distinctive aspect of energy metabolism in breast cancer, and key glycometabolism enzymes/pathways (glycolysis, hexosamine biosynthetic pathway, and pentose phosphate pathway) may directly or indirectly affect the clinical features. In this study, we analyzed the particular correlation between the altered glycometabolism and clinical features of breast cancer to instruct research and clinical treatment. Tissue microarrays containing 189 hollow needle aspiration samples and 295 triple-negative breast cancer tissues were used to test the expression of M2 isoform of pyruvate kinase (PKM2), glutamine-fructose-6-phosphate transaminase 1 (GFPT1), glucose-6-phosphate dehydrogenase (G6PD), and p53 by immunohistochemistry and the intensity of these glycometabolism-related protein was evaluated. Chi-square test, Kaplan-Meier estimates, and Cox proportional hazards model were used to analyze the relationship between the expression of these factors and major clinical features. PKM2, GFPT1, and G6PD affect the pathologic complete response rate of neoadjuvant chemotherapy patients in different ways; pyruvate kinase muscle isozyme 2 (PKM2) and G6PD are closely associated with the molecular subtypes, whereas GFPT1 is correlated with cancer size. All these three factors as well as p53 have impacts on the progression-free survival and overall survival of triple-negative breast cancer patients. Cancer size shows significant association with PKM2 and GFPT1 expression, while the pN stage and grade are associated with PKM2 and G6PD expression. Our study support that clinical characteristics are reflections of specific glycometabolism pathways, so their relationships may shed light on the orientation of research or clinical treatment. The expression of PKM2, GFPT1, and G6PD are hazardous factors for prognosis: high expression of these proteins predict worse progression-free survival and overall survival in triple-negative breast cancer, as well as worse pathologic complete response rate in neoadjuvant chemotherapy breast cancer. However, p53 appears as a protective factor only in the patients receiving neoadjuvant chemotherapy. All the four proteins, PKM2, GFPT1, G6PD and p53, are prognostic markers of breast cancer. The correlation among them suggests that there may be crosstalk of the four proteins in breast cancer.
[Mh] Termos MeSH primário: Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico
Biomarcadores Tumorais/metabolismo
Proteínas de Transporte/metabolismo
Glucosefosfato Desidrogenase/metabolismo
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/metabolismo
Proteínas de Membrana/metabolismo
Terapia Neoadjuvante
Hormônios Tireóideos/metabolismo
Neoplasias de Mama Triplo Negativas/patologia
Proteína Supressora de Tumor p53/metabolismo
[Mh] Termos MeSH secundário: Adulto
Idoso
Estudos de Casos e Controles
Feminino
Seguimentos
Seres Humanos
Técnicas Imunoenzimáticas
Meia-Idade
Mutação/genética
Estadiamento de Neoplasias
Prognóstico
Taxa de Sobrevida
Neoplasias de Mama Triplo Negativas/tratamento farmacológico
Neoplasias de Mama Triplo Negativas/metabolismo
Proteína Supressora de Tumor p53/genética
Adulto Jovem
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (Carrier Proteins); 0 (Membrane Proteins); 0 (TP53 protein, human); 0 (Thyroid Hormones); 0 (Tumor Suppressor Protein p53); 0 (thyroid hormone-binding proteins); EC 1.1.1.49 (Glucosephosphate Dehydrogenase); EC 2.6.1.16 (GFPT1 protein, human); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing))
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151231
[St] Status:MEDLINE
[do] DOI:10.1007/s13277-015-4729-8


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[PMID]:26668120
[Au] Autor:Nikiforov YE
[Ad] Endereço:Department of Pathology, University of Pittsburgh, 3477 Euler Way, Room 8031, Pittsburgh, Pennsylvania 15213, USA.
[Ti] Título:Thyroid cancer in 2015: Molecular landscape of thyroid cancer continues to be deciphered.
[So] Source:Nat Rev Endocrinol;12(2):67-8, 2016 Feb.
[Is] ISSN:1759-5037
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Carcinoma Neuroendócrino/genética
Carcinoma Anaplásico da Tireoide/genética
Neoplasias da Glândula Tireoide/genética
[Mh] Termos MeSH secundário: Enzimas Reparadoras do DNA/genética
Genes da Neurofibromatose 1
Genes da Neurofibromatose 2
Genômica
Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/genética
Seres Humanos
Proteínas de Fusão Oncogênicas/genética
Proteínas Proto-Oncogênicas B-raf/genética
Proteínas Proto-Oncogênicas c-ret/genética
Receptores Proteína Tirosina Quinases/genética
Serina Endopeptidases/genética
Serina-Treonina Quinases TOR/genética
Proteínas ras/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (EML4-ALK fusion protein, human); 0 (Oncogene Proteins, Fusion); EC 2.6.1.16 (GFPT1 protein, human); EC 2.6.1.16 (Glutamine-Fructose-6-Phosphate Transaminase (Isomerizing)); EC 2.7.1.1 (MTOR protein, human); EC 2.7.1.1 (TOR Serine-Threonine Kinases); EC 2.7.10.1 (Proto-Oncogene Proteins c-ret); EC 2.7.10.1 (RET protein, human); EC 2.7.10.1 (Receptor Protein-Tyrosine Kinases); EC 2.7.10.1 (anaplastic lymphoma kinase); EC 2.7.11.1 (BRAF protein, human); EC 2.7.11.1 (Proto-Oncogene Proteins B-raf); EC 3.4.21.- (HABP2 protein, human); EC 3.4.21.- (Serine Endopeptidases); EC 3.6.5.2 (ras Proteins); EC 6.5.1.- (DNA Repair Enzymes)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151216
[St] Status:MEDLINE
[do] DOI:10.1038/nrendo.2015.217



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