Base de dados : MEDLINE
Pesquisa : D08.811.913.400.725.100 [Categoria DeCS]
Referências encontradas : 1003 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 101 ir para página                         

  1 / 1003 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
[PMID]:29240373
[Au] Autor:Goldstein B; Goldfarb DS
[Ti] Título:Early Recognition and Management of Rare Kidney Stone Disorders.
[So] Source:Urol Nurs;37(2):81-9, 102, 2017 Mar-Apr.
[Is] ISSN:1053-816X
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Kidney stones, especially those that present in childhood/adolescence, may be due to rare inherited disorders such as cystinuria. Early recognition and prompt treatment can help reduce or even prevent the serious long-term complications of these rare stone disorders.
[Mh] Termos MeSH primário: Adenina Fosforribosiltransferase/deficiência
Cistinúria/diagnóstico
Doença de Dent/diagnóstico
Hiperoxalúria Primária/diagnóstico
Cálculos Renais/etiologia
Erros Inatos do Metabolismo/diagnóstico
Doenças Raras
Urolitíase/diagnóstico
[Mh] Termos MeSH secundário: Cistinúria/complicações
Cistinúria/terapia
Doença de Dent/complicações
Doença de Dent/terapia
Diagnóstico Precoce
Intervenção Médica Precoce
Seres Humanos
Hiperoxalúria Primária/complicações
Hiperoxalúria Primária/terapia
Erros Inatos do Metabolismo/complicações
Erros Inatos do Metabolismo/terapia
Urolitíase/complicações
Urolitíase/terapia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.2.7 (Adenine Phosphoribosyltransferase)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180123
[Lr] Data última revisão:
180123
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE


  2 / 1003 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28566603
[Au] Autor:Nanmoku K; Kurosawa A; Shinzato T; Shimizu T; Kimura T; Yagisawa T
[Ad] Endereço:Surgical Branch, Institute of Kidney Diseases, Jichi Medical University Hospital, Japan.
[Ti] Título:Febuxostat for the Prevention of Recurrent 2,8-dihydroxyadenine Nephropathy due to Adenine Phosphoribosyltransferase Deficiency Following Kidney Transplantation.
[So] Source:Intern Med;56(11):1387-1391, 2017.
[Is] ISSN:1349-7235
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Adenine phosphoribosyltransferase (APRT) deficiency is a rare autosomal recessive disorder that results in irreversible renal damage due to 2,8-dihydroxyadenine (DHA) nephropathy. A 28-year-old man underwent living-related kidney transplantation for chronic kidney disease of unknown etiology. Numerous spherical brownish crystals observed in his urinary sediment on postoperative day 3 and were observed within the tubular lumen of renal allograft biopsy specimens on postoperative day 7. After a genetic diagnosis, febuxostat treatment was started on postoperative day 7, with the dosage gradually increased to 80 mg/day until complete the disappearance of 2,8-DHA crystals. Febuxostat prevented secondary 2,8-DHA nephropathy after kidney transplantation.
[Mh] Termos MeSH primário: Adenina Fosforribosiltransferase/deficiência
Febuxostat/administração & dosagem
Supressores da Gota/administração & dosagem
Transplante de Rim/métodos
Erros Inatos do Metabolismo/prevenção & controle
Urolitíase/prevenção & controle
[Mh] Termos MeSH secundário: Adenina/análogos & derivados
Adenina/metabolismo
Adulto
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Gout Suppressants); 101V0R1N2E (Febuxostat); 30377-37-8 (2,8-dihydroxyadenine); EC 2.4.2.7 (Adenine Phosphoribosyltransferase); JAC85A2161 (Adenine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171108
[Lr] Data última revisão:
171108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170602
[St] Status:MEDLINE
[do] DOI:10.2169/internalmedicine.56.8142


  3 / 1003 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27838384
[Au] Autor:Rumsby G
[Ad] Endereço:Clinical Biochemistry, UCL Hospitals, 60 Whitfield St, London W1T 4EU, United Kingdom. Electronic address: gill.rumsby@nhs.net.
[Ti] Título:Genetic defects underlying renal stone disease.
[So] Source:Int J Surg;36(Pt D):590-595, 2016 Dec.
[Is] ISSN:1743-9159
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Renal stones are common and are usually secondary to risk factors affecting the solubility of substances in the urinary tract. Primary, that is genetic, causes are rare but nevertheless are important to recognise so that appropriate treatments can be instigated and the risks to other family members acknowledged. A brief overview of the investigation of renal stones from a biochemical point of view is presented with emphasis on the problems that can arise. The genetic basis of renal stone disease caused by (i) derangement of a metabolic pathway, (ii) diversion to an insoluble product, (iii) failure of transport and (iv) renal tubular acidosis is described by reference to the disorders of adenine phosphoribosyl transferase (APRT) deficiency, primary hyperoxaluria, cystinuria and autosomal dominant distal renal tubular acidosis.
[Mh] Termos MeSH primário: Cálculos Renais/genética
[Mh] Termos MeSH secundário: Acidose Tubular Renal/genética
Adenina Fosforribosiltransferase/deficiência
Adenina Fosforribosiltransferase/genética
Adulto
Predisposição Genética para Doença
Seres Humanos
Hiperoxalúria Primária/genética
Cálculos Renais/metabolismo
Erros Inatos do Metabolismo/genética
Urolitíase/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 2.4.2.7 (Adenine Phosphoribosyltransferase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170124
[Lr] Data última revisão:
170124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161114
[St] Status:MEDLINE


  4 / 1003 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27055360
[Au] Autor:Grygoryev D; Gauny S; Lasarev M; Ohlrich A; Kronenberg A; Turker MS
[Ad] Endereço:Oregon Institute of Occupational Health Sciences, Oregon Health & Science University, Portland, OR 97239, United States.
[Ti] Título:Charged particle mutagenesis at low dose and fluence in mouse splenic T cells.
[So] Source:Mutat Res;788:32-40, 2016 06.
[Is] ISSN:1873-135X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:High-energy heavy charged particles (HZE ions) found in the deep space environment can significantly affect human health by inducing mutations and related cancers. To better understand the relation between HZE ion exposure and somatic mutation, we examined cell survival fraction, Aprt mutant frequencies, and the types of mutations detected for mouse splenic T cells exposed in vivo to graded doses of densely ionizing (48)Ti ions (1GeV/amu, LET=107 keV/µm), (56)Fe ions (1GeV/amu, LET=151 keV/µm) ions, or sparsely ionizing protons (1GeV, LET=0.24 keV/µm). The lowest doses for (48)Ti and (56)Fe ions were equivalent to a fluence of approximately 1 or 2 particle traversals per nucleus. In most cases, Aprt mutant frequencies in the irradiated mice were not significantly increased relative to the controls for any of the particles or doses tested at the pre-determined harvest time (3-5 months after irradiation). Despite the lack of increased Aprt mutant frequencies in the irradiated splenocytes, a molecular analysis centered on chromosome 8 revealed the induction of radiation signature mutations (large interstitial deletions and complex mutational patterns), with the highest levels of induction at 2 particles nucleus for the (48)Ti and (56)Fe ions. In total, the results show that densely ionizing HZE ions can induce characteristic mutations in splenic T cells at low fluence, and that at least a subset of radiation-induced mutant cells are stably retained despite the apparent lack of increased mutant frequencies at the time of harvest.
[Mh] Termos MeSH primário: Adenina Fosforribosiltransferase
Radiação Cósmica/efeitos adversos
Mutação/efeitos da radiação
Baço/efeitos da radiação
Linfócitos T/efeitos da radiação
[Mh] Termos MeSH secundário: Adenina Fosforribosiltransferase/genética
Animais
Deleção Cromossômica
Relação Dose-Resposta à Radiação
Feminino
Transferência Linear de Energia
Masculino
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos DBA
Camundongos Knockout
Taxa de Mutação
Radioisótopos
Baço/patologia
Linfócitos T/patologia
Irradiação Corporal Total
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.
[Nm] Nome de substância:
0 (Radioisotopes); EC 2.4.2.7 (Adenine Phosphoribosyltransferase)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171117
[Lr] Data última revisão:
171117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160409
[St] Status:MEDLINE


  5 / 1003 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26969706
[Au] Autor:Zhang C; She Q; Bi H; Whitaker RJ
[Ad] Endereço:Department of Microbiology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA cyz@illinois.edu.
[Ti] Título:The apt/6-Methylpurine Counterselection System and Its Applications in Genetic Studies of the Hyperthermophilic Archaeon Sulfolobus islandicus.
[So] Source:Appl Environ Microbiol;82(10):3070-81, 2016 May 15.
[Is] ISSN:1098-5336
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:UNLABELLED: Sulfolobus islandicus serves as a model for studying archaeal biology as well as linking novel biology to evolutionary ecology using functional population genomics. In the present study, we developed a new counterselectable genetic marker in S. islandicus to expand the genetic toolbox for this species. We show that resistance to the purine analog 6-methylpurine (6-MP) in S. islandicus M.16.4 is due to the inactivation of a putative adenine phosphoribosyltransferase encoded by M164_0158 (apt). The application of the apt gene as a novel counterselectable marker was first illustrated by constructing an unmarked α-amylase deletion mutant. Furthermore, the 6-MP counterselection feature was employed in a forward (loss-of-function) mutation assay to reveal the profile of spontaneous mutations in S. islandicus M.16.4 at the apt locus. Moreover, the general conservation of apt genes in the crenarchaea suggests that the same strategy can be broadly applied to other crenarchaeal model organisms. These results demonstrate that the apt locus represents a new tool for genetic manipulation and sequence analysis of the hyperthermophilic crenarchaeon S. islandicus IMPORTANCE: Currently, the pyrEF/5-fluoroorotic acid (5-FOA) counterselection system remains the sole counterselection marker in crenarchaeal genetics. Since most Sulfolobus mutants constructed by the research community were derived from genetic hosts lacking the pyrEF genes, the pyrEF/5-FOA system is no longer available for use in forward mutation assays. Demonstration of the apt/6-MP counterselection system for the Sulfolobus model renders it possible to again study the mutation profiles in mutants that have already been constructed by the use of strains with a pyrEF-deficient background. Furthermore, additional counterselectable markers will allow us to conduct more sophisticated genetic studies, i.e., investigate mechanisms of chromosomal DNA transfer and quantify recombination frequencies among S. islandicus strains.
[Mh] Termos MeSH primário: Adenina Fosforribosiltransferase/genética
Marcação de Genes/métodos
Purinas/farmacologia
Seleção Genética
Sulfolobus/genética
[Mh] Termos MeSH secundário: Adenina Fosforribosiltransferase/metabolismo
Resistência Microbiana a Medicamentos
Sulfolobus/enzimologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Purines); 2004-03-7 (6-methylpurine); EC 2.4.2.7 (Adenine Phosphoribosyltransferase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170920
[Lr] Data última revisão:
170920
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160313
[St] Status:MEDLINE
[do] DOI:10.1128/AEM.00455-16


  6 / 1003 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26724837
[Au] Autor:Runolfsdottir HL; Palsson R; Agustsdottir IM; Indridason OS; Edvardsson VO
[Ad] Endereço:Faculty of Medicine, School of Health Sciences, University of Iceland, Reykjavik, Iceland.
[Ti] Título:Kidney Disease in Adenine Phosphoribosyltransferase Deficiency.
[So] Source:Am J Kidney Dis;67(3):431-8, 2016 Mar.
[Is] ISSN:1523-6838
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Adenine phosphoribosyltransferase (APRT) deficiency is a purine metabolism disorder causing kidney stones and chronic kidney disease (CKD). The course of nephrolithiasis and CKD has not been well characterized. The objective of this study was to examine long-term kidney outcomes in patients with APRT deficiency. STUDY DESIGN: An observational cohort study. SETTING & PARTICIPANTS: All patients enrolled in the APRT Deficiency Registry of the Rare Kidney Stone Consortium. OUTCOMES: Kidney stones, acute kidney injury (AKI), stage of CKD, end-stage renal disease, estimated glomerular filtration rate (eGFR), and changes in eGFR. MEASUREMENTS: Serum creatinine and eGFR calculated using creatinine-based equations. RESULTS: Of 53 patients, 30 (57%) were females and median age at diagnosis was 37.0 (range, 0.6-67.9) years. Median duration of follow-up was 10.3 (range, 0.0-31.5) years. At diagnosis, kidney stones had developed in 29 (55%) patients and 20 (38%) had CKD stages 3 to 5, including 11 (21%) patients with stage 5. At latest follow-up, 33 (62%) patients had experienced kidney stones; 18 (34%), AKI; and 22 (42%), CKD stages 3 to 5. Of 14 (26%) patients with stage 5 CKD, 12 had initiated renal replacement therapy. Kidney stones recurred in 18 of 33 (55%) patients. The median eGFR slope was -0.38 (range, -21.99 to 1.42) mL/min/1.73m(2) per year in patients receiving treatment with an xanthine dehydrogenase inhibitor and -5.74 (range, -75.8 to -0.10) mL/min/1.73m(2) per year in those not treated prior to the development of stage 5 CKD (P=0.001). LIMITATIONS: Use of observational registry data. CONCLUSIONS: Progressive CKD and AKI episodes are major features of APRT deficiency, whereas nephrolithiasis is the most common presentation. Advanced CKD without a history of kidney stones is more prevalent than previously reported. Our data suggest that timely therapy may retard CKD progression.
[Mh] Termos MeSH primário: Lesão Renal Aguda
Adenina Fosforribosiltransferase/deficiência
Cálculos Renais
Falência Renal Crônica
Erros Inatos do Metabolismo
Terapia de Substituição Renal
Urolitíase
[Mh] Termos MeSH secundário: Lesão Renal Aguda/diagnóstico
Lesão Renal Aguda/epidemiologia
Lesão Renal Aguda/etiologia
Adenina Fosforribosiltransferase/metabolismo
Adulto
Progressão da Doença
Intervenção Médica Precoce/métodos
Intervenção Médica Precoce/estatística & dados numéricos
Feminino
Seguimentos
Taxa de Filtração Glomerular
Seres Humanos
Islândia/epidemiologia
Rim/metabolismo
Rim/fisiopatologia
Cálculos Renais/diagnóstico
Cálculos Renais/epidemiologia
Cálculos Renais/etiologia
Cálculos Renais/prevenção & controle
Falência Renal Crônica/diagnóstico
Falência Renal Crônica/epidemiologia
Falência Renal Crônica/etiologia
Testes de Função Renal
Masculino
Erros Inatos do Metabolismo/complicações
Erros Inatos do Metabolismo/diagnóstico
Erros Inatos do Metabolismo/epidemiologia
Erros Inatos do Metabolismo/metabolismo
Prevalência
Terapia de Substituição Renal/métodos
Terapia de Substituição Renal/estatística & dados numéricos
Urolitíase/complicações
Urolitíase/diagnóstico
Urolitíase/epidemiologia
Urolitíase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; OBSERVATIONAL STUDY; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
EC 2.4.2.7 (Adenine Phosphoribosyltransferase)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170301
[Lr] Data última revisão:
170301
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160104
[St] Status:MEDLINE


  7 / 1003 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:26684317
[Au] Autor:Chong SL; Ng YH
[Ad] Endereço:Department of Pediatrics (Nephrology Service), KK Women's and Children's Hospital, Singapore, Singapore.
[Ti] Título:Obstructive uropathy and severe acute kidney injury from renal calculi due to adenine phosphoribosyltransferase deficiency.
[So] Source:World J Pediatr;12(2):243-5, 2016 May.
[Is] ISSN:1867-0687
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Adenine phosphoribosyltransferase (APRT) deficiency is an uncommon genetic cause of chronic kidney disease due to crystalline nephropathy. METHODS: A case of a Chinese boy with APRT deficiency presenting with severe acute kidney injury secondary to obstructive uropathy from multiple renal calculi was reviewed. RESULTS: The patient underwent staged removal of the calculi. Infrared spectrometry of the renal calculi showed 2,8-dihydroxyadenine. APRT deficiency was confirmed with abolished APRT enzyme activity in red blood cells. He was started on allopurinol and low purine diet with complete resolution of the residual calculi. CONCLUSION: APRT deficiency should be considered in patients with multiple radiolucent renal calculi.
[Mh] Termos MeSH primário: Lesão Renal Aguda/etiologia
Adenina Fosforribosiltransferase/deficiência
Cálculos Renais/complicações
Cálculos Renais/etiologia
Erros Inatos do Metabolismo/complicações
Obstrução Ureteral/etiologia
Obstrução do Colo da Bexiga Urinária/etiologia
Urolitíase/complicações
[Mh] Termos MeSH secundário: China
Seres Humanos
Lactente
Masculino
Índice de Gravidade de Doença
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.2.7 (Adenine Phosphoribosyltransferase)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151220
[St] Status:MEDLINE
[do] DOI:10.1007/s12519-015-0073-8


  8 / 1003 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25862022
[Au] Autor:Ueno K; Shimizu M; Kubo T; Igarashi N; Hatasaki K
[Ad] Endereço:Department of Pediatrics, Toyama Prefectural Central Hospital, Toyama, Japan.
[Ti] Título:An infant with nephrolithiasis and renal failure: Answers.
[So] Source:Pediatr Nephrol;31(7):1083-4, 2016 07.
[Is] ISSN:1432-198X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Cálculos Renais
Insuficiência Renal
[Mh] Termos MeSH secundário: Adenina
Adenina Fosforribosiltransferase
Alopurinol
Seres Humanos
Lactente
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
63CZ7GJN5I (Allopurinol); EC 2.4.2.7 (Adenine Phosphoribosyltransferase); JAC85A2161 (Adenine)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150412
[St] Status:MEDLINE
[do] DOI:10.1007/s00467-015-3100-z


  9 / 1003 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:25862021
[Au] Autor:Ueno K; Shimizu M; Kubo T; Igarashi N; Hatasaki K
[Ad] Endereço:Department of Pediatrics, Toyama Prefectural Central Hospital, Toyama, Japan.
[Ti] Título:An infant with nephrolithiasis and renal failure: Questions.
[So] Source:Pediatr Nephrol;31(7):1081-2, 2016 07.
[Is] ISSN:1432-198X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Adenina Fosforribosiltransferase/deficiência
Erros Inatos do Metabolismo/complicações
Erros Inatos do Metabolismo/diagnóstico
Nefrolitíase/etiologia
Insuficiência Renal/etiologia
Urolitíase/complicações
Urolitíase/diagnóstico
[Mh] Termos MeSH secundário: Seres Humanos
Lactente
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
EC 2.4.2.7 (Adenine Phosphoribosyltransferase)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171027
[Lr] Data última revisão:
171027
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150412
[St] Status:MEDLINE
[do] DOI:10.1007/s00467-015-3099-1


  10 / 1003 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
PubMed Central Texto completo
Texto completo
[PMID]:26544976
[Au] Autor:Cheng YF; Young GH; Lin JT; Jang HH; Chen CC; Nong JY; Chen PK; Kuo CY; Kao SH; Liang YJ; Chen HM
[Ad] Endereço:Energenesis Biomedical Co., Ltd., New Taipei City, Taiwan.
[Ti] Título:Activation of AMP-Activated Protein Kinase by Adenine Alleviates TNF-Alpha-Induced Inflammation in Human Umbilical Vein Endothelial Cells.
[So] Source:PLoS One;10(11):e0142283, 2015.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The AMP-activated protein kinase (AMPK) signaling system plays a key role in cellular stress by repressing the inflammatory responses induced by the nuclear factor-kappa B (NF-κB) system. Previous studies suggest that the anti-inflammatory role of AMPK involves activation by adenine, but the mechanism that allows adenine to produce these effects has not yet been elucidated. In human umbilical vein endothelial cells (HUVECs), adenine was observed to induce the phosphorylation of AMPK in both a time- and dose-dependent manner as well as its downstream target acetyl Co-A carboxylase (ACC). Adenine also attenuated NF-κB targeting of gene expression in a dose-dependent manner and decreased monocyte adhesion to HUVECs following tumor necrosis factor (TNF-α) treatment. The short hairpin RNA (shRNA) against AMPK α1 in HUVECs attenuated the adenine-induced inhibition of NF-κB activation in response to TNF-α, thereby suggesting that the anti-inflammatory role of adenine is mediated by AMPK. Following the knockdown of adenosyl phosphoribosyl transferase (APRT) in HUVECs, adenine supplementation failed to induce the phosphorylation of AMPK and ACC. Similarly, the expression of a shRNA against APRT nullified the anti-inflammatory effects of adenine in HUVECs. These results suggested that the role of adenine as an AMPK activator is related to catabolism by APRT, which increases the cellular AMP levels to activate AMPK.
[Mh] Termos MeSH primário: Proteínas Quinases Ativadas por AMP/metabolismo
Adenina/farmacologia
Inflamação/tratamento farmacológico
Inflamação/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Adenina/toxicidade
Adenina Fosforribosiltransferase/genética
Adenina Fosforribosiltransferase/metabolismo
Aminoimidazol Carboxamida/análogos & derivados
Aminoimidazol Carboxamida/farmacologia
Adesão Celular/efeitos dos fármacos
Células Cultivadas
Ativação Enzimática/efeitos dos fármacos
Expressão Gênica/efeitos dos fármacos
Células Endoteliais da Veia Umbilical Humana
Seres Humanos
Monócitos/metabolismo
NF-kappa B/metabolismo
Fosforilação/efeitos dos fármacos
Transporte Proteico/efeitos dos fármacos
RNA Interferente Pequeno/metabolismo
Ribonucleotídeos/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Ribonucleotides); 0 (Tumor Necrosis Factor-alpha); 360-97-4 (Aminoimidazole Carboxamide); EC 2.4.2.7 (Adenine Phosphoribosyltransferase); EC 2.7.11.31 (AMP-Activated Protein Kinases); F0X88YW0YK (AICA ribonucleotide); JAC85A2161 (Adenine)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151107
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0142283



página 1 de 101 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