Base de dados : MEDLINE
Pesquisa : A05.810.453.736 [Categoria DeCS]
Referências encontradas : 4593 [refinar]
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  1 / 4593 MEDLINE  
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[PMID]:29240767
[Au] Autor:Phelep A; Laouari D; Bharti K; Burtin M; Tammaccaro S; Garbay S; Nguyen C; Vasseur F; Blanc T; Berissi S; Langa-Vives F; Fischer E; Druilhe A; Arnheiter H; Friedlander G; Pontoglio M; Terzi F
[Ad] Endereço:INSERM U1151-CNRS UMR 8253, Université Paris Descartes, Institut Necker Enfants Malades, Département « Croissance et Signalisation ¼, Hôpital Necker Enfants Malades, Paris, France.
[Ti] Título:MITF - A controls branching morphogenesis and nephron endowment.
[So] Source:PLoS Genet;13(12):e1007093, 2017 12.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Congenital nephron number varies widely in the human population and individuals with low nephron number are at risk of developing hypertension and chronic kidney disease. The development of the kidney occurs via an orchestrated morphogenetic process where metanephric mesenchyme and ureteric bud reciprocally interact to induce nephron formation. The genetic networks that modulate the extent of this process and set the final nephron number are mostly unknown. Here, we identified a specific isoform of MITF (MITF-A), a bHLH-Zip transcription factor, as a novel regulator of the final nephron number. We showed that overexpression of MITF-A leads to a substantial increase of nephron number and bigger kidneys, whereas Mitfa deficiency results in reduced nephron number. Furthermore, we demonstrated that MITF-A triggers ureteric bud branching, a phenotype that is associated with increased ureteric bud cell proliferation. Molecular studies associated with an in silico analyses revealed that amongst the putative MITF-A targets, Ret was significantly modulated by MITF-A. Consistent with the key role of this network in kidney morphogenesis, Ret heterozygosis prevented the increase of nephron number in mice overexpressing MITF-A. Collectively, these results uncover a novel transcriptional network that controls branching morphogenesis during kidney development and identifies one of the first modifier genes of nephron endowment.
[Mh] Termos MeSH primário: Rim/fisiologia
Fator de Transcrição Associado à Microftalmia/metabolismo
Néfrons/fisiologia
[Mh] Termos MeSH secundário: Animais
Feminino
Seres Humanos
Rim/embriologia
Rim/metabolismo
Masculino
Camundongos
Camundongos Transgênicos
Fator de Transcrição Associado à Microftalmia/genética
Morfogênese
Néfrons/anatomia & histologia
Néfrons/crescimento & desenvolvimento
Néfrons/metabolismo
Organogênese
Isoformas de Proteínas
Proteínas Proto-Oncogênicas c-ret/genética
Proteínas Proto-Oncogênicas c-ret/metabolismo
Ureter/metabolismo
Ureter/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Microphthalmia-Associated Transcription Factor); 0 (Protein Isoforms); EC 2.7.10.1 (Proto-Oncogene Proteins c-ret); EC 2.7.10.1 (RET protein, human); EC 2.7.10.1 (Ret protein, mouse)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171215
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1007093


  2 / 4593 MEDLINE  
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[PMID]:29198839
[Au] Autor:Ma Q; Wang Y; Zhang T; Zuo W
[Ad] Endereço:School of Medicine, Tongji University, Shanghai 200433, China.
[Ti] Título:Notch-mediated Sox9 cell activation contributes to kidney repair after partial nephrectomy.
[So] Source:Life Sci;193:104-109, 2018 Jan 15.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:AIMS: Partial nephrectomy is a surgical technique as an alternative for traditional radical nephrectomy. The advantage of partial nephrectomy technique is nephron-sparing, however, whether the remaining kidney tissue could regenerate the lost nephron is still unknown. The current work is to investigate the kidney tissue repair process and the related cellular and molecular mechanism. MAIN METHODS: We used a novel unilateral partial nephrectomy mouse model to study kidney repair, and focused on a population of Sox9 progenitor cells to study their pivotal role in the regenerative process. Kidney function after nephrectomy was measured using creatinine and urea nitrogen assay kit. Wound healing was assessed by Masson Trichrome Staining. Tissue regeneration was tested by Sox9 cells immunofluorescence staining. The differentiation potential of Sox9 cells were assessed by immunoanalysis with various tubular cell markers. Notch activation was determined by qPCR and Western blotting. KEY FINDINGS: After partial nephrectomy, we found that massive Sox9 cells emerged one day after the surgery and lasted for up to 20days. The Sox9 cells had proliferative capacity and could give rise to epithelial cells of proximal tubule, Henle's loop, distal tubule, collecting duct, and the parietal layer of glomerulus. We also found that the activation of Sox9 cells was mediated by Notch signaling pathway. SIGNIFICANCE: The current study reveals that Notch-mediated Sox9 cell activation can contribute to kidney tubule regeneration after unilateral partial nephrectomy in mice.
[Mh] Termos MeSH primário: Rim/metabolismo
Nefrectomia/métodos
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Creatinina/metabolismo
Células Epiteliais/metabolismo
Rim/fisiologia
Túbulos Renais
Túbulos Renais Proximais/fisiologia
Camundongos
Camundongos Endogâmicos C57BL
Nefrectomia/reabilitação
Néfrons
Receptores Notch/metabolismo
Regeneração/fisiologia
Fatores de Transcrição SOX9/genética
Fatores de Transcrição SOX9/metabolismo
Transdução de Sinais
Cicatrização/genética
Cicatrização/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, Notch); 0 (SOX9 Transcription Factor); 0 (SOX9 protein, human); AYI8EX34EU (Creatinine)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171205
[St] Status:MEDLINE


  3 / 4593 MEDLINE  
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[PMID]:28933142
[Au] Autor:Rosenberg ME; Hostetter TH
[Ad] Endereço:University of Minnesota Medical School, Minneapolis, MN rosen001@umn.edu
[Ti] Título:Single-Nephron Glomerular Filtration Rate in Healthy Adults.
[So] Source:N Engl J Med;377(12):1202-3, 2017 09 21.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Taxa de Filtração Glomerular
Néfrons
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1709128


  4 / 4593 MEDLINE  
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[PMID]:28933141
[Au] Autor:Agarwal A
[Ad] Endereço:University of Utah, Salt Lake City, UT adhish.agarwal@hsc.utah.edu
[Ti] Título:Single-Nephron Glomerular Filtration Rate in Healthy Adults.
[So] Source:N Engl J Med;377(12):1202, 2017 09 21.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Taxa de Filtração Glomerular
Néfrons
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Rim
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1709128


  5 / 4593 MEDLINE  
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[PMID]:28931009
[Au] Autor:Trimpert C; Wesche D; de Groot T; Pimentel Rodriguez MM; Wong V; van den Berg DTM; Cheval L; Ariza CA; Doucet A; Stagljar I; Deen PMT
[Ad] Endereço:Department of Physiology, Radboud University Medical Center, Nijmegen, The Netherlands.
[Ti] Título:NDFIP allows NEDD4/NEDD4L-induced AQP2 ubiquitination and degradation.
[So] Source:PLoS One;12(9):e0183774, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Regulation of our water homeostasis is fine-tuned by dynamic translocation of Aquaporin-2 (AQP2)-bearing vesicles to and from the plasma membrane of renal principal cells. Whereas binding of vasopressin to its type-2 receptor initiates a cAMP-protein kinase A cascade and AQP2 translocation to the apical membrane, this is counteracted by protein kinase C-activating hormones, resulting in ubiquitination-dependent internalization of AQP2. The proteins targeting AQP2 for ubiquitin-mediated degradation are unknown. In collecting duct mpkCCD cells, siRNA knockdown of NEDD4 and NEDD4L E3 ligases yielded increased AQP2 abundance, but they did not bind AQP2. Membrane Yeast Two-Hybrid assays using full-length AQP2 as bait, identified NEDD4 family interacting protein 2 (NDFIP2) to bind AQP2. NDFIP2 and its homologue NDFIP1 have PY motifs by which they bind NEDD4 family members and bring them close to target proteins. In HEK293 cells, NDFIP1 and NDFIP2 bound AQP2 and were essential for NEDD4/NEDD4L-mediated ubiquitination and degradation of AQP2, an effect not observed with PY-lacking NDFIP1/2 proteins. In mpkCCD cells, downregulation of NDFIP1, NEDD4 and NEDD4L, but not NDFIP2, increased AQP2 abundance. In mouse kidney, Ndfip1 and Ndfip2 mRNA distribution was similar and high in proximal tubules and collecting ducts, which was also found for NDFIP1 proteins. Our results reveal that NEDD4/NEDD4L mediate ubiquitination and degradation of AQP2, but that NDFIP proteins are needed to connect NEDD4/NEDD4L to AQP2. As NDFIP1/2 bind many NEDD4 family E3 ligases, which are implicated in several cellular processes, NDFIP1/2 may be the missing link for AQP2 ubiquitination and degradation from different subcellular locations.
[Mh] Termos MeSH primário: Aquaporina 2/metabolismo
Proteínas de Transporte/metabolismo
Complexos Endossomais de Distribuição Requeridos para Transporte/metabolismo
Proteínas de Membrana/metabolismo
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteínas de Transporte/genética
Linhagem Celular
Regulação para Baixo
Complexos Endossomais de Distribuição Requeridos para Transporte/antagonistas & inibidores
Complexos Endossomais de Distribuição Requeridos para Transporte/genética
Células HEK293
Seres Humanos
Imunoprecipitação
Masculino
Proteínas de Membrana/genética
Camundongos
Camundongos Endogâmicos C57BL
Ubiquitina-Proteína Ligases Nedd4
Néfrons/metabolismo
Ligação Proteica
Interferência de RNA
RNA Mensageiro/metabolismo
RNA Interferente Pequeno/metabolismo
Técnicas do Sistema de Duplo-Híbrido
Ubiquitina-Proteína Ligases/antagonistas & inibidores
Ubiquitina-Proteína Ligases/genética
Ubiquitinação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aquaporin 2); 0 (Carrier Proteins); 0 (Endosomal Sorting Complexes Required for Transport); 0 (Membrane Proteins); 0 (NDFIP1 protein, human); 0 (NDFIP2 protein, human); 0 (RNA, Messenger); 0 (RNA, Small Interfering); EC 2.3.2.26 (Nedd4 Ubiquitin Protein Ligases); EC 2.3.2.26 (Nedd4 protein, human); EC 2.3.2.26 (Nedd4L protein, human); EC 2.3.2.26 (Nedd4l protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0183774


  6 / 4593 MEDLINE  
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[PMID]:28930503
[Au] Autor:Denic A; Glassock RJ; Rule AD
[Ad] Endereço:Mayo Clinic, Rochester, MN
[Ti] Título:Single-Nephron Glomerular Filtration Rate in Healthy Adults.
[So] Source:N Engl J Med;377(12):1203-4, 2017 09 21.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Taxa de Filtração Glomerular
Néfrons
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Rim
Glomérulos Renais
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1709128


  7 / 4593 MEDLINE  
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[PMID]:28930504
[Au] Autor:Zarogiannis SG; Liakopoulos V; Schmitt CP
[Ad] Endereço:University of Thessaly, Larissa, Greece szarog@med.uth.gr.
[Ti] Título:Single-Nephron Glomerular Filtration Rate in Healthy Adults.
[So] Source:N Engl J Med;377(12):1203, 2017 09 21.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Taxa de Filtração Glomerular
Néfrons
[Mh] Termos MeSH secundário: Adulto
Seres Humanos
Rim
Glomérulos Renais
[Pt] Tipo de publicação:LETTER; COMMENT
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1056/NEJMc1709128


  8 / 4593 MEDLINE  
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[PMID]:28860115
[Au] Autor:Gao L; Yang Z; Hiremath C; Zimmerman SE; Long B; Brakeman PR; Mostov KE; Bryant DM; Luby-Phelps K; Marciano DK
[Ad] Endereço:Department of Medicine, Division of Nephrology, University of Texas Southwestern Medical Center, Dallas, TX, 75390, USA.
[Ti] Título:Afadin orients cell division to position the tubule lumen in developing renal tubules.
[So] Source:Development;144(19):3511-3520, 2017 10 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In many types of tubules, continuity of the lumen is paramount to tubular function, yet how tubules generate lumen continuity is not known. We recently found that the F-actin-binding protein afadin is required for lumen continuity in developing renal tubules, though its mechanism of action remains unknown. Here, we demonstrate that afadin is required for lumen continuity by orienting the mitotic spindle during cell division. Using an 3D cyst model, we find that afadin localizes to the cell cortex adjacent to the spindle poles and orients the mitotic spindle. In tubules, cell division may be oriented relative to two axes: longitudinal and apical-basal. Unexpectedly, examination of early-stage developing nephron tubules reveals that cell division is not oriented in the longitudinal (or planar-polarized) axis. However, cell division is oriented perpendicular to the apical-basal axis. Absence of afadin leads to misorientation of apical-basal cell division in nephron tubules. Together, these results support a model whereby afadin determines lumen placement by directing apical-basal spindle orientation, resulting in a continuous lumen and normal tubule morphogenesis.
[Mh] Termos MeSH primário: Divisão Celular
Túbulos Renais/embriologia
Túbulos Renais/metabolismo
Proteínas dos Microfilamentos/metabolismo
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Cães
Células Epiteliais/metabolismo
Células Epiteliais/patologia
Feminino
Doenças Renais Císticas/patologia
Túbulos Renais/patologia
Células Madin Darby de Rim Canino
Masculino
Camundongos
Morfogênese
Néfrons/metabolismo
Néfrons/patologia
Fuso Acromático/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Microfilament Proteins); 0 (afadin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171126
[Lr] Data última revisão:
171126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170902
[St] Status:MEDLINE
[do] DOI:10.1242/dev.148908


  9 / 4593 MEDLINE  
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[PMID]:28783044
[Au] Autor:Ware JS; Wain LV; Channavajjhala SK; Jackson VE; Edwards E; Lu R; Siew K; Jia W; Shrine N; Kinnear S; Jalland M; Henry AP; Clayton J; O'Shaughnessy KM; Tobin MD; Schuster VL; Cook S; Hall IP; Glover M
[Ad] Endereço:NIHR Biomedical Research Unit in Cardiovascular Disease at Royal Brompton & Harefield, NHS Foundation Trust and Imperial College London, London, United Kingdom.
[Ti] Título:Phenotypic and pharmacogenetic evaluation of patients with thiazide-induced hyponatremia.
[So] Source:J Clin Invest;127(9):3367-3374, 2017 Sep 01.
[Is] ISSN:1558-8238
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thiazide diuretics are among the most widely used treatments for hypertension, but thiazide-induced hyponatremia (TIH), a clinically significant adverse effect, is poorly understood. Here, we have studied the phenotypic and genetic characteristics of patients hospitalized with TIH. In a cohort of 109 TIH patients, those with severe TIH displayed an extended phenotype of intravascular volume expansion, increased free water reabsorption, urinary prostaglandin E2 excretion, and reduced excretion of serum chloride, magnesium, zinc, and antidiuretic hormone. GWAS in a separate cohort of 48 TIH patients and 2,922 controls from the 1958 British birth cohort identified an additional 14 regions associated with TIH. We identified a suggestive association with a variant in SLCO2A1, which encodes a prostaglandin transporter in the distal nephron. Resequencing of SLCO2A1 revealed a nonsynonymous variant, rs34550074 (p.A396T), and association with this SNP was replicated in a second cohort of TIH cases. TIH patients with the p.A396T variant demonstrated increased urinary excretion of prostaglandin E2 and metabolites. Moreover, the SLCO2A1 phospho-mimic p.A396E showed loss of transporter function in vitro. These findings indicate that the phenotype of TIH involves a more extensive metabolic derangement than previously recognized. We propose one mechanism underlying TIH development in a subgroup of patients in which SLCO2A1 regulation is altered.
[Mh] Termos MeSH primário: Hiponatremia/induzido quimicamente
Inibidores de Simportadores de Cloreto de Sódio/efeitos adversos
Tiazidas/efeitos adversos
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Aquaporina 1/genética
Aquaporina 2/genética
Estudos de Coortes
Dinoprostona/metabolismo
Feminino
Estudo de Associação Genômica Ampla
Seres Humanos
Hiponatremia/genética
Masculino
Meia-Idade
Néfrons/metabolismo
Transportadores de Ânions Orgânicos/genética
Farmacogenética
Fenótipo
Polimorfismo de Nucleotídeo Único
Prostaglandinas/metabolismo
Reino Unido
Água/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AQP1 protein, human); 0 (AQP2 protein, human); 0 (Aquaporin 2); 0 (Organic Anion Transporters); 0 (Prostaglandins); 0 (SLCO2A1 protein, human); 0 (Sodium Chloride Symporter Inhibitors); 0 (Thiazides); 059QF0KO0R (Water); 146410-94-8 (Aquaporin 1); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170808
[St] Status:MEDLINE


  10 / 4593 MEDLINE  
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[PMID]:28754792
[Au] Autor:Liu J; Edgington-Giordano F; Dugas C; Abrams A; Katakam P; Satou R; Saifudeen Z
[Ad] Endereço:Department of Pediatrics, Section of Nephrology.
[Ti] Título:Regulation of Nephron Progenitor Cell Self-Renewal by Intermediary Metabolism.
[So] Source:J Am Soc Nephrol;28(11):3323-3335, 2017 Nov.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Nephron progenitor cells (NPCs) show an age-dependent capacity to balance self-renewal with differentiation. Older NPCs (postnatal day 0) exit the progenitor niche at a higher rate than younger (embryonic day 13.5) NPCs do. This behavior is reflected in the transcript profiles of young and old NPCs. Bioenergetic pathways have emerged as important regulators of stem cell fate. Here, we investigated the mechanisms underlying this regulation in murine NPCs. Upon isolation and culture in NPC renewal medium, younger NPCs displayed a higher glycolysis rate than older NPCs. Inhibition of glycolysis enhanced nephrogenesis in cultured embryonic kidneys, without increasing ureteric tree branching, and promoted mesenchymal-to-epithelial transition in cultured isolated metanephric mesenchyme. Cotreatment with a canonical Wnt signaling inhibitor attenuated but did not entirely block the increase in nephrogenesis observed after glycolysis inhibition. Furthermore, inhibition of the phosphatidylinositol 3-kinase/Akt self-renewal signaling pathway or stimulation of differentiation pathways in the NPC decreased glycolytic flux. Our findings suggest that glycolysis is a pivotal, cell-intrinsic determinant of NPC fate, with a high glycolytic flux supporting self-renewal and inhibition of glycolysis stimulating differentiation.
[Mh] Termos MeSH primário: Autorrenovação Celular/fisiologia
Néfrons/citologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular
Células Cultivadas
Glicólise
Rim/embriologia
Rim/metabolismo
Camundongos
Néfrons/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170730
[St] Status:MEDLINE
[do] DOI:10.1681/ASN.2016111246



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