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  1 / 141766 MEDLINE  
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[PMID]:29399882
[Au] Autor:Mitra S; Chatterjee D; Das A; Gupta K; Radotra BD; Mandal AK
[Ad] Endereço:Department of Histopathology, PGIMER, Chandigarh, India.
[Ti] Título:Urothelial tumors with villous morphology: Histomorphology and role of immunohistochemistry in diagnosis.
[So] Source:APMIS;126(3):191-200, 2018 Mar.
[Is] ISSN:1600-0463
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Ab] Resumo:Villous adenoma and urothelial carcinoma with villoglandular differentiation (UCVGD) are rare urothelial tumours showing villous morphology, the former being a preneoplastic entity and the latter being a malignant one. The detailed immunohistochemistry of these entities is previously not described in the literature. Moreover, a limited biopsy sample of UCVGD or a villous adenoma with or without adenocarcinoma may be difficult to distinguish on the basis of the histomorphology alone. An immunohistochemical panel comprising of GATA3, p63, ß-catenin, CK7 and CK20 was performed on five cases of UCVGD and three cases of villous adenoma with the aim of studying the expression of the proteins thereby aiding in the diagnosis of these entities in a limited surgical pathology specimen. The mean age of UCVGD was 66.8 years and all the patients were male. All the cases of UCVGD were associated with high grade papillary urothelial carcinoma with lamina propria invasion. The immunohistochemical panel showed strong nuclear GATA3 expression in the urothelial component of UCVGD. Interestingly, the high grade and the low grade villoglandular components of UCVGD also expressed GATA3 (nuclear) with a progressive loss of expression from the high grade to the low grade component. The villous adenomas showed negativity or aberrant cytoplasmic positivity for GATA3. The ß-catenin showed a gradual loss of membranous expression from villous adenoma to low grade and high grade villoglandular components of UCVGD with a patchy membranous expression in the urothelial component of the UCVGD. p63 showed strong nuclear positivity in the urothelial component and uniform negativity in the villous adenoma and villoglandular component of UCVGD irrespective of its grade, thereby distinguishing the villoglandular component from the urothelial component. The urothelial component of UCVGD showed strong membranous CK7 expression and was higher than the CK20 expression in the urothelial component. In contrast, CK20 expression was higher in villous adenoma as compared to CK7. There was no difference in the expression of CK7 and CK20 in the villoglandular components and low grade and high grade villoglandular areas. The above-mentioned immunohistochemical pattern may help to distinguish the UCVGD from the villous adenoma.
[Mh] Termos MeSH primário: Adenoma Viloso/diagnóstico
Fator de Transcrição GATA3/metabolismo
Queratina-7/metabolismo
Proteínas de Membrana/metabolismo
Neoplasias Urológicas/diagnóstico
beta Catenina/metabolismo
[Mh] Termos MeSH secundário: Adenoma Viloso/patologia
Idoso
Biomarcadores Tumorais/metabolismo
Feminino
Hematúria/patologia
Seres Humanos
Imuno-Histoquímica
Queratina-20/metabolismo
Masculino
Meia-Idade
Neoplasias Urológicas/patologia
Urotélio/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers, Tumor); 0 (CKAP4 protein, human); 0 (GATA3 Transcription Factor); 0 (GATA3 protein, human); 0 (KRT20 protein, human); 0 (KRT7 protein, human); 0 (Keratin-20); 0 (Keratin-7); 0 (Membrane Proteins); 0 (beta Catenin)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180206
[St] Status:MEDLINE
[do] DOI:10.1111/apm.12799


  2 / 141766 MEDLINE  
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[PMID]:29353037
[Au] Autor:Lu Z; Liu Y; Shi Y; Shi X; Wang X; Xu C; Zhao H; Dong Q
[Ad] Endereço:Department of Neurology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 200437, PR China.
[Ti] Título:Curcumin protects cortical neurons against oxygen and glucose deprivation/reoxygenation injury through flotillin-1 and extracellular signal-regulated kinase1/2 pathway.
[So] Source:Biochem Biophys Res Commun;496(2):515-522, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:In this study, we provided evidence that curcumin could be a promising therapeutic agent for ischemic stroke by activating neuroprotective signaling pathways. Post oxygen and glucose deprivation/reoxygenation (OGD/R), primary mouse cortical neurons treated with curcumin exhibited a significant decrease in cell death, LDH release and enzyme caspase-3 activity under OGD/R circumstances, which were abolished by flotillin-1 downregulation or extracellular signal-regulated kinase (ERK) inhibitor. Moreover, flotillin-1 knockdown led to suppression of curcumin-mediated ERK phosphorylation under OGD/R condition. Based on these findings, we concluded that curcumin could confer neuroprotection against OGD/R injury through a novel flotillin-1 and ERK1/2 pathway.
[Mh] Termos MeSH primário: Isquemia Encefálica/tratamento farmacológico
Curcumina/farmacologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Proteínas de Membrana/metabolismo
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
[Mh] Termos MeSH secundário: Animais
Isquemia Encefálica/metabolismo
Células Cultivadas
Córtex Cerebelar/citologia
Córtex Cerebelar/efeitos dos fármacos
Feminino
Glucose/metabolismo
Masculino
Camundongos Endogâmicos BALB C
Neurônios/metabolismo
Oxigênio/metabolismo
Traumatismo por Reperfusão/tratamento farmacológico
Traumatismo por Reperfusão/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (Neuroprotective Agents); 0 (flotillins); IT942ZTH98 (Curcumin); IY9XDZ35W2 (Glucose); S88TT14065 (Oxygen)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180122
[St] Status:MEDLINE


  3 / 141766 MEDLINE  
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[PMID]:28452222
[Au] Autor:Zhu Y; Serra A; Guo T; Park JE; Zhong Q; Sze SK
[Ad] Endereço:School of Biological Sciences, Nanyang Technological University , 60 Nanyang Drive 637551, Singapore.
[Ti] Título:Application of Nanosecond Laser Photolysis Protein Footprinting to Study EGFR Activation by EGF in Cells.
[So] Source:J Proteome Res;16(6):2282-2293, 2017 Jun 02.
[Is] ISSN:1535-3907
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mass spectrometry-based protein footprinting emerged as a useful technology to understand protein ligand interactions in vitro. We have previously demonstrated the application of footprinting in live E. coli cells. Here, we further optimized an ultrafast laser photolysis hydroxyl radical footprinting method and applied it to study the interaction of EGF and EGFR in live mammalian cells. This method used a nanosecond laser to photochemically generate a burst of hydroxyl radicals in situ in-cell suspension to oxidize the amino acids on the protein surface. Mass spectrometric analysis of the thus modified peptides was interpreted to probe the solvent-accessible surface areas of the protein in its native biological state with and without EGF activation. Our footprinting data agreed with the two relevant EGFR crystal structures, indicating that this in-cell laser photolysis footprinting technique is a valid approach to study the structural properties of integral membrane proteins directly in the native environment.
[Mh] Termos MeSH primário: Fator de Crescimento Epidérmico/metabolismo
Pegadas de Proteínas/métodos
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Mh] Termos MeSH secundário: Aminoácidos/química
Ativação Enzimática
Células HEK293
Seres Humanos
Radical Hidroxila
Lasers
Proteínas de Membrana/metabolismo
Estrutura Molecular
Oxirredução
Fotólise
Receptor do Fator de Crescimento Epidérmico/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; VALIDATION STUDIES
[Nm] Nome de substância:
0 (Amino Acids); 0 (Membrane Proteins); 3352-57-6 (Hydroxyl Radical); 62229-50-9 (Epidermal Growth Factor); EC 2.7.10.1 (EGFR protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180309
[Lr] Data última revisão:
180309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1021/acs.jproteome.7b00154


  4 / 141766 MEDLINE  
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[PMID]:29182013
[Au] Autor:Dickerson T; Jauregui CE; Teng Y
[Ad] Endereço:College of Science & Mathematics, Augusta University, Augusta, GA 30912, USA.
[Ti] Título:Friend or foe? Mitochondria as a pharmacological target in cancer treatment.
[So] Source:Future Med Chem;9(18):2197-2210, 2017 12.
[Is] ISSN:1756-8927
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Mitochondria have acquired numerous functions over the course of evolution, such as those involved in controlling energy production, cellular metabolism, cell survival, apoptosis and autophagy within host cells. Tumor cells can develop defects in mitochondrial function, presenting a potential strategy for designing selective anticancer therapies. Therefore, cancer has been the main focus of recent research to uncover possible mitochondrial targets for therapeutic benefit. This comprehensive review covers not only the recent discoveries of the roles of mitochondria in cancer development, progression and therapeutic implications but also the findings regarding emerging mitochondrial therapeutic targets and mitochondria-targeted agents. Current challenges and future directions for developments and applications of mitochondrial-targeted therapeutics are also discussed.
[Mh] Termos MeSH primário: Mitocôndrias/metabolismo
Neoplasias/tratamento farmacológico
[Mh] Termos MeSH secundário: ATPases Associadas a Diversas Atividades Celulares/metabolismo
Trifosfato de Adenosina/metabolismo
Animais
Antineoplásicos/farmacologia
Antineoplásicos/uso terapêutico
DNA Mitocondrial/efeitos dos fármacos
DNA Mitocondrial/metabolismo
Metabolismo Energético/efeitos dos fármacos
Seres Humanos
Proteínas de Membrana/metabolismo
Mitocôndrias/genética
Proteínas Mitocondriais/metabolismo
Neoplasias/metabolismo
Neoplasias/patologia
Espécies Reativas de Oxigênio/metabolismo
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ATAD3A protein, human); 0 (Antineoplastic Agents); 0 (DNA, Mitochondrial); 0 (Membrane Proteins); 0 (Mitochondrial Proteins); 0 (Reactive Oxygen Species); 8L70Q75FXE (Adenosine Triphosphate); EC 3.6.4.- (ATPases Associated with Diverse Cellular Activities)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171129
[St] Status:MEDLINE
[do] DOI:10.4155/fmc-2017-0110


  5 / 141766 MEDLINE  
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[PMID]:28453858
[Au] Autor:McCormack SE; Li D; Kim YJ; Lee JY; Kim SH; Rapaport R; Levine MA
[Ad] Endereço:Division of Endocrinology and Diabetes, Children's Hospital of Philadelphia, Philadelphia, Pennsylvania 19104.
[Ti] Título:Digenic Inheritance of PROKR2 and WDR11 Mutations in Pituitary Stalk Interruption Syndrome.
[So] Source:J Clin Endocrinol Metab;102(7):2501-2507, 2017 Jul 01.
[Is] ISSN:1945-7197
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Context: Pituitary stalk interruption syndrome (PSIS, ORPHA95496) is a congenital defect of the pituitary gland characterized by the triad of a very thin/interrupted pituitary stalk, an ectopic (or absent) posterior pituitary gland, and hypoplasia or aplasia of the anterior pituitary gland. Complex genetic patterns of inheritance of this disorder are increasingly recognized. Objective: The objective of this study was to identify a genetic cause of PSIS in an affected child. Methods: Whole exome sequencing (WES) was performed by using standard techniques, with prioritized genetic variants confirmed via Sanger sequencing. To investigate the effects of one candidate variant on mutant WDR11 function, Western blotting and coimmunofluorescence were used to assess binding capacity, and leptomycin B exposure along with immunofluorescence was used to assess nuclear localization. Results: We describe a child who presented in infancy with combined pituitary hormone deficiencies and whose brain imaging demonstrated a small anterior pituitary, ectopic posterior pituitary, and a thin, interrupted stalk. WES demonstrated heterozygous missense mutations in two genes required for pituitary development, a known loss-of-function mutation in PROKR2 (c.253C>T;p.R85C) inherited from an unaffected mother, and a WDR11 (c.1306A>G;p.I436V) mutation inherited from an unaffected father. Mutant WDR11 loses its capacity to bind to its functional partner, EMX1, and to localize to the nucleus. Conclusions: WES in a child with PSIS and his unaffected family implicates a digenic mechanism of inheritance. In cases of hypopituitarism in which there is incomplete segregation of a monogenic genotype with the phenotype, the possibility that a second genetic locus is involved should be considered.
[Mh] Termos MeSH primário: Predisposição Genética para Doença
Hipopituitarismo/genética
Proteínas de Membrana/genética
Mutação
Hipófise/anormalidades
Proteínas Proto-Oncogênicas/genética
Receptores Acoplados a Proteínas-G/genética
Receptores de Peptídeos/genética
[Mh] Termos MeSH secundário: Exoma/genética
Genótipo
Heterozigoto
Seres Humanos
Hipopituitarismo/congênito
Hipopituitarismo/patologia
Recém-Nascido
Masculino
Linhagem
Síndrome
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (PROKR2 protein, human); 0 (Proto-Oncogene Proteins); 0 (Receptors, G-Protein-Coupled); 0 (Receptors, Peptide); 0 (WDR11 protein, human)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE
[do] DOI:10.1210/jc.2017-00332


  6 / 141766 MEDLINE  
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[PMID]:28747460
[Au] Autor:Schallner N; Lieberum JL; Gallo D; LeBlanc RH; Fuller PM; Hanafy KA; Otterbein LE
[Ad] Endereço:From the Department of Surgery (N.S., J.-L.L., D.G., L.E.O.) and Department of Neurology (R.H.L., P.M.F., K.A.H.), Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA; Department of Anesthesiology and Critical Care, Medical Center-University Freiburg, Faculty of Medicine, German
[Ti] Título:Carbon Monoxide Preserves Circadian Rhythm to Reduce the Severity of Subarachnoid Hemorrhage in Mice.
[So] Source:Stroke;48(9):2565-2573, 2017 09.
[Is] ISSN:1524-4628
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND AND PURPOSE: Subarachnoid hemorrhage (SAH) is associated with a temporal pattern of stroke incidence. We hypothesized that natural oscillations in gene expression controlling circadian rhythm affect the severity of neuronal injury. We moreover predict that heme oxygenase-1 (HO-1/ ) and its product carbon monoxide (CO) contribute to the restoration of rhythm and neuroprotection. METHODS: Murine SAH model was used where blood was injected at various time points of the circadian cycle. Readouts included circadian clock gene expression, locomotor activity, vasospasm, neuroinflammatory markers, and apoptosis. In addition, cerebrospinal fluid and peripheral blood leukocytes from SAH patients and controls were analyzed for clock gene expression. RESULTS: Significant elevations in the clock genes , , and were observed in the hippocampus, cortex, and suprachiasmatic nucleus in mice subjected to SAH at zeitgeber time (ZT) 12 when compared with ZT2. Clock gene expression amplitude correlated with basal expression of HO-1, which was also significantly greater at ZT12. SAH animals showed a significant reduction in cerebral vasospasm, neuronal apoptosis, and microglial activation at ZT12 compared with ZT2. In animals with myeloid-specific HO-1 deletion ( ), , and expression was reduced in the suprachiasmatic nucleus, which correlated with increased injury. Treatment with low-dose CO rescued mice, restored , expression, and reduced neuronal apoptosis. CONCLUSIONS: Clock gene expression regulates, in part, the severity of SAH and requires myeloid HO-1 activity to clear the erythrocyte burden and inhibit neuronal apoptosis. Exposure to CO rescues the loss of HO-1 and thus merits further investigation in patients with SAH.
[Mh] Termos MeSH primário: Monóxido de Carbono/metabolismo
Ritmo Circadiano/genética
Expressão Gênica/efeitos dos fármacos
Heme Oxigenase-1/genética
Proteínas de Membrana/genética
Hemorragia Subaracnóidea/genética
[Mh] Termos MeSH secundário: Fatores de Transcrição ARNTL/genética
Animais
Apoptose
Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética
Proteínas CLOCK/genética
Líquido Cefalorraquidiano/metabolismo
Heme Oxigenase-1/metabolismo
Seres Humanos
Imuno-Histoquímica
Inflamação
Leucócitos/metabolismo
Locomoção
Proteínas de Membrana/metabolismo
Camundongos
Proteínas do Tecido Nervoso/genética
Proteínas Circadianas Period/genética
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Índice de Gravidade de Doença
Núcleo Supraquiasmático/metabolismo
Vasoespasmo Intracraniano
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, U.S. GOV'T, NON-P.H.S.; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ARNTL Transcription Factors); 0 (Arntl protein, mouse); 0 (Basic Helix-Loop-Helix Transcription Factors); 0 (Membrane Proteins); 0 (Nerve Tissue Proteins); 0 (Npas2 protein, mouse); 0 (PER2 protein, human); 0 (Per1 protein, mouse); 0 (Per2 protein, mouse); 0 (Period Circadian Proteins); 7U1EE4V452 (Carbon Monoxide); EC 1.14.14.18 (Heme Oxygenase-1); EC 1.14.14.18 (Hmox1 protein, mouse); EC 2.3.1.48 (CLOCK Proteins); EC 2.3.1.48 (Clock protein, mouse)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.1161/STROKEAHA.116.016165


  7 / 141766 MEDLINE  
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[PMID]:28458469
[Au] Autor:Ryu J; Lee JW
[Ad] Endereço:Department of Pharmacy, Research Institute of Pharmaceutical Sciences, Tumor Microenvironment Global Core Research Center, Medicinal Bioconvergence Research Center, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
[Ti] Título:TM4SF5-Mediated Roles in the Development of Fibrotic Phenotypes.
[So] Source:Mediators Inflamm;2017:5108525, 2017.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Transmembrane 4 L six family member 5 (TM4SF5) can form tetraspanin-enriched microdomains (TERMs) on the cell's surface. TERMs contain protein-protein complexes comprised of tetraspanins, growth factor receptors, and integrins. These complexes regulate communication between extracellular and intracellular spaces to control diverse cellular functions. TM4SF5 influences the epithelial-mesenchymal transition (EMT), aberrant multilayer cellular growth, drug resistance, enhanced migration and invasion, circulation through the bloodstream, tumor-initiation property, metastasis, and muscle development in zebrafish. Here, current data on TM4SF5's roles in the development of fibrotic phenotypes are reviewed. TM4SF5 is induced by transforming growth factor 1 (TGF 1) signaling via a collaboration with epidermal growth factor receptor (EGFR) activation. TM4SF5, by itself or in concert with other receptors, transduces signals intracellularly. In hepatocytes, TM4SF5 expression regulates cell cycle progression, migration, and expression of extracellular matrix components. In CCl -treated mice, TM4SF5, -smooth muscle actin ( -SMA), and collagen I expression are observed together along the fibrotic septa regions of the liver. These fibrotic phenotypes are diminished by anti-TM4SF5 reagents, such as a specific small compound [TSAHC, 4'-( -toluenesulfonylamido)-4-hydroxychalcone] or a chimeric antibody. This review discusses the antifibrotic strategies that target TM4SF5 and its associated protein networks that regulate the intracellular signaling necessary for fibrotic functions of hepatocytes.
[Mh] Termos MeSH primário: Fibrose/metabolismo
Proteínas de Membrana/metabolismo
[Mh] Termos MeSH secundário: Actinas/metabolismo
Animais
Fibrose/genética
Hepatócitos/metabolismo
Seres Humanos
Proteínas de Membrana/genética
Camundongos
Receptor do Fator de Crescimento Epidérmico/genética
Receptor do Fator de Crescimento Epidérmico/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Actins); 0 (Membrane Proteins); 0 (TM4SF5 protein, human); EC 2.7.10.1 (Receptor, Epidermal Growth Factor)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1155/2017/5108525


  8 / 141766 MEDLINE  
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[PMID]:29416037
[Au] Autor:Zabara A; Chong JTY; Martiel I; Stark L; Cromer BA; Speziale C; Drummond CJ; Mezzenga R
[Ad] Endereço:Department of Health Sciences and Technology, ETH Zurich, Schmelzbergstrasse 9 LFO E23, 8092, Zürich, Switzerland.
[Ti] Título:Design of ultra-swollen lipidic mesophases for the crystallization of membrane proteins with large extracellular domains.
[So] Source:Nat Commun;9(1):544, 2018 02 07.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In meso crystallization of membrane proteins from lipidic mesophases is central to protein structural biology but limited to membrane proteins with small extracellular domains (ECDs), comparable to the water channels (3-5 nm) of the mesophase. Here we present a strategy expanding the scope of in meso crystallization to membrane proteins with very large ECDs. We combine monoacylglycerols and phospholipids to design thermodynamically stable ultra-swollen bicontinuous cubic phases of double-gyroid (Ia3d), double-diamond (Pn3m), and double-primitive (Im3m) space groups, with water channels five times larger than traditional lipidic mesophases, and showing re-entrant behavior upon increasing hydration, of sequences Ia3d→Pn3m→Ia3d and Pn3m→Im3m→Pn3m, unknown in lipid self-assembly. We use these mesophases to crystallize membrane proteins with ECDs inaccessible to conventional in meso crystallization, demonstrating the methodology on the Gloeobacter ligand-gated ion channel (GLIC) protein, and show substantial modulation of packing, molecular contacts and activation state of the ensued proteins crystals, illuminating a general strategy in protein structural biology.
[Mh] Termos MeSH primário: Membrana Celular
Proteínas de Membrana/química
Fosfatidilgliceróis/química
[Mh] Termos MeSH secundário: Cristalização/métodos
Ácidos Graxos Monoinsaturados/química
Canais Iônicos
Transição de Fase
Domínios Proteicos
Termodinâmica
Água
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fatty Acids, Monounsaturated); 0 (Ion Channels); 0 (Membrane Proteins); 0 (Phosphatidylglycerols); 059QF0KO0R (Water); 4271ZA8WXO (distearoyl phosphatidylglycerol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02996-5


  9 / 141766 MEDLINE  
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[PMID]:29410425
[Au] Autor:Cervero P; Wiesner C; Bouissou A; Poincloux R; Linder S
[Ad] Endereço:Institut für Medizinische Mikrobiologie, Virologie und Hygiene, Universitätsklinikum Eppendorf, Martinistr. 52, 20246, Hamburg, Germany.
[Ti] Título:Lymphocyte-specific protein 1 regulates mechanosensory oscillation of podosomes and actin isoform-based actomyosin symmetry breaking.
[So] Source:Nat Commun;9(1):515, 2018 02 06.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Subcellular fine-tuning of the actomyosin cytoskeleton is a prerequisite for polarized cell migration. We identify LSP (lymphocyte-specific protein) 1 as a critical regulator of actomyosin contractility in primary macrophages. LSP1 regulates adhesion and migration, including the parameters cell area and speed, and also podosome turnover, oscillation and protrusive force. LSP1 recruits myosin IIA and its regulators, including myosin light chain kinase and calmodulin, and competes with supervillin, a myosin hyperactivator, for myosin regulators, and for actin isoforms, notably ß-actin. Actin isoforms are anisotropically distributed in myosin IIA-expressing macrophages, and contribute to the differential recruitment of LSP1 and supervillin, thus enabling an actomyosin symmetry break, analogous to the situation in cells expressing two myosin II isoforms. Collectively, these results show that the cellular pattern of actin isoforms builds the basis for the differential distribution of two actomyosin machineries with distinct properties, leading to the establishment of discrete zones of actomyosin contractility.
[Mh] Termos MeSH primário: Actinas/metabolismo
Actomiosina/metabolismo
Macrófagos/metabolismo
Mecanotransdução Celular/fisiologia
Proteínas dos Microfilamentos/metabolismo
Podossomos/fisiologia
[Mh] Termos MeSH secundário: Actomiosina/química
Regulação da Expressão Gênica/fisiologia
Seres Humanos
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Proteínas dos Microfilamentos/genética
Miosina não Muscular Tipo IIA/metabolismo
Conformação Proteica
Isoformas de Proteínas
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Actins); 0 (LSP1 protein, human); 0 (Membrane Proteins); 0 (Microfilament Proteins); 0 (Protein Isoforms); 0 (SVIL protein, human); 9013-26-7 (Actomyosin); EC 3.6.1.- (Nonmuscle Myosin Type IIA)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180208
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02904-x


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[PMID]:29330478
[Au] Autor:Williams JJL; Alotaiq N; Mullen W; Burchmore R; Liu L; Baillie GS; Schaper F; Pilch PF; Palmer TM
[Ad] Endereço:School of Pharmacy and Medical Sciences, University of Bradford, Bradford, BD7 1DP, UK. j.j.l.williams@bradford.ac.uk.
[Ti] Título:Interaction of suppressor of cytokine signalling 3 with cavin-1 links SOCS3 function and cavin-1 stability.
[So] Source:Nat Commun;9(1):168, 2018 01 12.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Effective suppression of JAK-STAT signalling by the inducible inhibitor "suppressor of cytokine signalling 3" (SOCS3) is essential for limiting signalling from cytokine receptors. Here we show that cavin-1, a component of caveolae, is a functionally significant SOCS3-interacting protein. Biochemical and confocal imaging demonstrate that SOCS3 localisation to the plasma membrane requires cavin-1. SOCS3 is also critical for cavin-1 stabilisation, such that deletion of SOCS3 reduces the expression of cavin-1 and caveolin-1 proteins, thereby reducing caveola abundance in endothelial cells. Moreover, the interaction of cavin-1 and SOCS3 is essential for SOCS3 function, as loss of cavin-1 enhances cytokine-stimulated STAT3 phosphorylation and abolishes SOCS3-dependent inhibition of IL-6 signalling by cyclic AMP. Together, these findings reveal a new functionally important mechanism linking SOCS3-mediated inhibition of cytokine signalling to localisation at the plasma membrane via interaction with and stabilisation of cavin-1.
[Mh] Termos MeSH primário: Proteínas de Membrana/metabolismo
Proteínas de Ligação a RNA/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Cavéolas/fisiologia
Deleção de Genes
Regulação da Expressão Gênica
Células HEK293
Seres Humanos
Janus Quinases/genética
Janus Quinases/metabolismo
Proteínas de Membrana/genética
Camundongos
Ligação Proteica
Proteínas de Ligação a RNA/genética
Fatores de Transcrição STAT/genética
Fatores de Transcrição STAT/metabolismo
Proteína 3 Supressora da Sinalização de Citocinas/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (PTRF protein, human); 0 (Ptrf protein, mouse); 0 (RNA-Binding Proteins); 0 (SOCS3 protein, human); 0 (STAT Transcription Factors); 0 (Socs3 protein, mouse); 0 (Suppressor of Cytokine Signaling 3 Protein); EC 2.7.10.2 (Janus Kinases)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180114
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02585-y



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