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Referências encontradas : 116 [refinar]
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[PMID]:27650733
[Au] Autor:Moktefi A; Zhang SY; Vachin P; Ory V; Henique C; Audard V; Rucker-Martin C; Gouadon E; Eccles M; Schedl A; Heidet L; Ollero M; Sahali D; Pawlak A
[Ad] Endereço:Institut National de la Santé et de la Recherche Médicale, Créteil, France; Université Paris Est, Faculté de Médecine, Créteil, France.
[Ti] Título:Repression of CMIP transcription by WT1 is relevant to podocyte health.
[So] Source:Kidney Int;90(6):1298-1311, 2016 Dec.
[Is] ISSN:1523-1755
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The WT1 (Wilm's tumor suppressor) gene is expressed throughout life in podocytes and is essential for the functional integrity of the glomerular filtration barrier. We have previously shown that CMIP (C-Maf inducing protein) is overproduced in podocyte diseases and alters intracellular signaling. Here we isolated the proximal region of the human CMIP promoter and showed by chromatin immunoprecipitation assays and electrophoretic-mobility shift that Wilm's tumor protein (WT1) bound to 2 WT1 response elements, located at positions -290/-274 and -57/-41 relative to transcription start site. Unlike the human CMIP gene, only one Wt1 response element was identified in the mouse Cmip proximal promoter located at position -217/-206. Luciferase reporter assays indicated that WT1 dose-dependently inhibited the transcriptional induction of the CMIP promoter. Transfection of decoy oligonucleotides mimicking the WT1 response elements prevented the inhibition of WT1 on CMIP promoter activity. Furthermore, WT1 silencing promoted Cmip expression. In line with these findings, the abundance of Cmip was early and significantly increased at the transcript and protein level in podocytes displaying a primary defect in Wt1, including Denys-Drash syndrome and Frasier syndrome. Thus, WT1 is a major repressor of the CMIP gene in physiological situations, while conditional deletion of CMIP in the developing kidney did not affect the development of mature glomeruli.
[Mh] Termos MeSH primário: Proteínas Adaptadoras de Transdução de Sinal/genética
Proteínas Adaptadoras de Transdução de Sinal/metabolismo
Podócitos/metabolismo
Proteínas WT1/metabolismo
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Síndrome de Denys-Drash/metabolismo
Feminino
Síndrome de Frasier/metabolismo
Regulação da Expressão Gênica
Seres Humanos
Rim/embriologia
Masculino
Camundongos
Regiões Promotoras Genéticas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (CMIP protein, human); 0 (Cmip protein, mouse); 0 (WT1 Proteins); 0 (WT1 protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160922
[St] Status:MEDLINE


  2 / 116 MEDLINE  
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[PMID]:27596598
[Au] Autor:Hashimoto H; Zhang X; Zheng Y; Wilson GG; Cheng X
[Ad] Endereço:Department of Biochemistry, Emory University School of Medicine, Atlanta, GA 30322, USA.
[Ti] Título:Denys-Drash syndrome associated WT1 glutamine 369 mutants have altered sequence-preferences and altered responses to epigenetic modifications.
[So] Source:Nucleic Acids Res;44(21):10165-10176, 2016 Dec 01.
[Is] ISSN:1362-4962
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mutations in human zinc-finger transcription factor WT1 result in abnormal development of the kidneys and genitalia and an array of pediatric problems including nephropathy, blastoma, gonadal dysgenesis and genital discordance. Several overlapping phenotypes are associated with WT1 mutations, including Wilms tumors, Denys-Drash syndrome (DDS), Frasier syndrome (FS) and WAGR syndrome (Wilms tumor, aniridia, genitourinary malformations, and mental retardation). These conditions vary in severity from individual to individual; they can be fatal in early childhood, or relatively benign into adulthood. DDS mutations cluster predominantly in zinc fingers (ZF) 2 and 3 at the C-terminus of WT1, which together with ZF4 determine the sequence-specificity of DNA binding. We examined three DDS associated mutations in ZF2 of human WT1 where the normal glutamine at position 369 is replaced by arginine (Q369R), lysine (Q369K) or histidine (Q369H). These mutations alter the sequence-specificity of ZF2, we find, changing its affinity for certain bases and certain epigenetic forms of cytosine. X-ray crystallography of the DNA binding domains of normal WT1, Q369R and Q369H in complex with preferred sequences revealed the molecular interactions responsible for these affinity changes. DDS is inherited in an autosomal dominant fashion, implying a gain of function by mutant WT1 proteins. This gain, we speculate, might derive from the ability of the mutant proteins to sequester WT1 into unproductive oligomers, or to erroneously bind to variant target sequences.
[Mh] Termos MeSH primário: Síndrome de Denys-Drash/genética
Epigênese Genética
Mutação
Proteínas WT1/genética
Proteínas WT1/metabolismo
[Mh] Termos MeSH secundário: Adenina/metabolismo
Substituição de Aminoácidos
Cristalografia por Raios X
Citosina/química
Citosina/metabolismo
DNA/química
DNA/metabolismo
Glutamina/genética
Guanina/metabolismo
Seres Humanos
Proteínas WT1/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (WT1 Proteins); 0 (WT1 protein, human); 0RH81L854J (Glutamine); 5Z93L87A1R (Guanine); 8J337D1HZY (Cytosine); 9007-49-2 (DNA); JAC85A2161 (Adenine)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170613
[Lr] Data última revisão:
170613
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160907
[St] Status:MEDLINE


  3 / 116 MEDLINE  
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[PMID]:26914782
[Au] Autor:Smith SC; Chang B; Fleming LB
[Ad] Endereço:At Cardon Children's Medical Center in Mesa, Ariz., Shawn C. Smith practices pediatric urology, Barry Chang is a pediatric urologist and director of robotic and minimally invasive surgery, and Laura Beth Fleming is a pediatric nurse practitioner in pediatric urology. The authors have disclosed no potential conflicts of interest, financial or otherwise.
[Ti] Título:A 3-year-old with a renal mass and large cystic bladder mass.
[So] Source:JAAPA;29(3):54-6, 2016 Mar.
[Is] ISSN:1547-1896
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Cistocele/diagnóstico por imagem
Síndrome de Denys-Drash/diagnóstico
Neoplasias Renais/diagnóstico por imagem
Síndrome Nefrótica/diagnóstico
Uretra/diagnóstico por imagem
Anormalidades Urogenitais/diagnóstico por imagem
Tumor de Wilms/diagnóstico por imagem
[Mh] Termos MeSH secundário: Pré-Escolar
Cistocele/etiologia
Cistografia
Cistoscopia
Síndrome de Denys-Drash/complicações
Seres Humanos
Neoplasias Renais/etiologia
Masculino
Síndrome Nefrótica/etiologia
Tomografia Computadorizada por Raios X
Uretra/anormalidades
Anormalidades Urogenitais/etiologia
Tumor de Wilms/etiologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:T
[Da] Data de entrada para processamento:160226
[St] Status:MEDLINE
[do] DOI:10.1097/01.JAA.0000480580.08498.25


  4 / 116 MEDLINE  
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[PMID]:26882358
[Au] Autor:Hillen LM; Kamsteeg EJ; Schoots J; Tiebosch AT; Speel EJ; Roemen GM; Peutz-Koostra CJ; Stumpel CT
[Ad] Endereço:a Department of Pathology , Maastricht University Medical Center , Maastricht , The Netherlands.
[Ti] Título:Refining the Diagnosis of Congenital Nephrotic Syndrome on Long-term Stored Tissue: c.1097G>A (p.(Arg366His)) WT1 Mutation Causing Denys Drash Syndrome.
[So] Source:Fetal Pediatr Pathol;35(2):112-9, 2016.
[Is] ISSN:1551-3823
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Congenital nephrotic syndrome (CNS) caused by a mutation in the Wilms tumor 1 suppressor gene (WT1) is part of Denys Drash Syndrome or Frasier syndrome. In the framework of genetic counseling, the diagnosis of CNS can be refined with gene mutation studies on long-term stored formalin-fixed paraffin-embedded tissue from postmortem examination. We report a case of diffuse mesangial sclerosis with perinatal death caused by a de novo mutation in the WT1 gene in a girl with an XY-genotype. This is the first case of Denys Drash Syndrome with the uncommon missense c.1097G>A [p.(Arg366His)] mutation in the WT1 gene which has been diagnosed on long-term stored formalin-fixed paraffin-embedded tissue in 1993. This emphasizes the importance of retained and adequately stored tissue as a resource in the ongoing medical care and counseling.
[Mh] Termos MeSH primário: Síndrome de Denys-Drash/genética
Genes do Tumor de Wilms
Síndrome Nefrótica/diagnóstico
Síndrome Nefrótica/genética
[Mh] Termos MeSH secundário: Feminino
Seres Humanos
Hibridização in Situ Fluorescente
Mutação de Sentido Incorreto
Inclusão em Parafina
Fixação de Tecidos
Proteínas WT1/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (WT1 Proteins)
[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:160217
[St] Status:MEDLINE
[do] DOI:10.3109/15513815.2016.1139018


  5 / 116 MEDLINE  
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[PMID]:24924335
[Au] Autor:Carson JM; Okamura K; Wakashin H; McFann K; Dobrinskikh E; Kopp JB; Blaine J
[Ad] Endereço:University of Colorado Health Sciences Center, Aurora, Colorado, United States of America.
[Ti] Título:Podocytes degrade endocytosed albumin primarily in lysosomes.
[So] Source:PLoS One;9(6):e99771, 2014.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Albuminuria is a strong, independent predictor of chronic kidney disease progression. We hypothesize that podocyte processing of albumin via the lysosome may be an important determinant of podocyte injury and loss. A human urine derived podocyte-like epithelial cell (HUPEC) line was used for in vitro experiments. Albumin uptake was quantified by Western blot after loading HUPECs with fluorescein-labeled (FITC) albumin. Co-localization of albumin with lysosomes was determined by confocal microscopy. Albumin degradation was measured by quantifying FITC-albumin abundance in HUPEC lysates by Western blot. Degradation experiments were repeated using HUPECs treated with chloroquine, a lysosome inhibitor, or MG-132, a proteasome inhibitor. Lysosome activity was measured by fluorescence recovery after photo bleaching (FRAP). Cytokine production was measured by ELISA. Cell death was determined by trypan blue staining. In vivo, staining with lysosome-associated membrane protein-1 (LAMP-1) was performed on tissue from a Denys-Drash trangenic mouse model of nephrotic syndrome. HUPECs endocytosed albumin, which co-localized with lysosomes. Choloroquine, but not MG-132, inhibited albumin degradation, indicating that degradation occurs in lysosomes. Cathepsin B activity, measured by FRAP, significantly decreased in HUPECs exposed to albumin (12.5% of activity in controls) and chloroquine (12.8%), and declined further with exposure to albumin plus chloroquine (8.2%, p<0.05). Cytokine production and cell death were significantly increased in HUPECs exposed to albumin and chloroquine alone, and these effects were potentiated by exposure to albumin plus chloroquine. Compared to wild-type mice, glomerular staining of LAMP-1 was significantly increased in Denys-Drash mice and appeared to be most prominent in podocytes. These data suggest lysosomes are involved in the processing of endocytosed albumin in podocytes, and lysosomal dysfunction may contribute to podocyte injury and glomerulosclerosis in albuminuric diseases. Modifiers of lysosomal activity may have therapeutic potential in slowing the progression of glomerulosclerosis by enhancing the ability of podocytes to process and degrade albumin.
[Mh] Termos MeSH primário: Albuminas/metabolismo
Lisossomos/metabolismo
Podócitos/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Síndrome de Denys-Drash/genética
Síndrome de Denys-Drash/patologia
Modelos Animais de Doenças
Endocitose
Fluoresceína-5-Isotiocianato/análogos & derivados
Fluoresceína-5-Isotiocianato/metabolismo
Fluoresceína-5-Isotiocianato/farmacocinética
Seres Humanos
Camundongos
Camundongos Transgênicos
Proteólise
Proteínas Repressoras/genética
Proteínas Repressoras/metabolismo
Albumina Sérica/metabolismo
Albumina Sérica/farmacocinética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, N.I.H., INTRAMURAL
[Nm] Nome de substância:
0 (Albumins); 0 (FITC-albumin); 0 (Repressor Proteins); 0 (Serum Albumin); 0 (WT1 protein, mouse); I223NX31W9 (Fluorescein-5-isothiocyanate)
[Em] Mês de entrada:1512
[Cu] Atualização por classe:170222
[Lr] Data última revisão:
170222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140614
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0099771


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[PMID]:24913517
[Au] Autor:Hutson JM; Grover SR; O'Connell M; Pennell SD
[Ad] Endereço:Department of Urology, The Royal Children's Hospital, Flemington Road, Melbourne, VIC 3051, Australia.
[Ti] Título:Malformation syndromes associated with disorders of sex development.
[So] Source:Nat Rev Endocrinol;10(8):476-87, 2014 Aug.
[Is] ISSN:1759-5037
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:When embryological development of the internal and/or external genitalia is disrupted, the patient presents with a disorder of sex development (DSD) in the neonatal period or sometime later in life. Some of these patients have other, nongenital malformations, which makes their overall management more complex than if they just had a DSD. This Review summarises these malformation syndromes and discusses the recent research into their aetiology. The genetic causes of these malformation syndromes, when they are known, will also be described. Many specific genetic mutations are now known in malformation syndromes with a defect in hormonal function. By contrast, the genetic causes remain unknown in many nonhormonal morphological anomalies that affect the genitalia.
[Mh] Termos MeSH primário: Transtornos do Desenvolvimento Sexual/genética
Genitália/anormalidades
[Mh] Termos MeSH secundário: Animais
Fissura Palatina/genética
Síndrome de Denys-Drash/genética
Esôfago/anormalidades
Feminino
Síndrome de Frasier/genética
Doenças Genéticas Ligadas ao Cromossomo X/genética
Disgenesia Gonadal/genética
Disgenesia Gonadal 46 XY/genética
Seres Humanos
Hipertelorismo/genética
Hipogonadismo/genética
Hipospadia/genética
Masculino
Retardo Mental Ligado ao Cromossomo X/genética
Síndrome de Turner/genética
Síndrome WAGR/genética
Talassemia alfa/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1411
[Cu] Atualização por classe:170606
[Lr] Data última revisão:
170606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140611
[St] Status:MEDLINE
[do] DOI:10.1038/nrendo.2014.83


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[PMID]:24856573
[Au] Autor:Ikezumi Y; Suzuki T; Karasawa T; Kaneko U; Yamada T; Hasegawa H; Nagata M; Saitoh A
[Ad] Endereço:Department of Pediatrics, Niigata University Medical and Dental Hospital, 1-784 Asahimachi-dori, Cyuo-ku, Niigata, 951-8520, Japan. Electronic address: ikezumi@med.niigata-u.ac.jp.
[Ti] Título:Glomerular epithelial cell phenotype in diffuse mesangial sclerosis: a report of 2 cases with markedly increased urinary podocyte excretion.
[So] Source:Hum Pathol;45(8):1778-83, 2014 Aug.
[Is] ISSN:1532-8392
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We report 2 cases of diffuse mesangial sclerosis (DMS) accompanied by severe podocyte excretion in urine. Patient 1 was a 9-day-old girl with a WT1 mutation who developed Wilms tumor at 6 months of age and was subsequently diagnosed with Denys-Drash syndrome. Patient 2 was a 1-year-old boy without a WT1 abnormality but presenting with heavy proteinuria. In both patients, histological examination showed findings of DMS. Immunohistochemical staining for synaptopodin (a podocyte marker) revealed a reduced number of podocytes in the glomeruli with severe sclerosis; however, podocytes persisted in the relatively intact glomeruli. Some glomeruli were accompanied by sclerotic lesions surrounded by proliferating cells; immunofluorescence staining revealed a majority of these proliferating cells to be positive for claudin-1 (a parietal cell marker) but negative for synaptopodin. These findings suggest that podocyte loss and the consequent proliferation of parietal cells are common processes in the pathogenesis of DMS.
[Mh] Termos MeSH primário: Síndrome de Denys-Drash/patologia
Glomérulos Renais/patologia
Síndrome Nefrótica/patologia
Podócitos/patologia
Esclerose/patologia
Tumor de Wilms/patologia
[Mh] Termos MeSH secundário: Síndrome de Denys-Drash/genética
Síndrome de Denys-Drash/fisiopatologia
Feminino
Seres Humanos
Lactente
Recém-Nascido
Glomérulos Renais/fisiopatologia
Masculino
Síndrome Nefrótica/genética
Síndrome Nefrótica/fisiopatologia
Fenótipo
Podócitos/fisiologia
Esclerose/genética
Esclerose/fisiopatologia
Proteínas WT1/genética
Tumor de Wilms/genética
Tumor de Wilms/fisiopatologia
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (WT1 Proteins)
[Em] Mês de entrada:1409
[Cu] Atualização por classe:140721
[Lr] Data última revisão:
140721
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140527
[St] Status:MEDLINE


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[PMID]:24625882
[Au] Autor:Wang HY; Yue ZH; Sun LZ; Mo JC; Mo Y; Sun JJ
[Ti] Título:Clinical features and an atypical WT1 mutant site in a child with incomplete Denys-Drash syndrome.
[So] Source:Asian J Androl;16(4):647-9, 2014 Jul-Aug.
[Is] ISSN:1745-7262
[Cp] País de publicação:China
[La] Idioma:eng
[Mh] Termos MeSH primário: Síndrome de Denys-Drash/diagnóstico
Proteínas WT1/genética
[Mh] Termos MeSH secundário: Criança
Síndrome de Denys-Drash/genética
Seres Humanos
Masculino
Mutação
[Pt] Tipo de publicação:CASE REPORTS; LETTER; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (WT1 Proteins); 0 (WT1 protein, human)
[Em] Mês de entrada:1508
[Cu] Atualização por classe:140704
[Lr] Data última revisão:
140704
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140315
[St] Status:MEDLINE
[do] DOI:10.4103/1008-682X.125396


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[PMID]:24379226
[Au] Autor:Eneman B; Mekahli D; Audrezet MP; Lerut E; Van Damme-Lombaerts R; Van den Heuvel L; Levtchenko E
[Ad] Endereço:Pediatric Nephrology, University Hospitals Leuven, Herestraat 49, 3000 Leuven, Belgium. benedicte.eneman@uzleuven.be.
[Ti] Título:An unusual presentation of Denys-Drash syndrome due to bigenic disease.
[So] Source:Pediatrics;133(1):e252-6, 2014 Jan.
[Is] ISSN:1098-4275
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We report a case of Denys-Drash syndrome (DDS) in a 3-month-old girl presenting with bilateral renal cortical cysts mimicking polycystic kidney disease. Genetic analysis revealed a de novo heterozygous missense mutation c.1186G>A (p.Asp396Asn) in the WT1 gene, confirming the diagnosis of DDS. Because multiple renal cysts have never been reported in DDS, we explored several genes responsible for these renal manifestations, such as HNF-1ß, PAX2, PKD1, and PKD2. Remarkably, we identified a heterozygous missense variant c.12439A>G (p.Lys4147Glu) in the PKD1 gene. The same variant was found in the patient's mother, who had no renal cysts, and in the grandfather, who had several renal cysts. Mutation prediction programs classified the c.12439A>G variant as being "likely pathogenic." We hypothesize that the severe cystic phenotype in the index patient could be due to the WT1 mutation, enhancing pathogenicity of the "hypomorph" PKD1 allele. A possible role for Wilms tumor suppressor 1 (WT1) in renal cyst development should be considered. From a conceptual point of view, this case shows that an unusual presentation of a known genetic syndrome might point to bigenic inheritance, with unexpected interference of mutated genes causing an uncommon clinical phenotype.
[Mh] Termos MeSH primário: Síndrome de Denys-Drash/diagnóstico
Genes do Tumor de Wilms
Mutação de Sentido Incorreto
Rim Policístico Autossômico Dominante/diagnóstico
Canais de Cátion TRPP/genética
[Mh] Termos MeSH secundário: Síndrome de Denys-Drash/genética
Diagnóstico Diferencial
Feminino
Marcadores Genéticos
Heterozigoto
Seres Humanos
Lactente
Rim Policístico Autossômico Dominante/genética
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Genetic Markers); 0 (TRPP Cation Channels); 0 (polycystic kidney disease 1 protein)
[Em] Mês de entrada:1402
[Cu] Atualização por classe:140103
[Lr] Data última revisão:
140103
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:140101
[St] Status:MEDLINE
[do] DOI:10.1542/peds.2013-1524


  10 / 116 MEDLINE  
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[PMID]:23835859
[Au] Autor:Yang Y; Zhao F; Huang J; Nie X; Yu Z
[Ad] Endereço:Department of Pediatrics, Fuzhou Dongfang Hospital, No. 156 Xi Er Huan Bei Lu, Fuzhou, Fujian, 350025, People's Republic of China.
[Ti] Título:Patients with different or identical genotypes of the WT1 gene present different phenotypes.
[So] Source:Eur J Pediatr;172(12):1707-8, 2013 Dec.
[Is] ISSN:1432-1076
[Cp] País de publicação:Germany
[La] Idioma:eng
[Mh] Termos MeSH primário: Síndrome de Denys-Drash/genética
Síndrome de Frasier/genética
Falência Renal Crônica/genética
Síndrome Nefrótica/genética
Proteínas WT1/genética
[Mh] Termos MeSH secundário: Seres Humanos
Masculino
[Pt] Tipo de publicação:COMMENT; LETTER
[Nm] Nome de substância:
0 (WT1 Proteins)
[Em] Mês de entrada:1407
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:130710
[St] Status:MEDLINE
[do] DOI:10.1007/s00431-013-2086-4



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