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Pesquisa : G05.360.340 [Categoria DeCS]
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  1 / 24976 MEDLINE  
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[PMID]:28931564
[Au] Autor:Padmanabhan S; Joe B
[Ad] Endereço:Institute of Cardiovascular and Medical Sciences, College of Medical, Veterinary and Life Sciences, University of Glasgow, Glasgow, United Kingdom; and Center for Hypertension and Personalized Medicine; Department of Physiology and Pharmacology, University of Toledo College of Medicine and Life Sciences, Toledo, Ohio.
[Ti] Título:Towards Precision Medicine for Hypertension: A Review of Genomic, Epigenomic, and Microbiomic Effects on Blood Pressure in Experimental Rat Models and Humans.
[So] Source:Physiol Rev;97(4):1469-1528, 2017 Oct 01.
[Is] ISSN:1522-1210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Compelling evidence for the inherited nature of essential hypertension has led to extensive research in rats and humans. Rats have served as the primary model for research on the genetics of hypertension resulting in identification of genomic regions that are causally associated with hypertension. In more recent times, genome-wide studies in humans have also begun to improve our understanding of the inheritance of polygenic forms of hypertension. Based on the chronological progression of research into the genetics of hypertension as the "structural backbone," this review catalogs and discusses the rat and human genetic elements mapped and implicated in blood pressure regulation. Furthermore, the knowledge gained from these genetic studies that provide evidence to suggest that much of the genetic influence on hypertension residing within noncoding elements of our DNA and operating through pervasive epistasis or gene-gene interactions is highlighted. Lastly, perspectives on current thinking that the more complex "triad" of the genome, epigenome, and the microbiome operating to influence the inheritance of hypertension, is documented. Overall, the collective knowledge gained from rats and humans is disappointing in the sense that major hypertension-causing genes as targets for clinical management of essential hypertension may not be a clinical reality. On the other hand, the realization that the polygenic nature of hypertension prevents any single locus from being a relevant clinical target for all humans directs future studies on the genetics of hypertension towards an individualized genomic approach.
[Mh] Termos MeSH primário: Epigênese Genética
Genoma/fisiologia
Hipertensão/genética
Hipertensão/patologia
Microbiota
[Mh] Termos MeSH secundário: Animais
Humanos
Hipertensão/microbiologia
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170921
[St] Status:MEDLINE
[do] DOI:10.1152/physrev.00035.2016


  2 / 24976 MEDLINE  
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[PMID]:28230237
[Au] Autor:Bourgeois Y; Roulin AC; Müller K; Ebert D
[Ad] Endereço:Zoological Institute, Basel University, Vesalgasse 1, 4051, Basel, Switzerland.
[Ti] Título:Parasitism drives host genome evolution: Insights from the Pasteuria ramosa-Daphnia magna system.
[So] Source:Evolution;71(4):1106-1113, 2017 Apr.
[Is] ISSN:1558-5646
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Because parasitism is thought to play a major role in shaping host genomes, it has been predicted that genomic regions associated with resistance to parasites should stand out in genome scans, revealing signals of selection above the genomic background. To test whether parasitism is indeed such a major factor in host evolution and to better understand host-parasite interaction at the molecular level, we studied genome-wide polymorphisms in 97 genotypes of the planktonic crustacean Daphnia magna originating from three localities across Europe. Daphnia magna is known to coevolve with the bacterial pathogen Pasteuria ramosa for which host genotypes (clonal lines) are either resistant or susceptible. Using association mapping, we identified two genomic regions involved in resistance to P. ramosa, one of which was already known from a previous QTL analysis. We then performed a naïve genome scan to test for signatures of positive selection and found that the two regions identified with the association mapping further stood out as outliers. Several other regions with evidence for selection were also found, but no link between these regions and phenotypic variation could be established. Our results are consistent with the hypothesis that parasitism is driving host genome evolution.
[Mh] Termos MeSH primário: Daphnia/genética
Daphnia/microbiologia
Evolução Molecular
Genoma
Pasteuria/fisiologia
[Mh] Termos MeSH secundário: Animais
Interações Hospedeiro-Patógeno
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170223
[St] Status:MEDLINE
[do] DOI:10.1111/evo.13209


  3 / 24976 MEDLINE  
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[PMID]:28067418
[Au] Autor:Flanagan SP; Jones AG
[Ad] Endereço:Department of Biology, Texas A&M University, College Station, TX, 77843.
[Ti] Título:Genome-wide selection components analysis in a fish with male pregnancy.
[So] Source:Evolution;71(4):1096-1105, 2017 Apr.
[Is] ISSN:1558-5646
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A major goal of evolutionary biology is to identify the genome-level targets of natural and sexual selection. With the advent of next-generation sequencing, whole-genome selection components analysis provides a promising avenue in the search for loci affected by selection in nature. Here, we implement a genome-wide selection components analysis in the sex role reversed Gulf pipefish, Syngnathus scovelli. Our approach involves a double-digest restriction-site associated DNA sequencing (ddRAD-seq) technique, applied to adult females, nonpregnant males, pregnant males, and their offspring. An F comparison of allele frequencies among these groups reveals 47 genomic regions putatively experiencing sexual selection, as well as 468 regions showing a signature of differential viability selection between males and females. A complementary likelihood ratio test identifies similar patterns in the data as the F analysis. Sexual selection and viability selection both tend to favor the rare alleles in the population. Ultimately, we conclude that genome-wide selection components analysis can be a useful tool to complement other approaches in the effort to pinpoint genome-level targets of selection in the wild.
[Mh] Termos MeSH primário: Genoma
Genômica/métodos
Polimorfismo de Nucleotídeo Único
Seleção Genética
Smegmamorpha/genética
[Mh] Termos MeSH secundário: Animais
Feminino
Frequência do Gene
Masculino
Reprodução
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170109
[St] Status:MEDLINE
[do] DOI:10.1111/evo.13173


  4 / 24976 MEDLINE  
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[PMID]:28918748
[Au] Autor:Malygin AG
[Ad] Endereço:Bach Institute of Biochemistry, Research Center of Biotechnology, Russian Academy of Sciences, Moscow, 119071, Russia. agmalygin@mail.ru.
[Ti] Título:New Data on Programmed Risks of Death in Normal Mice and Mutants with Growth Delay.
[So] Source:Biochemistry (Mosc);82(7):834-843, 2017 Jul.
[Is] ISSN:1608-3040
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Study of the lifespans of normal (non mutant) mice and growth delay mutants has shown that mortality rates for both kinds of animals exhibit reproducible fluctuations. In the case of the mutant mice, the positions of peaks on the differential mortality curves (mortality rate plotted against lifespan) coincided in different-sex groups of animals and in same-sex subgroups of animals. Differential mortality curves of the mutant mice also had a peak at 1 month of age that was absent from the differential mortality curves of the normal mice. In the case of normal animals, positions of most peaks were the same in the studied independent subgroups of males, and to a lesser extent - independent subgroups of females, which might be explained by a shift in mortality peak positions due to the reproductive activity of females. Similar positions of mortality rate peaks in the differential mortality curves for animals from independent groups and subgroups indicate the existence of increased risks of death at specific ages. The observed pattern could be due to the programming in the genome of both the periods of increased risk of death and the intermitting intervals of stable development.
[Mh] Termos MeSH primário: Genoma
Longevidade
[Mh] Termos MeSH secundário: Animais
Feminino
Longevidade/genética
Masculino
Camundongos
Reprodução
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170918
[St] Status:MEDLINE
[do] DOI:10.1134/S0006297917070094


  5 / 24976 MEDLINE  
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[PMID]:28811666
[Au] Autor:Saldivar JC; Cortez D; Cimprich KA
[Ad] Endereço:Department of Chemical and Systems Biology, Stanford University School of Medicine, 318 Campus Drive, Stanford, California 94305-5441, USA.
[Ti] Título:The essential kinase ATR: ensuring faithful duplication of a challenging genome.
[So] Source:Nat Rev Mol Cell Biol;18(10):622-636, 2017 Oct.
[Is] ISSN:1471-0080
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:One way to preserve a rare book is to lock it away from all potential sources of damage. Of course, an inaccessible book is also of little use, and the paper and ink will continue to degrade with age in any case. Like a book, the information stored in our DNA needs to be read, but it is also subject to continuous assault and therefore needs to be protected. In this Review, we examine how the replication stress response that is controlled by the kinase ataxia telangiectasia and Rad3-related (ATR) senses and resolves threats to DNA integrity so that the DNA remains available to read in all of our cells. We discuss the multiple data that have revealed an elegant yet increasingly complex mechanism of ATR activation. This involves a core set of components that recruit ATR to stressed replication forks, stimulate kinase activity and amplify ATR signalling. We focus on the activities of ATR in the control of cell cycle checkpoints, origin firing and replication fork stability, and on how proper regulation of these processes is crucial to ensure faithful duplication of a challenging genome.
[Mh] Termos MeSH primário: Proteínas Mutadas de Ataxia Telangiectasia/metabolismo
Replicação do DNA
Eucariotos/metabolismo
[Mh] Termos MeSH secundário: Animais
Genoma
Genoma Humano
Humanos
Transdução de Sinal
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 2.7.11.1 (ATR protein, human); EC 2.7.11.1 (Ataxia Telangiectasia Mutated Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170816
[St] Status:MEDLINE
[do] DOI:10.1038/nrm.2017.67


  6 / 24976 MEDLINE  
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[PMID]:28777078
[Au] Autor:Lam SD; Das S; Sillitoe I; Orengo C
[Ad] Endereço:Institute of Structural and Molecular Biology, UCL, Darwin Building, Gower Street, London WC1E 6BT, England.
[Ti] Título:An overview of comparative modelling and resources dedicated to large-scale modelling of genome sequences.
[So] Source:Acta Crystallogr D Struct Biol;73(Pt 8):628-640, 2017 Aug 01.
[Is] ISSN:2059-7983
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Computational modelling of proteins has been a major catalyst in structural biology. Bioinformatics groups have exploited the repositories of known structures to predict high-quality structural models with high efficiency at low cost. This article provides an overview of comparative modelling, reviews recent developments and describes resources dedicated to large-scale comparative modelling of genome sequences. The value of subclustering protein domain superfamilies to guide the template-selection process is investigated. Some recent cases in which structural modelling has aided experimental work to determine very large macromolecular complexes are also cited.
[Mh] Termos MeSH primário: Genoma
Genômica/métodos
Proteínas/química
[Mh] Termos MeSH secundário: Animais
Bases de Dados Genéticas
Genômica/economia
Humanos
Conformação Proteica
Proteínas/genética
Homologia Estrutural de Proteína
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170804
[St] Status:MEDLINE
[do] DOI:10.1107/S2059798317008920


  7 / 24976 MEDLINE  
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[PMID]:28708842
[Au] Autor:Casillas-Espinosa PM; Powell KL; Zhu M; Campbell CR; Maia JM; Ren Z; Jones NC; O'Brien TJ; Petrovski S
[Ad] Endereço:Department of Medicine, The Royal Melbourne Hospital, The University of Melbourne, Parkville, Victoria, Australia.
[Ti] Título:Evaluating whole genome sequence data from the Genetic Absence Epilepsy Rat from Strasbourg and its related non-epileptic strain.
[So] Source:PLoS One;12(7):e0179924, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: The Genetic Absence Epilepsy Rats from Strasbourg (GAERS) are an inbreed Wistar rat strain widely used as a model of genetic generalised epilepsy with absence seizures. As in humans, the genetic architecture that results in genetic generalized epilepsy in GAERS is poorly understood. Here we present the strain-specific variants found among the epileptic GAERS and their related Non-Epileptic Control (NEC) strain. The GAERS and NEC represent a powerful opportunity to identify neurobiological factors that are associated with the genetic generalised epilepsy phenotype. METHODS: We performed whole genome sequencing on adult epileptic GAERS and adult NEC rats, a strain derived from the same original Wistar colony. We also generated whole genome sequencing on four double-crossed (GAERS with NEC) F2 selected for high-seizing (n = 2) and non-seizing (n = 2) phenotypes. RESULTS: Specific to the GAERS genome, we identified 1.12 million single nucleotide variants, 296.5K short insertion-deletions, and 354 putative copy number variants that result in complete or partial loss/duplication of 41 genes. Of the GAERS-specific variants that met high quality criteria, 25 are annotated as stop codon gain/loss, 56 as putative essential splice sites, and 56 indels are predicted to result in a frameshift. Subsequent screening against the two F2 progeny sequenced for having the highest and two F2 progeny for having the lowest seizure burden identified only the selected Cacna1h GAERS-private protein-coding variant as exclusively co-segregating with the two high-seizing F2 rats. SIGNIFICANCE: This study highlights an approach for using whole genome sequencing to narrow down to a manageable candidate list of genetic variants in a complex genetic epilepsy animal model, and suggests utility of this sequencing design to investigate other spontaneously occurring animal models of human disease.
[Mh] Termos MeSH primário: Canais de Cálcio Tipo T/genética
Epilepsia Tipo Ausência/genética
Genoma
[Mh] Termos MeSH secundário: Animais
Encéfalo/diagnóstico por imagem
Encéfalo/metabolismo
Encéfalo/patologia
DNA/química
DNA/isolamento & purificação
DNA/metabolismo
Modelos Animais de Doenças
Eletroencefalografia
Epilepsia Tipo Ausência/patologia
Feminino
Genótipo
Sequenciamento de Nucleotídeos em Larga Escala
Masculino
Polimorfismo de Nucleotídeo Único
Ratos
Ratos Wistar
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cacna1h protein, rat); 0 (Calcium Channels, T-Type); 9007-49-2 (DNA)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170926
[Lr] Data última revisão:
170926
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170714
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179924


  8 / 24976 MEDLINE  
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[PMID]:28587593
[Au] Autor:Pedersen SH; Ferchaud AL; Bertelsen MS; Bekkevold D; Hansen MM
[Ad] Endereço:Department of Bioscience, Aarhus University, Ny Munkegade 114, DK-8000, Aarhus C, Denmark.
[Ti] Título:Low genetic and phenotypic divergence in a contact zone between freshwater and marine sticklebacks: gene flow constrains adaptation.
[So] Source:BMC Evol Biol;17(1):130, 2017 Jun 06.
[Is] ISSN:1471-2148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Distinct hybrid zones and phenotypic and genomic divergence is often observed between marine and freshwater threespine sticklebacks (Gasterosteus aculeatus). Nevertheless, cases also exist where marine-freshwater divergence is diffuse despite seemingly similar environmental settings. In order to assess what characterizes these highly different outcomes, we focused on the latter kind of system in the Odder River, Denmark. Here, a previous study based on RAD (Restriction site Associated DNA) sequencing found non-significant genome-wide differentiation between marine and freshwater sticklebacks. In the present study, we analyzed samples on a finer geographical scale. We assessed if the system should be regarded as panmictic, or if fine-scale genetic structure and local selection was present but dominated by strong migration. We also asked if specific population components, that is the two sexes and different lateral plate morphs, contributed disproportionally more to dispersal. RESULTS: We assessed variation at 96 SNPs and the Eda gene that affects lateral plate number, conducted molecular sex identification, and analyzed morphological traits. Genetic differentiation estimated by F was non-significant throughout the system. Nevertheless, spatial autocorrelation analysis suggested fine scale genetic structure with a genetic patch size of 770 m. There was no evidence for sex-biased dispersal, but full-plated individuals showed higher dispersal than low- and partial-plated individuals. The system was dominated by full-plated morphs characteristic of marine sticklebacks, but in the upstream part of the river body shape and frequency of low-plated morphs changed in the direction expected for freshwater sticklebacks. Five markers including Eda were under possible diversifying selection. However, only subtle clinal patterns were observed for traits and markers. CONCLUSIONS: We suggest that gene flow from marine sticklebacks overwhelms adaptation to freshwater conditions, but the short genetic patch size means that the effect of gene flow on the most upstream region must be indirect and occurs over generations. The occurrence of both weak unimodal and strong bimodal hybrid zones within the same species is striking. We suggest environmental and demographic factors that could determine these outcomes, but also highlight the possibility that long-term population history and the presence or absence of genomic incompatibilities could be a contributing factor.
[Mh] Termos MeSH primário: Smegmamorpha/genética
Smegmamorpha/fisiologia
[Mh] Termos MeSH secundário: Aclimatação
Animais
Dinamarca
Feminino
Água Doce
Fluxo Gênico
Variação Genética
Genoma
Masculino
Polimorfismo de Nucleotídeo Único
Rios
Água do Mar
Smegmamorpha/parasitologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170607
[St] Status:MEDLINE
[do] DOI:10.1186/s12862-017-0982-3


  9 / 24976 MEDLINE  
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[PMID]:28535375
[Au] Autor:Weiser NE; Yang DX; Feng S; Kalinava N; Brown KC; Khanikar J; Freeberg MA; Snyder MJ; Csankovszki G; Chan RC; Gu SG; Montgomery TA; Jacobsen SE; Kim JK
[Ad] Endereço:Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA; Program in Cellular and Molecular Biology, University of Michigan, Ann Arbor, MI 48109, USA.
[Ti] Título:MORC-1 Integrates Nuclear RNAi and Transgenerational Chromatin Architecture to Promote Germline Immortality.
[So] Source:Dev Cell;41(4):408-423.e7, 2017 May 22.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Germline-expressed endogenous small interfering RNAs (endo-siRNAs) transmit multigenerational epigenetic information to ensure fertility in subsequent generations. In Caenorhabditis elegans, nuclear RNAi ensures robust inheritance of endo-siRNAs and deposition of repressive H3K9me3 marks at target loci. How target silencing is maintained in subsequent generations is poorly understood. We discovered that morc-1 is essential for transgenerational fertility and acts as an effector of endo-siRNAs. Unexpectedly, morc-1 is dispensable for siRNA inheritance but is required for target silencing and maintenance of siRNA-dependent chromatin organization. A forward genetic screen identified mutations in met-1, which encodes an H3K36 methyltransferase, as potent suppressors of morc-1(-) and nuclear RNAi mutant phenotypes. Further analysis of nuclear RNAi and morc-1(-) mutants revealed a progressive, met-1-dependent enrichment of H3K36me3, suggesting that robust fertility requires repression of MET-1 activity at nuclear RNAi targets. Without MORC-1 and nuclear RNAi, MET-1-mediated encroachment of euchromatin leads to detrimental decondensation of germline chromatin and germline mortality.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/metabolismo
Caenorhabditis elegans/metabolismo
Cromatina/metabolismo
Células Germinativas/metabolismo
Padrões de Herança/genética
Proteínas Nucleares/metabolismo
Interferência de RNA
[Mh] Termos MeSH secundário: Animais
Núcleo Celular/metabolismo
Genoma
Células Germinativas/citologia
Heterocromatina/metabolismo
Histonas/metabolismo
Lisina/metabolismo
Metilação
Modelos Biológicos
Mutação/genética
RNA Interferente Pequeno/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Chromatin); 0 (Heterochromatin); 0 (Histones); 0 (MORC-1 protein, C elegans); 0 (Nuclear Proteins); 0 (RNA, Small Interfering); K3Z4F929H6 (Lysine)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE


  10 / 24976 MEDLINE  
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[PMID]:28535374
[Au] Autor:Liu H; Dowdle JA; Khurshid S; Sullivan NJ; Bertos N; Rambani K; Mair M; Daniel P; Wheeler E; Tang X; Toth K; Lause M; Harrigan ME; Eiring K; Sullivan C; Sullivan MJ; Chang SW; Srivastava S; Conway JS; Kladney R; McElroy J; Bae S; Lu Y; Tofigh A; Saleh SMI; Fernandez SA; Parvin JD; Coppola V; Macrae ER; Majumder S; Shapiro CL; Yee LD; Ramaswamy B; Hallett M; Ostrowski MC; Park M; Chamberlin HM; Leone G
[Ad] Endereço:Solid Tumor Biology Program, Comprehensive Cancer Center, The Ohio State University, Columbus, OH 43210, USA; Department of Molecular Genetics, The Ohio State University, 484 West 12th Avenue, Columbus, OH 43210, USA; Department of Cancer Biology and Genetics, McGill University, Montreal, QC H3A 1A1
[Ti] Título:Discovery of Stromal Regulatory Networks that Suppress Ras-Sensitized Epithelial Cell Proliferation.
[So] Source:Dev Cell;41(4):392-407.e6, 2017 May 22.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesodermal cells signal to neighboring epithelial cells to modulate their proliferation in both normal and disease states. We adapted a Caenorhabditis elegans organogenesis model to enable a genome-wide mesodermal-specific RNAi screen and discovered 39 factors in mesodermal cells that suppress the proliferation of adjacent Ras pathway-sensitized epithelial cells. These candidates encode components of protein complexes and signaling pathways that converge on the control of chromatin dynamics, cytoplasmic polyadenylation, and translation. Stromal fibroblast-specific deletion of mouse orthologs of several candidates resulted in the hyper-proliferation of mammary gland epithelium. Furthermore, a 33-gene signature of human orthologs was selectively enriched in the tumor stroma of breast cancer patients, and depletion of these factors from normal human breast fibroblasts increased proliferation of co-cultured breast cancer cells. This cross-species approach identified unanticipated regulatory networks in mesodermal cells with growth-suppressive function, exposing the conserved and selective nature of mesodermal-epithelial communication in development and cancer.
[Mh] Termos MeSH primário: Células Epiteliais/citologia
Células Epiteliais/metabolismo
Redes Reguladoras de Genes
Proteínas ras/metabolismo
[Mh] Termos MeSH secundário: Animais
Neoplasias da Mama/genética
Neoplasias da Mama/patologia
Caenorhabditis elegans/citologia
Caenorhabditis elegans/metabolismo
Proteínas de Caenorhabditis elegans/metabolismo
Linhagem da Célula
Proliferação de Células
Feminino
Fibroblastos/metabolismo
Fibroblastos/patologia
Perfilação da Expressão Gênica
Genoma
Humanos
Glândulas Mamárias Animais/citologia
Mesoderma/metabolismo
Camundongos
Mutação/genética
Proteínas Nucleares
Especificidade de Órgãos
Fenótipo
Proteínas Quinases
Proteínas Serina-Treonina Quinases/metabolismo
Interferência de RNA
Transdução de Sinal/genética
Células Estromais/citologia
Células Estromais/metabolismo
Proteínas Ativadoras de ras GTPase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (GAP-1 protein, C elegans); 0 (Nuclear Proteins); 0 (ras GTPase-Activating Proteins); EC 2.7.- (Protein Kinases); EC 2.7.1.- (Tlk1 protein, mouse); EC 2.7.1.- (protein kinase U); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.6.5.2 (ras Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170927
[Lr] Data última revisão:
170927
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170523
[St] Status:MEDLINE



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