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[PMID]:29111207
[Au] Autor:Oczkowicz M; Szmatola T; Piórkowska K; Ropka-Molik K
[Ad] Endereço:National Research Institute of Animal Production, Department of Genomics and Molecular Biology of Animals, Krakowska 1, 32-083 Balice, Poland. Electronic address: maria.oczkowicz@izoo.krakow.pl.
[Ti] Título:Variant calling from RNA-seq data of the brain transcriptome of pigs and its application for allele-specific expression and imprinting analysis.
[So] Source:Gene;641:367-375, 2018 Jan 30.
[Is] ISSN:1879-0038
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Identification of new polymorphic variants from RNA-seq data is difficult mainly because of the errors arising during bioinformatic analysis. Therefore, new experiments in this area are very profitable for improving new statistical methods. In our study of the porcine brain transcriptome, we have identified 10966 polymorphic variants, among which 7277 were single nucleotide polymorphisms (SNPs). Further, we have calculated allelic ratios for the SNPs identified and estimated that 52% of genes in porcine brain are subjected to allele-specific expression (ASE), a phenomenon in which one allele is preferentially expressed. Our investigation presents the first estimates of ASE in porcine brain. In addition, we have used the results of RNA-seq for the identification of SNPs in putatively imprinted genes. Finally, we have used these SNPs for the verification of the imprinted status of the INPP5f variant 2, LRRTM1 and HM13 genes in pigs by Sanger sequencing. We observed that INPP5f variant 2 is paternally expressed, while HM13 and LRRTM1 are biallelically expressed in porcine brain. We have also confirmed maternal expression of the MEG3 gene in pigs. Our results present how RNA-seq data may be used for imprinting studies without sequencing of parental genomes.
[Mh] Termos MeSH primário: Encéfalo/fisiologia
Expressão Gênica/genética
Impressão Genômica/genética
Polimorfismo de Nucleotídeo Único/genética
[Mh] Termos MeSH secundário: Alelos
Animais
Feminino
Inositol Polifosfato 5-Fosfatases/genética
Masculino
Proteínas de Membrana/genética
Análise de Sequência de RNA/métodos
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Membrane Proteins); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171108
[St] Status:MEDLINE


  2 / 610 MEDLINE  
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[PMID]:28669993
[Au] Autor:De Matteis MA; Staiano L; Emma F; Devuyst O
[Ad] Endereço:Telethon Institute of Genetics and Medicine, Via Campi Flegrei 34, 80078, Pozzuoli, Italy.
[Ti] Título:The 5-phosphatase OCRL in Lowe syndrome and Dent disease 2.
[So] Source:Nat Rev Nephrol;13(8):455-470, 2017 Aug.
[Is] ISSN:1759-507X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Lowe syndrome is an X-linked disease that is characterized by congenital cataracts, central hypotonia, intellectual disability and renal Fanconi syndrome. The disease is caused by mutations in OCRL, which encodes an inositol polyphosphate 5-phosphatase (OCRL) that acts on phosphoinositides - quantitatively minor constituents of cell membranes that are nonetheless pivotal regulators of intracellular trafficking. In this Review we summarize the considerable progress made over the past decade in understanding the cellular roles of OCRL in regulating phosphoinositide balance along the endolysosomal pathway, a fundamental system for the reabsorption of proteins and solutes by proximal tubular cells. We discuss how studies of OCRL have led to important discoveries about the basic mechanisms of membrane trafficking and describe the key features and limitations of the currently available animal models of Lowe syndrome. Mutations in OCRL can also give rise to a milder pathology, Dent disease 2, which is characterized by renal Fanconi syndrome in the absence of extrarenal pathologies. Understanding how mutations in OCRL give rise to two clinical entities with differing extrarenal manifestations represents an opportunity to identify molecular pathways that could be targeted to develop treatments for these conditions.
[Mh] Termos MeSH primário: Doenças Genéticas Ligadas ao Cromossomo X/genética
Mutação
Nefrolitíase/genética
Síndrome Oculocerebrorrenal/genética
Monoéster Fosfórico Hidrolases/genética
[Mh] Termos MeSH secundário: Animais
Vesículas Revestidas por Clatrina
Modelos Animais de Doenças
Endocitose
Seres Humanos
Inositol Polifosfato 5-Fosfatases/genética
Túbulos Renais Proximais/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.36 (OCRL protein, human); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170704
[St] Status:MEDLINE
[do] DOI:10.1038/nrneph.2017.83


  3 / 610 MEDLINE  
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[PMID]:27719911
[Au] Autor:Jin X; Yang R; Guo L; Wang X; Yan X; Gu Z
[Ad] Endereço:College of Food Science and Technology, Nanjing Agricultural University, Nanjing, Jiangsu 210095, People's Republic of China; College of Life Science, Shandong Normal University, Jinan 250000, People's Republic of China. Electronic address: 2013208009@njau.edu.cn.
[Ti] Título:iTRAQ analysis of low-phytate mung bean sprouts treated with sodium citrate, sodium acetate and sodium tartrate.
[So] Source:Food Chem;218:285-293, 2017 Mar 01.
[Is] ISSN:0308-8146
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The effects of sodium citrate (SC), sodium acetate (SA) and sodium tartrate (ST) spraying on mung bean germination were investigated. Exogenous SC, ST and SA treatments significantly reduced the phytic acid content and increased the antioxidant enzyme activities. In this study, an iTRAQ-based proteomic approach was employed to explore the proteomes of mung bean sprouts, and 81, 101 and 90 differentially expressed proteins were identified in 4-day-old SC-, SA- and ST-treated mung bean sprouts, with 38 proteins present in all samples. Functional classification analysis showed that most of the differentially expressed proteins in mung bean sprouts subjected to the three treatments were involved in carbohydrate and energy metabolism. The inhibitory effect of the SA treatment was probably due to impairments in protein biosynthesis, whereas enhanced energy metabolism, accelerated reserve hydrolysis and protein processing were very important strategies for growth stimulation in response to ST and SC treatments.
[Mh] Termos MeSH primário: Citratos/química
Regulação da Expressão Gênica de Plantas
Ácido Fítico/análise
Acetato de Sódio/química
Tartaratos/química
Vigna/metabolismo
[Mh] Termos MeSH secundário: Fosfatase Ácida/genética
Fosfatase Ácida/metabolismo
Aditivos Alimentares/química
Manipulação de Alimentos
Glicoproteínas/genética
Glicoproteínas/metabolismo
Inositol Polifosfato 5-Fosfatases/genética
Inositol Polifosfato 5-Fosfatases/metabolismo
Proteínas de Plantas/genética
Proteínas de Plantas/metabolismo
Biossíntese de Proteínas/efeitos dos fármacos
Proteômica
Regulação para Cima
Vigna/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Citrates); 0 (Food Additives); 0 (Glycoproteins); 0 (Plant Proteins); 0 (Tartrates); 1Q73Q2JULR (sodium citrate); 4550K0SC9B (Sodium Acetate); 7IGF0S7R8I (Phytic Acid); EC 3.1.3.- (purple acid phosphatase); EC 3.1.3.2 (Acid Phosphatase); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases); W4888I119H (tartaric acid)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:171008
[Lr] Data última revisão:
171008
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161011
[St] Status:MEDLINE


  4 / 610 MEDLINE  
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[PMID]:27063899
[Au] Autor:Niwa F; Bannai H; Mikoshiba K
[Ti] Título:[Stabilization of GABAAR synaptic structure by IP3-induced calcium release].
[So] Source:Nihon Yakurigaku Zasshi;147(4):184-9, 2016 Apr.
[Is] ISSN:0015-5691
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Mh] Termos MeSH primário: Cálcio/metabolismo
Monoéster Fosfórico Hidrolases/metabolismo
Receptores de GABA-A/metabolismo
Sinapses/metabolismo
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio
Inositol Polifosfato 5-Fosfatases
Fosforilação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Receptors, GABA-A); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:161126
[Lr] Data última revisão:
161126
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160412
[St] Status:MEDLINE
[do] DOI:10.1254/fpj.147.184


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[PMID]:27063844
[Au] Autor:Fansa EK; Kösling SK; Zent E; Wittinghofer A; Ismail S
[Ad] Endereço:Max Planck Institute of Molecular Physiology, Otto-Hahn-Strasse 11, 44227 Dortmund, Germany.
[Ti] Título:PDE6δ-mediated sorting of INPP5E into the cilium is determined by cargo-carrier affinity.
[So] Source:Nat Commun;7:11366, 2016 Apr 11.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The phosphodiesterase 6 delta subunit (PDE6δ) shuttles several farnesylated cargos between membranes. The cargo sorting mechanism between cilia and other compartments is not understood. Here we show using the inositol polyphosphate 5'-phosphatase E (INPP5E) and the GTP-binding protein (Rheb) that cargo sorting depends on the affinity towards PDE6δ and the specificity of cargo release. High-affinity cargo is exclusively released by the ciliary transport regulator Arl3, while low-affinity cargo is released by Arl3 and its non-ciliary homologue Arl2. Structures of PDE6δ/cargo complexes reveal the molecular basis of the sorting signal which depends on the residues at the -1 and -3 positions relative to farnesylated cysteine. Structure-guided mutation allows the generation of a low-affinity INPP5E mutant which loses exclusive ciliary localization. We postulate that the affinity to PDE6δ and the release by Arl2/3 in addition to a retention signal are the determinants for cargo sorting and enrichment at its destination.
[Mh] Termos MeSH primário: Cílios/metabolismo
Nucleotídeo Cíclico Fosfodiesterase do Tipo 6/metabolismo
Monoéster Fosfórico Hidrolases/metabolismo
[Mh] Termos MeSH secundário: Fatores de Ribosilação do ADP/química
Fatores de Ribosilação do ADP/metabolismo
Animais
Linhagem Celular
Polarização de Fluorescência
Proteínas de Fluorescência Verde/metabolismo
Guanosina Trifosfato/metabolismo
Inositol Polifosfato 5-Fosfatases
Cinética
Camundongos
Modelos Biológicos
Proteínas Monoméricas de Ligação ao GTP/metabolismo
Proteínas Mutantes/metabolismo
Neuropeptídeos/metabolismo
Ligação Proteica
Prenilação de Proteína
Sinais Direcionadores de Proteínas
Estrutura Secundária de Proteína
Transporte Proteico
Proteína Enriquecida em Homólogo de Ras do Encéfalo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Mutant Proteins); 0 (Neuropeptides); 0 (Protein Sorting Signals); 0 (Ras Homolog Enriched in Brain Protein); 0 (Rheb protein, mouse); 147336-22-9 (Green Fluorescent Proteins); 86-01-1 (Guanosine Triphosphate); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases); EC 3.1.4.35 (Cyclic Nucleotide Phosphodiesterases, Type 6); EC 3.6.1.2 (Arl3 protein, mouse); EC 3.6.5.2 (ADP-Ribosylation Factors); EC 3.6.5.2 (Monomeric GTP-Binding Proteins)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160412
[St] Status:MEDLINE
[do] DOI:10.1038/ncomms11366


  6 / 610 MEDLINE  
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[PMID]:26908121
[Au] Autor:Bai D; Zhang Y; Shen M; Sun Y; Xia Q; Zhang Y; Liu X; Wang H; Yuan L
[Ad] Endereço:Department of Cardiology, Xijing Hospital, the Fourth Military Medical University, Xi'an 710032, China.
[Ti] Título:Hyperglycemia and hyperlipidemia blunts the Insulin-Inpp5f negative feedback loop in the diabetic heart.
[So] Source:Sci Rep;6:22068, 2016 Feb 24.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The leading cause of death in diabetic patients is diabetic cardiomyopathy, in which alteration of Akt signal plays an important role. Inpp5f is recently found to be a negative regulator of Akt signaling, while its expression and function in diabetic heart is largely unknown. In this study, we found that in both the streptozotocin (STZ) and high fat diet (HFD) induced diabetic mouse models, Inpp5f expression was coordinately regulated by insulin, blood glucose and lipid levels. Increased Inpp5f was inversely correlated with the cardiac function. Further studies revealed that Insulin transcriptionally activated Inpp5f in an Sp1 dependent manner, and increased Inpp5f in turn reduced the phosphorylation of Akt, forming a negative feedback loop. The negative feedback plays a protective role under diabetic condition. However, high blood glucose and lipid, which are characteristics of uncontrolled diabetes and type 2 diabetes, increased Inpp5f expression through activation of NF-κB, blunts the protective feedback. Thus, our study has revealed that Inpp5f provides as a negative feedback regulator of insulin signaling and downregulation of Inpp5f in diabetes is cardioprotective. Increased Inpp5f by hyperglycemia and hyperlipidemia is an important mediator of diabetic cardiomyopathy and is a promising therapeutic target for the disease.
[Mh] Termos MeSH primário: Diabetes Mellitus Experimental/genética
Cardiomiopatias Diabéticas/genética
Hiperglicemia/genética
Hiperlipidemias/genética
Inositol Polifosfato 5-Fosfatases/genética
Insulina/genética
Miocárdio/metabolismo
[Mh] Termos MeSH secundário: Animais
Glicemia/metabolismo
Colesterol/sangue
Diabetes Mellitus Experimental/sangue
Diabetes Mellitus Experimental/etiologia
Diabetes Mellitus Experimental/patologia
Diabetes Mellitus Tipo 2/sangue
Diabetes Mellitus Tipo 2/genética
Diabetes Mellitus Tipo 2/patologia
Cardiomiopatias Diabéticas/sangue
Cardiomiopatias Diabéticas/etiologia
Cardiomiopatias Diabéticas/patologia
Dieta Hiperlipídica/efeitos adversos
Retroalimentação Fisiológica
Regulação da Expressão Gênica
Seres Humanos
Hiperglicemia/sangue
Hiperglicemia/patologia
Hiperlipidemias/sangue
Hiperlipidemias/patologia
Inositol Polifosfato 5-Fosfatases/sangue
Insulina/sangue
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Miocárdio/patologia
NF-kappa B/sangue
NF-kappa B/genética
Proteínas Proto-Oncogênicas c-akt/sangue
Proteínas Proto-Oncogênicas c-akt/genética
Transdução de Sinais
Fator de Transcrição Sp1/sangue
Fator de Transcrição Sp1/genética
Estreptozocina
Triglicerídeos/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Blood Glucose); 0 (Insulin); 0 (NF-kappa B); 0 (Sp1 Transcription Factor); 0 (Triglycerides); 5W494URQ81 (Streptozocin); 97C5T2UQ7J (Cholesterol); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases); EC 3.1.3.56 (Inpp5f protein, mouse)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160225
[St] Status:MEDLINE
[do] DOI:10.1038/srep22068


  7 / 610 MEDLINE  
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[PMID]:26862211
[Au] Autor:Eramo MJ; Mitchell CA
[Ad] Endereço:Department of Biochemistry and Molecular Biology, Monash University, Clayton, VIC 3800, Australia.
[Ti] Título:Regulation of PtdIns(3,4,5)P3/Akt signalling by inositol polyphosphate 5-phosphatases.
[So] Source:Biochem Soc Trans;44(1):240-52, 2016 Feb.
[Is] ISSN:1470-8752
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The phosphoinositide 3-kinase (PI3K) generated lipid signals, PtdIns(3,4,5)P3 and PtdIns(3,4)P2, are both required for the maximal activation of the serine/threonine kinase proto-oncogene Akt. The inositol polyphosphate 5-phosphatases (5-phosphatases) hydrolyse the 5-position phosphate from the inositol head group of PtdIns(3,4,5)P3 to yield PtdIns(3,4)P2. Extensive work has revealed several 5-phosphatases inhibit PI3K-driven Akt signalling, by decreasing PtdIns(3,4,5)P3 despite increasing cellular levels of PtdIns(3,4)P2. The roles that 5-phosphatases play in suppressing cell proliferation and transformation are slow to emerge; however, the 5-phosphatase PIPP [proline-rich inositol polyphosphate 5-phosphatase; inositol polyphosphate 5-phosphatase (INPP5J)] has recently been identified as a putative tumour suppressor in melanoma and breast cancer and SHIP1 [SH2 (Src homology 2)-containing inositol phosphatase 1] inhibits haematopoietic cell proliferation. INPP5E regulates cilia stability and INPP5E mutations have been implicated ciliopathy syndromes. This review will examine 5-phosphatase regulation of PI3K/Akt signalling, focussing on the role PtdIns(3,4,5)P3 5-phosphatases play in developmental diseases and cancer.
[Mh] Termos MeSH primário: Fosfatos de Fosfatidilinositol/metabolismo
Monoéster Fosfórico Hidrolases/metabolismo
Proteínas Proto-Oncogênicas c-akt/metabolismo
Transdução de Sinais
[Mh] Termos MeSH secundário: Animais
Cílios/metabolismo
Seres Humanos
Inositol Polifosfato 5-Fosfatases
Especificidade de Órgãos
Fosfatidilinositol-3,4,5-Trifosfato 5-Fosfatases
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Phosphatidylinositol Phosphates); 0 (phosphatidylinositol 3,4,5-triphosphate); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases); EC 3.1.3.86 (INPP5D protein, human); EC 3.1.3.86 (Phosphatidylinositol-3,4,5-Trisphosphate 5-Phosphatases)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:170103
[Lr] Data última revisão:
170103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160211
[St] Status:MEDLINE
[do] DOI:10.1042/BST20150214


  8 / 610 MEDLINE  
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[PMID]:26767748
[Au] Autor:Avila LM; Cerrudo D; Swanton C; Lukens L
[Ad] Endereço:Department of Plant Agriculture, University of Guelph, 50 Stone Road East, Guelph, Ontario N1G 2W1, Canada.
[Ti] Título:Brevis plant1, a putative inositol polyphosphate 5-phosphatase, is required for internode elongation in maize.
[So] Source:J Exp Bot;67(5):1577-88, 2016 Mar.
[Is] ISSN:1460-2431
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In maize (Zea mays L.), as in other grass species, stem elongation occurs during growth and most noticeably upon the transition to flowering. Genes that reduce stem elongation have been important to reduce stem breakage, or lodging. Stem elongation has been mediated by dwarf and brachytic/brevis plant mutants that affect giberellic acid and auxin pathways, respectively. Maize brevis plant1 (bv1) mutants, first identified over 80 years ago, strongly resemble brachytic2 mutants that have shortened internodes, short internode cells, and are deficient in auxin transport. Here, we characterized two novel bv1 maize mutants. We found that an inositol polyphosphate 5-phosphatase orthologue of the rice gene dwarf50 was the molecular basis for the bv1 phenotype, implicating auxin-mediated inositol polyphosphate and/or phosphoinositide signalling in stem elongation. We suggest that auxin-mediated internode elongation involves processes that also contribute to stem gravitropism. Genes misregulated in bv1 mutants included genes important for cell wall synthesis, transmembrane transport, and cytoskeletal function. Mutant and wild-type plants were indistinguishable early in development, responded similarly to changes in light quality, had unaltered flowering times, and had normal flower development. These attributes suggest that breeding could utilize bv1 alleles to increase crop grain yields.
[Mh] Termos MeSH primário: Genes de Plantas
Inositol Polifosfato 5-Fosfatases/metabolismo
Proteínas de Plantas/metabolismo
Caules de Planta/crescimento & desenvolvimento
Zea mays/enzimologia
Zea mays/genética
[Mh] Termos MeSH secundário: Alelos
Arabidopsis/metabolismo
Regulação da Expressão Gênica de Plantas
Loci Gênicos
Mutação/genética
Fenótipo
Proteínas de Plantas/genética
Polimorfismo de Nucleotídeo Único/genética
Zea mays/anatomia & histologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Plant Proteins); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160116
[St] Status:MEDLINE
[do] DOI:10.1093/jxb/erv554


  9 / 610 MEDLINE  
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[PMID]:26751515
[Au] Autor:Xiong D; Xiao S; Guo S; Lin Q; Nakatsu F; Wu M
[Ad] Endereço:Mechanobiology Institute, National University of Singapore, Singapore.
[Ti] Título:Frequency and amplitude control of cortical oscillations by phosphoinositide waves.
[So] Source:Nat Chem Biol;12(3):159-66, 2016 Mar.
[Is] ISSN:1552-4469
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Rhythmicity is prevalent in the cortical dynamics of diverse single and multicellular systems. Current models of cortical oscillations focus primarily on cytoskeleton-based feedbacks, but information on signals upstream of the actin cytoskeleton is limited. In addition, inhibitory mechanisms--especially local inhibitory mechanisms, which ensure proper spatial and kinetic controls of activation--are not well understood. Here, we identified two phosphoinositide phosphatases, synaptojanin 2 and SHIP1, that function in periodic traveling waves of rat basophilic leukemia (RBL) mast cells. The local, phase-shifted activation of lipid phosphatases generates sequential waves of phosphoinositides. By acutely perturbing phosphoinositide composition using optogenetic methods, we showed that pulses of PtdIns(4,5)P2 regulate the amplitude of cyclic membrane waves while PtdIns(3,4)P2 sets the frequency. Collectively, these data suggest that the spatiotemporal dynamics of lipid metabolism have a key role in governing cortical oscillations and reveal how phosphatidylinositol 3-kinases (PI3K) activity could be frequency-encoded by a phosphatase-dependent inhibitory reaction.
[Mh] Termos MeSH primário: Córtex Cerebral/metabolismo
Córtex Cerebral/fisiologia
Fosfatidilinositóis/metabolismo
Fosfatidilinositóis/fisiologia
[Mh] Termos MeSH secundário: Actinas/genética
Animais
Linhagem Celular Tumoral
Citoesqueleto/genética
Inositol Polifosfato 5-Fosfatases
Cinética
Leucemia Basofílica Aguda/patologia
Metabolismo dos Lipídeos/fisiologia
Mastócitos/metabolismo
Proteínas do Tecido Nervoso/genética
Fosfatidilinositol 3-Quinases/metabolismo
Fosfatidilinositol 4,5-Difosfato/metabolismo
Fosfatos de Fosfatidilinositol/metabolismo
Monoéster Fosfórico Hidrolases/genética
Monoéster Fosfórico Hidrolases/metabolismo
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (Nerve Tissue Proteins); 0 (Phosphatidylinositol 4,5-Diphosphate); 0 (Phosphatidylinositol Phosphates); 0 (Phosphatidylinositols); 0 (phosphatidylinositol 3,4-diphosphate); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 3.1.3.- (synaptojanin); EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases)
[Em] Mês de entrada:1607
[Cu] Atualização por classe:170603
[Lr] Data última revisão:
170603
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160112
[St] Status:MEDLINE
[do] DOI:10.1038/nchembio.2000


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[PMID]:26683227
[Au] Autor:Hamilton MJ; Halvorsen EC; LePard NE; Bosiljcic M; Ho VW; Lam V; Banáth J; Bennewith KL; Krystal G
[Ad] Endereço:Department of Integrative Oncology, British Columbia Cancer Agency Research Centre, Vancouver, BC, Canada.
[Ti] Título:SHIP represses lung inflammation and inhibits mammary tumor metastasis in BALB/c mice.
[So] Source:Oncotarget;7(4):3677-91, 2016 Jan 26.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:SH2-containing-inositol-5'-phosphatase (SHIP) is a negative regulator of the phosphatidylinositol-3-kinase pathway in hematopoietic cells and limits the development of leukemias and lymphomas. The potential role of SHIP in solid tumor development and metastasis remains unknown. While SHIP restricts the aberrant development of myeloid cells in C57BL/6 mice, there are conflicting reports regarding the effect of SHIP deletion in BALB/c mice with important consequences for determining the influence of SHIP in different model tumor systems. We generated SHIP-/- BALB/c mice and challenged them with syngeneic non-metastatic 67NR or metastatic 4T1 mammary tumors. We demonstrate that SHIP restricts the development, alternative-activation, and immunosuppressive function of myeloid cells in tumor-free and tumor-bearing BALB/c mice. Tumor-free SHIP-/- BALB/c mice exhibited pulmonary inflammation, myeloid hyperplasia, and M2-polarized macrophages and this phenotype was greatly exacerbated by 4T1, but not 67NR, tumors. 4T1-bearing SHIP-/- mice rapidly lost weight and died from necrohemorrhagic inflammatory pulmonary disease, characterized by massive infiltration of pulmonary macrophages and myeloid-derived suppressor cells that were more M2-polarized and immunosuppressive than wild-type cells. Importantly, while SHIP loss did not affect primary tumor growth, 4T1-bearing SHIP-/- mice had 7.5-fold more metastatic tumor cells in their lungs than wild-type mice, consistent with the influence of immunosuppressive myeloid cells on metastatic growth. Our findings identify the hematopoietic cell-restricted protein SHIP as an intriguing target to influence the development of solid tumor metastases, and support development of SHIP agonists to prevent the accumulation of immunosuppressive myeloid cells and tumor metastases in the lungs to improve treatment of metastatic breast cancer.
[Mh] Termos MeSH primário: Neoplasias Pulmonares/prevenção & controle
Neoplasias Mamárias Experimentais/prevenção & controle
Monoéster Fosfórico Hidrolases/fisiologia
Pneumonia/prevenção & controle
[Mh] Termos MeSH secundário: Animais
Apoptose
Western Blotting
Proliferação Celular
Feminino
Seres Humanos
Técnicas Imunoenzimáticas
Inositol Polifosfato 5-Fosfatases
Neoplasias Pulmonares/genética
Neoplasias Pulmonares/secundário
Macrófagos/metabolismo
Macrófagos/patologia
Neoplasias Mamárias Experimentais/genética
Neoplasias Mamárias Experimentais/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C3H
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Mieloides/metabolismo
Células Mieloides/patologia
Pneumonia/genética
Pneumonia/patologia
Células Tumorais Cultivadas
Ensaios Antitumorais Modelo de Xenoenxerto
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
EC 3.1.3.2 (Phosphoric Monoester Hydrolases); EC 3.1.3.56 (Inositol Polyphosphate 5-Phosphatases)
[Em] Mês de entrada:1611
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151220
[St] Status:MEDLINE
[do] DOI:10.18632/oncotarget.6611



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