Base de dados : MEDLINE
Pesquisa : A11.284.149.165 [Categoria DeCS]
Referências encontradas : 416 [refinar]
Mostrando: 1 .. 10   no formato [Detalhado]

página 1 de 42 ir para página                         

  1 / 416 MEDLINE  
              next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:29173819
[Au] Autor:Goudarzi M; Tarbashevich K; Mildner K; Begemann I; Garcia J; Paksa A; Reichman-Fried M; Mahabaleshwar H; Blaser H; Hartwig J; Zeuschner D; Galic M; Bagnat M; Betz T; Raz E
[Ad] Endereço:Institute for Cell Biology, ZMBE, Von-Esmarch-Strasse 56, 48149 Münster, Germany.
[Ti] Título:Bleb Expansion in Migrating Cells Depends on Supply of Membrane from Cell Surface Invaginations.
[So] Source:Dev Cell;43(5):577-587.e5, 2017 Dec 04.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell migration is essential for morphogenesis, organ formation, and homeostasis, with relevance for clinical conditions. The migration of primordial germ cells (PGCs) is a useful model for studying this process in the context of the developing embryo. Zebrafish PGC migration depends on the formation of cellular protrusions in form of blebs, a type of protrusion found in various cell types. Here we report on the mechanisms allowing the inflation of the membrane during bleb formation. We show that the rapid expansion of the protrusion depends on membrane invaginations that are localized preferentially at the cell front. The formation of these invaginations requires the function of Cdc42, and their unfolding allows bleb inflation and dynamic cell-shape changes performed by migrating cells. Inhibiting the formation and release of the invaginations strongly interfered with bleb formation, cell motility, and the ability of the cells to reach their target.
[Mh] Termos MeSH primário: Membrana Celular/metabolismo
Movimento Celular/fisiologia
Forma Celular/fisiologia
Células Germinativas/citologia
Peixe-Zebra
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Estruturas da Membrana Celular/metabolismo
Extensões da Superfície Celular/metabolismo
Células Germinativas/metabolismo
Peixe-Zebra/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180104
[Lr] Data última revisão:
180104
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


  2 / 416 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28468978
[Au] Autor:Valdivia A; Goicoechea SM; Awadia S; Zinn A; Garcia-Mata R
[Ad] Endereço:Department of Biological Sciences, University of Toledo, Toledo, OH 43606.
[Ti] Título:Regulation of circular dorsal ruffles, macropinocytosis, and cell migration by RhoG and its exchange factor, Trio.
[So] Source:Mol Biol Cell;28(13):1768-1781, 2017 Jul 01.
[Is] ISSN:1939-4586
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Circular dorsal ruffles (CDRs) are actin-rich structures that form on the dorsal surface of many mammalian cells in response to growth factor stimulation. CDRs represent a unique type of structure that forms transiently and only once upon stimulation. The formation of CDRs involves a drastic rearrangement of the cytoskeleton, which is regulated by the Rho family of GTPases. So far, only Rac1 has been consistently associated with CDR formation, whereas the role of other GTPases in this process is either lacking or inconclusive. Here we show that RhoG and its exchange factor, Trio, play a role in the regulation of CDR dynamics, particularly by modulating their size. RhoG is activated by Trio downstream of PDGF in a PI3K- and Src-dependent manner. Silencing RhoG expression decreases the number of cells that form CDRs, as well as the area of the CDRs. The regulation of CDR area by RhoG is independent of Rac1 function. In addition, our results show the RhoG plays a role in the cellular functions associated with CDR formation, including macropinocytosis, receptor internalization, and cell migration. Taken together, our results reveal a novel role for RhoG in the regulation of CDRs and the cellular processes associated with their formation.
[Mh] Termos MeSH primário: Fatores de Troca do Nucleotídeo Guanina/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas rho de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Linhagem Celular
Estruturas da Membrana Celular/metabolismo
Estruturas da Membrana Celular/fisiologia
Movimento Celular/fisiologia
Citoesqueleto/metabolismo
Seres Humanos
Microtúbulos/metabolismo
Fosfatidilinositol 3-Quinases/metabolismo
Pinocitose/fisiologia
Ratos
Proteínas rac1 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Guanine Nucleotide Exchange Factors); 147605-13-8 (RHOG protein, human); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 2.7.11.1 (TRIO protein, human); EC 3.6.5.2 (rac1 GTP-Binding Protein); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1091/mbc.E16-06-0412


  3 / 416 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28774893
[Au] Autor:Hinojosa LS; Holst M; Baarlink C; Grosse R
[Ad] Endereço:Institute of Pharmacology, Biochemisch-Pharmakologisches Centrum Marburg, University of Marburg, Marburg, Germany.
[Ti] Título:MRTF transcription and Ezrin-dependent plasma membrane blebbing are required for entotic invasion.
[So] Source:J Cell Biol;216(10):3087-3095, 2017 Oct 02.
[Is] ISSN:1540-8140
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Entosis is a nonapoptotic form of cell death initiated by actomyosin-dependent homotypic cell-in-cell invasion that can be observed in malignant exudates during tumor progression. We previously demonstrated formin-mediated actin dynamics at the rear of the invading cell as well as nonapoptotic plasma membrane (PM) blebbing in this cellular motile process. Although the contractile actin cortex involved in bleb-driven motility is well characterized, a role for transcriptional regulation in this process has not been studied. Here, we explore the impact of the actin-controlled MRTF-SRF (myocardin-related transcription factor-serum response factor) pathway for sustained PM blebbing and entotic invasion. We find that cortical blebbing is tightly coupled to MRTF nuclear shuttling to promote the SRF transcriptional activity required for entosis. Furthermore, PM blebbing triggered SRF-mediated up-regulation of the metastasis-associated ERM protein Ezrin. Notably, Ezrin is sufficient and important to sustain bleb dynamics for cell-in-cell invasion when SRF is suppressed. Our results highlight the critical role of the actin-regulated MRTF transcriptional pathway for bleb-associated invasive motility, such as during entosis.
[Mh] Termos MeSH primário: Estruturas da Membrana Celular/metabolismo
Proteínas do Citoesqueleto/biossíntese
Entose/fisiologia
Transativadores/metabolismo
Transcrição Genética/fisiologia
Regulação para Cima/fisiologia
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Estruturas da Membrana Celular/genética
Proteínas do Citoesqueleto/genética
Seres Humanos
Fator de Resposta Sérica/genética
Fator de Resposta Sérica/metabolismo
Transativadores/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cytoskeletal Proteins); 0 (MKL1 protein, human); 0 (SRF protein, human); 0 (Serum Response Factor); 0 (Trans-Activators); 0 (ezrin)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170805
[St] Status:MEDLINE
[do] DOI:10.1083/jcb.201702010


  4 / 416 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28079896
[Au] Autor:Chen TL; Yang HC; Hung CY; Ou MH; Pan YY; Cheng ML; Stern A; Lo SJ; Chiu DT
[Ad] Endereço:Graduate Institute of Biomedical Sciences, College of Medicine, Chang Gung University, Taoyuan, Taiwan.
[Ti] Título:Impaired embryonic development in glucose-6-phosphate dehydrogenase-deficient Caenorhabditis elegans due to abnormal redox homeostasis induced activation of calcium-independent phospholipase and alteration of glycerophospholipid metabolism.
[So] Source:Cell Death Dis;8(1):e2545, 2017 Jan 12.
[Is] ISSN:2041-4889
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a commonly pervasive inherited disease in many parts of the world. The complete lack of G6PD activity in a mouse model causes embryonic lethality. The G6PD-deficient Caenorhabditis elegans model also shows embryonic death as indicated by a severe hatching defect. Although increased oxidative stress has been implicated in both cases as the underlying cause, the exact mechanism has not been clearly delineated. In this study with C. elegans, membrane-associated defects, including enhanced permeability, defective polarity and cytokinesis, were found in G6PD-deficient embryos. The membrane-associated abnormalities were accompanied by impaired eggshell structure as evidenced by a transmission electron microscopic study. Such loss of membrane structural integrity was associated with abnormal lipid composition as lipidomic analysis revealed that lysoglycerophospholipids were significantly increased in G6PD-deficient embryos. Abnormal glycerophospholipid metabolism leading to defective embryonic development could be attributed to the increased activity of calcium-independent phospholipase A (iPLA) in G6PD-deficient embryos. This notion is further supported by the fact that the suppression of multiple iPLAs by genetic manipulation partially rescued the embryonic defects in G6PD-deficient embryos. In addition, G6PD deficiency induced disruption of redox balance as manifested by diminished NADPH and elevated lipid peroxidation in embryos. Taken together, disrupted lipid metabolism due to abnormal redox homeostasis is a major factor contributing to abnormal embryonic development in G6PD-deficient C. elegans.
[Mh] Termos MeSH primário: Caenorhabditis elegans/genética
Desenvolvimento Embrionário/genética
Glucosefosfato Desidrogenase/genética
Fosfolipases A2 Independentes de Cálcio/genética
[Mh] Termos MeSH secundário: Animais
Caenorhabditis elegans/crescimento & desenvolvimento
Estruturas da Membrana Celular/ultraestrutura
Casca de Ovo/ultraestrutura
Deficiência de Glucosefosfato Desidrogenase/genética
Glicerofosfolipídeos/metabolismo
Homeostase
Oxirredução
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Glycerophospholipids); EC 1.1.1.49 (Glucosephosphate Dehydrogenase); EC 3.1.1.4 (Phospholipases A2, Calcium-Independent)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171026
[Lr] Data última revisão:
171026
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE
[do] DOI:10.1038/cddis.2016.463


  5 / 416 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27435106
[Au] Autor:Wildenberg ME; Koelink PJ; Diederen K; Te Velde AA; Wolfkamp SC; Nuij VJ; Peppelenbosch MP; Nobis M; Sansom OJ; Anderson KI; van der Woude CJ; D'Haens GR; van den Brink GR
[Ad] Endereço:Tytgat Institute for Intestinal and Liver Research, Academic Medical Center, Amsterdam, The Netherlands.
[Ti] Título:The ATG16L1 risk allele associated with Crohn's disease results in a Rac1-dependent defect in dendritic cell migration that is corrected by thiopurines.
[So] Source:Mucosal Immunol;10(2):352-360, 2017 Mar.
[Is] ISSN:1935-3456
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thiopurines are commonly used drugs in the therapy of Crohn's disease, but unfortunately only show a 30% response rate. The biological basis for the thiopurine response is unclear, thus hampering patient selection prior to treatment. A genetic risk factor associated specifically with Crohn's disease is a variant in ATG16L1 that reduces autophagy. We have previously shown that autophagy is involved in dendritic cell (DC)-T-cell interactions and cytoskeletal regulation. Here we further investigated the role of autophagy in DC cytoskeletal modulation and cellular trafficking. Autophagy-deficient DC displayed loss of filopodia, altered podosome distribution, and increased membrane ruffling, all consistent with increased cellular adhesion. Consequently, autophagy-deficient DC showed reduced migration. The cytoskeletal aberrations were mediated through hyperactivation of Rac1, a known thiopurine target. Indeed thiopurines restored the migratory defects in autophagy-deficient DC. Clinically, the ATG16L1 risk variant associated with increased response to thiopurine treatment in patients with Crohn's disease but not ulcerative colitis. These results suggest that the association between ATG16L1 and Crohn's disease is mediated at least in part through Rac1 hyperactivation and subsequent defective DC migration. As this phenotype can be corrected using thiopurines, ATG16L1 genotyping may be useful in the identification of patients that will benefit most from thiopurine treatment.
[Mh] Termos MeSH primário: Proteínas Relacionadas à Autofagia/metabolismo
Autofagia
Doença de Crohn/imunologia
Células Dendríticas/fisiologia
Proteínas rac1 de Ligação ao GTP/metabolismo
[Mh] Termos MeSH secundário: Alelos
Animais
Autofagia/genética
Proteínas Relacionadas à Autofagia/genética
Estruturas da Membrana Celular/patologia
Movimento Celular
Células Cultivadas
Colite Ulcerativa/tratamento farmacológico
Doença de Crohn/tratamento farmacológico
Doença de Crohn/genética
Citoesqueleto/metabolismo
Células Dendríticas/patologia
Feminino
Predisposição Genética para Doença
Seres Humanos
Mercaptopurina/uso terapêutico
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Polimorfismo Genético
RNA Interferente Pequeno/genética
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ATG16L1 protein, human); 0 (Autophagy-Related Proteins); 0 (RNA, Small Interfering); E7WED276I5 (Mercaptopurine); EC 3.6.5.2 (rac1 GTP-Binding Protein)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160721
[St] Status:MEDLINE
[do] DOI:10.1038/mi.2016.65


  6 / 416 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:28076931
[Au] Autor:Makowiecka A; Simiczyjew A; Nowak D; Mazur AJ
[Ad] Endereço:University of Wroclaw, Department of Cell Pathology. aleksandra.makowiecka@uwr.edu.pl.
[Ti] Título:Varying effects of EGF, HGF and TGFß on formation of invadopodia and invasiveness of melanoma cell lines of different origin.
[So] Source:Eur J Histochem;60(4):2728, 2016 Dec 09.
[Is] ISSN:2038-8306
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:The understanding of melanoma malignancy mechanisms is essential for patient survival, because melanoma is responsible for ca. 75% of deaths related to skin cancers. Enhanced formation of invadopodia and extracellular matrix (ECM) degradation are two important drivers of cell invasion, and actin dynamics facilitate protrusive activity by providing a driving force to push through the ECM. We focused on the influence of epidermal growth factor (EGF), hepatocyte growth factor (HGF) and transforming growth factor ß (TGFß) on melanoma cell invasiveness, since they are observed in the melanoma microenvironment. All three factors stimulated invasion of A375 and WM1341D cells derived from primary tumor sites. In contrast, only EGF and HGF stimulated invasion of WM9 and Hs294T cells isolated from lymph node metastases. Enhanced formation of invadopodia and ECM degradation underlie the increased amount of invasive cells after stimulation with the tested agents. Generally, a rise in invasive potential was accompanied by a decrease in actin polymerization state (F:G ratio). The F:G ratio remained unchanged or was even increased in metastatic cell lines treated with TGFß. Our findings indicate that the effects of stimulation with EGF, HGF and TGFß on melanoma cell invasiveness could depend on melanoma cell progression stage.
[Mh] Termos MeSH primário: Estruturas da Membrana Celular/metabolismo
Fator de Crescimento Epidérmico/farmacologia
Fator de Crescimento de Hepatócito/farmacologia
Melanoma/metabolismo
Fator de Crescimento Transformador beta/farmacologia
Microambiente Tumoral/efeitos dos fármacos
[Mh] Termos MeSH secundário: Linhagem Celular Tumoral
Estruturas da Membrana Celular/patologia
Seres Humanos
Melanoma/patologia
Invasividade Neoplásica
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (HGF protein, human); 0 (Transforming Growth Factor beta); 62229-50-9 (Epidermal Growth Factor); 67256-21-7 (Hepatocyte Growth Factor)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170224
[Lr] Data última revisão:
170224
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170113
[St] Status:MEDLINE
[do] DOI:10.4081/ejh.2016.2728


  7 / 416 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
[PMID]:27807273
[Au] Autor:Hadjivasiliou Z; Hunter GL; Baum B
[Ad] Endereço:Centre for Mathematics, Physics, and Engineering in the Life Sciences and Experimental Biology, University College London, London WC1E 6BT, UK zena.hadjivasiliou@unige.ch.
[Ti] Título:A new mechanism for spatial pattern formation via lateral and protrusion-mediated lateral signalling.
[So] Source:J R Soc Interface;13(124), 2016 Nov.
[Is] ISSN:1742-5662
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Tissue organization and patterning are critical during development when genetically identical cells take on different fates. Lateral signalling plays an important role in this process by helping to generate self-organized spatial patterns in an otherwise uniform collection of cells. Recent data suggest that lateral signalling can be mediated both by junctional contacts between neighbouring cells and via cellular protrusions that allow non-neighbouring cells to interact with one another at a distance. However, it remains unclear precisely how signalling mediated by these distinct types of cell-cell contact can physically contribute to the generation of complex patterns without the assistance of diffusible morphogens or pre-patterns. To explore this question, in this work we develop a model of lateral signalling based on a single receptor/ligand pair as exemplified by Notch and Delta. We show that allowing the signalling kinetics to differ at junctional versus protrusion-mediated contacts, an assumption inspired by recent data which show that the cleavage of Notch in several systems requires both Delta binding and the application of mechanical force, permits individual cells to act to promote both lateral activation and lateral inhibition. Strikingly, under this model, in which Delta can sequester Notch, a variety of patterns resembling those typical of reaction-diffusion systems is observed, together with more unusual patterns that arise when we consider changes in signalling kinetics, and in the length and distribution of protrusions. Importantly, these patterns are self-organizing-so that local interactions drive tissue-scale patterning. Together, these data show that protrusions can, in principle, generate different types of patterns in addition to contributing to long-range signalling and to pattern refinement.
[Mh] Termos MeSH primário: Comunicação Celular/fisiologia
Estruturas da Membrana Celular/fisiologia
Modelos Biológicos
Transdução de Sinais/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Peptídeos e Proteínas de Sinalização Intracelular/metabolismo
Proteínas de Membrana/metabolismo
Receptores Notch/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Intracellular Signaling Peptides and Proteins); 0 (Membrane Proteins); 0 (Receptors, Notch); 0 (delta protein)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171019
[Lr] Data última revisão:
171019
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161104
[St] Status:MEDLINE


  8 / 416 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27638614
[Au] Autor:Marshall MS; Bongarzone ER
[Ad] Endereço:Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, Illinois. mmarsh22@uic.edu.
[Ti] Título:Beyond Krabbe's disease: The potential contribution of galactosylceramidase deficiency to neuronal vulnerability in late-onset synucleinopathies.
[So] Source:J Neurosci Res;94(11):1328-32, 2016 Nov.
[Is] ISSN:1097-4547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:New insights into the pathophysiological mechanisms behind late-onset neurodegenerative diseases have come from unexpected sources in recent years. Specifically, the group of inherited metabolic disorders known as lysosomal storage diseases that most commonly affect infants has been found to have surprising similarities with adult neurodegenerative disorders. Most notable has been the identification of Gaucher's disease as a comorbidity for Parkinson's disease. Prompted by the recent identification of neuronal aggregates of α-synuclein in another lysosomal storage disease, Krabbe's disease, we propose the idea that a similar connection exists between adult synucleinopathies and Krabbe's. Similarities between the two diseases, including the pattern of α-synuclein aggregation in the brain of the twitcher mouse (the authentic murine model of Krabbe's disease), changes to lipid membrane dynamics, and possible dysfunction in synaptic function and macroautophagy, underscore a link between Krabbe's disease and late-onset synucleinopathies. Silent GALC mutations may even constitute a risk factor for the development of Parkinson's in certain patients. More research is required to identify definitively any link and the validity of this hypothesis, but such a connection would prove invaluable for developing novel therapeutic targets for Parkinson's based on our current understanding of Krabbe's disease and for establishing new biomarkers for the identification of at-risk patients. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Encéfalo/patologia
Leucodistrofia de Células Globoides
Neurônios/patologia
alfa-Sinucleína/metabolismo
[Mh] Termos MeSH secundário: Animais
Estruturas da Membrana Celular/patologia
Galactosilceramidase/genética
Galactosilceramidase/metabolismo
Predisposição Genética para Doença
Seres Humanos
Leucodistrofia de Células Globoides/genética
Leucodistrofia de Células Globoides/metabolismo
Leucodistrofia de Células Globoides/patologia
Lipídeos/fisiologia
Mutação/genética
Neurônios/metabolismo
Agregados Proteicos/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Lipids); 0 (Protein Aggregates); 0 (alpha-Synuclein); EC 3.2.1.46 (Galactosylceramidase)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160918
[St] Status:MEDLINE
[do] DOI:10.1002/jnr.23751


  9 / 416 MEDLINE  
              first record previous record next record last record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27459068
[Au] Autor:Hind LE; Vincent WJ; Huttenlocher A
[Ad] Endereço:Departments of Pediatrics and Medical Microbiology and Immunology, University of Wisconsin-Madison, Madison, WI 53706, USA.
[Ti] Título:Leading from the Back: The Role of the Uropod in Neutrophil Polarization and Migration.
[So] Source:Dev Cell;38(2):161-9, 2016 Jul 25.
[Is] ISSN:1878-1551
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cell motility is required for diverse biological processes including development, homing of immune cells, wound healing, and cancer cell invasion. Motile neutrophils exhibit a polarized morphology characterized by the formation of leading-edge pseudopods and a highly contractile cell rear known as the uropod. Although it is known that perturbing uropod formation impairs neutrophil migration, the role of the uropod in cell polarization and motility remains incompletely understood. Here we discuss cell intrinsic mechanisms that regulate neutrophil polarization and motility, with a focus on the uropod, and examine how relationships among regulatory mechanisms change when cells change their direction of migration.
[Mh] Termos MeSH primário: Estruturas da Membrana Celular/fisiologia
Movimento Celular/fisiologia
Polaridade Celular/fisiologia
Neutrófilos/fisiologia
Pseudópodes/fisiologia
[Mh] Termos MeSH secundário: Adesão Celular
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170725
[Lr] Data última revisão:
170725
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160727
[St] Status:MEDLINE


  10 / 416 MEDLINE  
              first record previous record
seleciona
para imprimir
Fotocópia
Texto completo
[PMID]:27412703
[Au] Autor:Brejchova J; Vosahlikova M; Roubalova L; Parenti M; Mauri M; Chernyavskiy O; Svoboda P
[Ad] Endereço:Laboratory of Biochemistry of Membrane Receptors, Department of Biomathematics, Institute of Physiology of the Czech Academy of Sciences, Videnska 1083, 14220, Prague 4, Czech Republic.
[Ti] Título:Plasma membrane cholesterol level and agonist-induced internalization of δ-opioid receptors; colocalization study with intracellular membrane markers of Rab family.
[So] Source:J Bioenerg Biomembr;48(4):375-96, 2016 08.
[Is] ISSN:1573-6881
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Decrease of cholesterol level in plasma membrane of living HEK293 cells transiently expressing FLAG-δ-OR by ß-cyclodextrin (ß-CDX) resulted in a slight internalization of δ-OR. Massive internalization of δ-OR induced by specific agonist DADLE was diminished in cholesterol-depleted cells. These results suggest that agonist-induced internalization of δ-OR, which has been traditionally attributed exclusively to clathrin-mediated pathway, proceeds at least partially via membrane domains. Identification of internalized pools of FLAG-δ-OR by colocalization studies with proteins of Rab family indicated the decreased presence of receptors in early endosomes (Rab5), late endosomes and lysosomes (Rab7) and fast recycling vesicles (Rab4). Slow type of recycling (Rab11) was unchanged by cholesterol depletion. As expected, agonist-induced internalization of oxytocin receptors was totally suppressed in ß-CDX-treated cells. Determination of average fluorescence lifetime of TMA-DPH, the polar derivative of hydrophobic membrane probe diphenylhexatriene, in live cells by FLIM indicated a significant alteration of the overall PM structure which may be interpreted as an increased "water-accessible space" within PM area. Data obtained by studies of HEK293 cells transiently expressing FLAG-δ-OR by "antibody feeding" method were extended by analysis of the effect of cholesterol depletion on distribution of FLAG-δ-OR in sucrose density gradients prepared from HEK293 cells stably expressing FLAG-δ-OR. Major part of FLAG-δ-OR was co-localized with plasma membrane marker Na,K-ATPase and ß-CDX treatment resulted in shift of PM fragments containing both FLAG-δ-OR and Na,K-ATPase to higher density. Thus, the decrease in content of the major lipid constituent of PM resulted in increased density of resulting PM fragments.
[Mh] Termos MeSH primário: Membrana Celular/química
Colesterol/metabolismo
Receptores Opioides delta/metabolismo
[Mh] Termos MeSH secundário: Estruturas da Membrana Celular/química
Células HEK293
Seres Humanos
Membranas Intracelulares/química
Receptores Opioides delta/agonistas
Proteínas rab de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Receptors, Opioid, delta); 97C5T2UQ7J (Cholesterol); EC 3.6.5.2 (rab GTP-Binding Proteins)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170410
[Lr] Data última revisão:
170410
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160715
[St] Status:MEDLINE
[do] DOI:10.1007/s10863-016-9667-7



página 1 de 42 ir para página                         
   


Refinar a pesquisa
  Base de dados : MEDLINE Formulário avançado   

    Pesquisar no campo  
1  
2
3
 
           



Search engine: iAH v2.6 powered by WWWISIS

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