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[PMID]:28880872
[Au] Autor:Escobar-Aguirre M; Zhang H; Jamieson-Lucy A; Mullins MC
[Ad] Endereço:Department of Cell and Developmental Biology, University of Pennsylvania Perelman School of Medicine, 1152 BRBII/III, 421 Curie Blvd., Philadelphia, Pennsylvania, United States of America.
[Ti] Título:Microtubule-actin crosslinking factor 1 (Macf1) domain function in Balbiani body dissociation and nuclear positioning.
[So] Source:PLoS Genet;13(9):e1006983, 2017 Sep.
[Is] ISSN:1553-7404
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Animal-vegetal (AV) polarity of most vertebrate eggs is established during early oogenesis through the formation and disassembly of the Balbiani Body (Bb). The Bb is a structure conserved from insects to humans that appears as a large granule, similar to a mRNP granule composed of mRNA and proteins, that in addition contains mitochondria, ER and Golgi. The components of the Bb, which have amyloid-like properties, include germ cell and axis determinants of the embryo that are anchored to the vegetal cortex upon Bb disassembly. Our lab discovered in zebrafish the only gene known to function in Bb disassembly, microtubule-actin crosslinking factor 1a (macf1a). Macf1 is a conserved, giant multi-domain cytoskeletal linker protein that can interact with microtubules (MTs), actin filaments (AF), and intermediate filaments (IF). In macf1a mutant oocytes the Bb fails to dissociate, the nucleus is acentric, and AV polarity of the oocyte and egg fails to form. The cytoskeleton-dependent mechanism by which Macf1a regulates Bb mRNP granule dissociation was unknown. We found that disruption of AFs phenocopies the macf1a mutant phenotype, while MT disruption does not. We determined that cytokeratins (CK), a type of IF, are enriched in the Bb. We found that Macf1a localizes to the Bb, indicating a direct function in regulating its dissociation. We thus tested if Macf1a functions via its actin binding domain (ABD) and plectin repeat domain (PRD) to integrate cortical actin and Bb CK, respectively, to mediate Bb dissociation at the oocyte cortex. We developed a CRISPR/Cas9 approach to delete the exons encoding these domains from the macf1a endogenous locus, while maintaining the open reading frame. Our analysis shows that Macf1a functions via its ABD to mediate Bb granule dissociation and nuclear positioning, while the PRD is dispensable. We propose that Macf1a does not function via its canonical mechanism of linking two cytoskeletal systems together in dissociating the Bb. Instead our results suggest that Macf1a functions by linking one cytoskeletal system, cortical actin, to another structure, the Bb, where Macf1a is localized. Through this novel linking process, it dissociates the Bb at the oocyte cortex, thus specifying the AV axis of the oocyte and future egg. To our knowledge, this is also the first study to use genome editing to unravel the module-dependent function of a cytoskeletal linker.
[Mh] Termos MeSH primário: Polaridade Celular/genética
Oogênese/genética
Plaquinas/genética
Proteínas de Peixe-Zebra/genética
Peixe-Zebra/genética
[Mh] Termos MeSH secundário: Citoesqueleto de Actina/genética
Animais
Células Germinativas/crescimento & desenvolvimento
Complexo de Golgi/genética
Seres Humanos
Filamentos Intermediários/genética
Microtúbulos/genética
Microtúbulos/metabolismo
Oócitos/crescimento & desenvolvimento
Oócitos/metabolismo
Peixe-Zebra/crescimento & desenvolvimento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (MACF1 protein, zebrafish); 0 (Plakins); 0 (Zebrafish Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171110
[Lr] Data última revisão:
171110
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170908
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pgen.1006983


  2 / 131 MEDLINE  
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[PMID]:28068625
[Au] Autor:Li X; Zhang G; Wang Y; Elgehama A; Sun Y; Li L; Gu Y; Guo W; Xu Q
[Ad] Endereço:State Key Laboratory of Pharmaceutical Biotechnology, School of Life Science, Nanjing University, 163 Xianlin Avenue, Nanjing 210023, China.
[Ti] Título:Loss of periplakin expression is associated with the tumorigenesis of colorectal carcinoma.
[So] Source:Biomed Pharmacother;87:366-374, 2017 Mar.
[Is] ISSN:1950-6007
[Cp] País de publicação:France
[La] Idioma:eng
[Ab] Resumo:Periplakin (PPL), a member of the plakin protein family, has been reported to be down-expressed in urothelial carcinoma. The role of PPL in human colorectal cancer, however, remains largely unknown. Also little is known about the contribution of PPL to the malignant property of colorectal cancer and the intracellular function of PPL. In this study, we demonstrated that PPL was apparently down-expressed in colon carcinomas compared with normal and para-carcinoma tissues, which was correlated with the tumor size. Enforced expression of PPL in HT29 cells inhibited its proliferation evidenced by decreased expression of phosphorylated ERK and PCNA. Furthermore, PPL overexpression could reduce metastasis and epithelial-mesenchymal transition (EMT) of HT29 cells, with decreased expression of N-cadherin, Snail, Slug and α-SMA while increased expression of E-cadherin. On the contrary, the PPL knockdown could promote the cell proliferation, migratory, invasive and EMT ability of HT29 cells. Moreover, enforced expression of PPL induced G1/G0 cell cycle arrest, with decreased cyclin D1, p-Rb and increased expression of p27 , which could be reversed by PPL knockdown. In addition, PPL overexpression inhibited the growth of colon cancer allograft in vivo. Taken together, acted as a tumor suppressor in colon cancer progression, PPL could be a new biomarker or potential therapeutic target in colon cancer.
[Mh] Termos MeSH primário: Carcinogênese/genética
Neoplasias do Colo/genética
Neoplasias do Colo/patologia
Neoplasias Colorretais/genética
Neoplasias Colorretais/patologia
Plaquinas/genética
[Mh] Termos MeSH secundário: Actinas/genética
Animais
Caderinas/genética
Linhagem Celular Tumoral
Movimento Celular/genética
Proliferação Celular/genética
Colo/patologia
Progressão da Doença
Transição Epitelial-Mesenquimal/genética
Pontos de Checagem da Fase G1 do Ciclo Celular/genética
Regulação Neoplásica da Expressão Gênica/genética
Células HT29
Seres Humanos
Sistema de Sinalização das MAP Quinases/genética
Masculino
Camundongos
Camundongos Endogâmicos BALB C
Antígeno Nuclear de Célula em Proliferação/genética
Fase de Repouso do Ciclo Celular/genética
Fatores de Transcrição da Família Snail/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (ACTA2 protein, human); 0 (Actins); 0 (Cadherins); 0 (PPL protein, human); 0 (Plakins); 0 (Proliferating Cell Nuclear Antigen); 0 (SNAI1 protein, human); 0 (Snail Family Transcription Factors)
[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:170110
[St] Status:MEDLINE


  3 / 131 MEDLINE  
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[PMID]:28139597
[Au] Autor:Smolyannikova VA; Kubanova AA; Albanova VI; Nefedova MA; Karamova AE
[Ad] Endereço:State Research Center for Dermatovenereology and Cosmetology, Ministry of Health of Russia, Moscow, Russia; I.M. Sechenov First Moscow State Medical University, Ministry of Health of the Russian Federation, Moscow, Russia.
[Ti] Título:[Current approaches to the morphologic diagnosis of different types of congenital epidermolysis bullosa].
[Ti] Título:Sovremennye podkhody k morfologicheskoi diagnostike razlichnykh tipov vrozhdennogo bulleznogo epidermoliza..
[So] Source:Arkh Patol;78(6):9-16, 2016.
[Is] ISSN:0004-1955
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Congenital epidermolysis bullosa (CEB) is an extensive group of hereditary skin diseases, the differential diagnosis of which is a challenge due to the rarity of this pathology and the diversity of its clinical manifestations. The determination of the type of CEB makes it possible to estimate its prognosis and to facilitate a prenatal diagnosis. AIM: to optimize the morphological diagnosis of different types of CEB. MATERIAL AND METHODS: 28 skin biopsies from 14 patients with different types of CEB were investigated. The investigators performed routine histological examination of skin fragments taken from a bullous area and immunofluorescence antigen mapping using the indirect immunofluorescence test (IIFT) with antibodies against structural proteins of the dermal-epidermal junction (laminin α3, ß3, and γ2 chains, keratins 5 and 14, types VII and XVII collagen, α6 and ß4 integrin subunits, desmoplakin, plectin, kindlin-1, and plakophillin) of the apparently unaffected skin. The intact skin of healthy individuals, which had been obtained during cosmetic operations, was used as controls in IIFT. RESULTS: Immunofluorescence antigen mapping could determine the type of CEB in all cases and in 86% of cases identify the protein, the impaired production of which was responsible for the development of the disease. CONCLUSION: Immunofluorescence antigen mapping is an integral part of the comprehensive morphological diagnosis of CEB, acting as an intermediate between the morphological verification of CEB diagnosis and the targeted search for mutations by a molecular genetic method.
[Mh] Termos MeSH primário: Epidermólise Bolhosa/patologia
Pele/metabolismo
[Mh] Termos MeSH secundário: Adolescente
Adulto
Estudos de Casos e Controles
Criança
Colágeno/genética
Colágeno/metabolismo
Epidermólise Bolhosa/classificação
Epidermólise Bolhosa/genética
Epidermólise Bolhosa/metabolismo
Feminino
Seres Humanos
Integrinas/genética
Integrinas/metabolismo
Queratinas/genética
Queratinas/metabolismo
Laminina/genética
Laminina/metabolismo
Masculino
Meia-Idade
Plaquinas/genética
Plaquinas/metabolismo
Pele/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Integrins); 0 (Laminin); 0 (Plakins); 68238-35-7 (Keratins); 9007-34-5 (Collagen)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170629
[Lr] Data última revisão:
170629
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170201
[St] Status:MEDLINE
[do] DOI:10.17116/patol20167869-16


  4 / 131 MEDLINE  
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[PMID]:27790676
[Au] Autor:Chu CY
[Ad] Endereço:Department of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine, 7 Chung-Shan South Rd., Taipei, 10002, Taiwan. chiayu@ntu.edu.tw.
[Ti] Título:Autoantibodies against members of the plakin family in severe drug eruptions: does the phenomenon matter?
[So] Source:Br J Dermatol;175(5):866-867, 2016 11.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Autoanticorpos/imunologia
Plaquinas
[Mh] Termos MeSH secundário: Erupção por Droga
Seres Humanos
Pênfigo/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Plakins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161030
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.14940


  5 / 131 MEDLINE  
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[PMID]:27427436
[Au] Autor:Natsuga K; Watt FM
[Ad] Endereço:Department of Dermatology, Hokkaido University Graduate School of Medicine N15W7, Sapporo 060-8638, Japan; Centre for Stem Cells and Regenerative Medicine, King's College London, 28th floor, Guy's Tower Wing, London SE1 9RT, UK.
[Ti] Título:Galectin-6 is a novel skin anti-microbial peptide that is modulated by the skin barrier and microbiome.
[So] Source:J Dermatol Sci;84(1):97-99, 2016 Oct.
[Is] ISSN:1873-569X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Peptídeos Catiônicos Antimicrobianos/genética
Galectinas/genética
Microbiota
Pele/imunologia
[Mh] Termos MeSH secundário: Animais
Peptídeos Catiônicos Antimicrobianos/metabolismo
Dermatite Atópica/metabolismo
Galectinas/metabolismo
Perfilação da Expressão Gênica
Proteínas de Membrana/metabolismo
Camundongos
Plaquinas/metabolismo
Precursores de Proteínas/metabolismo
Pele/efeitos dos fármacos
Pele/metabolismo
[Pt] Tipo de publicação:LETTER
[Nm] Nome de substância:
0 (Antimicrobial Cationic Peptides); 0 (Galectins); 0 (Lgals6 protein, mouse); 0 (Membrane Proteins); 0 (Plakins); 0 (Ppl protein, mouse); 0 (Protein Precursors); 0 (envoplakin); 60108-77-2 (involucrin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160719
[St] Status:MEDLINE


  6 / 131 MEDLINE  
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[PMID]:27427435
[Au] Autor:Wang X; Chen T; Zhao J; Peng Y; Chen X; Tu P; Zhu X; Liu Z; Wang M
[Ad] Endereço:Department of Dermatology, Peking University First Hospital, Beijing 100034, China; Beijing Key Laboratory of Molecular Diagnosis of Dermatoses, Beijing 100034, China. Electronic address: xuewang@bjmu.edu.cn.
[Ti] Título:Extremities of the N-terminus of envoplakin and C-terminus of its linker subdomain are major epitopes of paraneoplastic pemphigus.
[So] Source:J Dermatol Sci;84(1):24-29, 2016 Oct.
[Is] ISSN:1873-569X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Autoantibodies against N-terminal domains and linker subdomains of envoplakin (EVPL) and periplakin (PPL) were frequently detected in sera of paraneoplastic pemphigus(PNP) patients. OBJECTIVES: To further investigate finer epitopes of EVPL and PPL, and evaluate their associations with clinical aspects of PNP. METHODS: We produced 12 overlapping truncated fragments of these regions in Escherichia coli, and measured their reactivities to sera of 65 PNP patients and 50 healthy volunteers by enzyme-linked immunosorbent assays (ELISA). Then appropriate statistics were performed to evaluate the correlation between antibodies against different fragments and clinical information of patients. RESULTS: EVPL-N1 (aa1-141) and EVPL-L3 (aa1684-1784) were recognized by PNP sera at the same sensitivity of 75.38% (49/65) with specificities of 98% and 92%, respectively. Although neoplasm types were not associated with any fragment, the ELISA of these fragments and indirect immunofluorescence on rat bladder complemented each other in detecting PNP. Meanwhile, levels of autoantibodies against EVPL-N3 were elevated with PNP accompanied with bronchiolitis obliterans or presented with lichen planus-like lesions (P<0.05). No influence of autoantibodies against any fragments on prognosis of the patients was observed by Cox regression test, though antibodies against some fragments were higher in the dead patients. CONCLUSIONS: The study proved antigenic epitopes were mainly concentrated on EVPL-N1 and EVPL-L3 in PNP. Autoantibodies against EVPL-N3 might associate with those patients accompanied with bronchiolitis obliterans or presented with lichen planus-like lesions.
[Mh] Termos MeSH primário: Proteínas de Membrana/química
Síndromes Paraneoplásicas/imunologia
Pênfigo/imunologia
Precursores de Proteínas/química
[Mh] Termos MeSH secundário: Animais
Antígenos/química
Área Sob a Curva
Autoanticorpos/química
Bronquiolite Obliterante/imunologia
Ensaio de Imunoadsorção Enzimática
Epitopos/química
Escherichia coli/metabolismo
Feminino
Técnica Indireta de Fluorescência para Anticorpo
Seres Humanos
Líquen Plano/imunologia
Masculino
Proteínas de Membrana/imunologia
Plaquinas/química
Plaquinas/imunologia
Modelos de Riscos Proporcionais
Domínios Proteicos
Precursores de Proteínas/imunologia
Curva ROC
Ratos
Proteínas Recombinantes/química
Sensibilidade e Especificidade
Bexiga Urinária/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antigens); 0 (Autoantibodies); 0 (Epitopes); 0 (Membrane Proteins); 0 (PPL protein, human); 0 (Plakins); 0 (Protein Precursors); 0 (Recombinant Proteins); 0 (envoplakin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:171109
[Lr] Data última revisão:
171109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160719
[St] Status:MEDLINE


  7 / 131 MEDLINE  
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[PMID]:27087170
[Au] Autor:Takehara A; Aoyama Y; Kurosawa M; Shirafuji Y; Umemura H; Kamiya K; Ushigome Y; Kano Y; Shiohara T; Iwatsuki K
[Ad] Endereço:Department of Dermatology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama, Japan.
[Ti] Título:Longitudinal analysis of antibody profiles against plakins in severe drug eruptions: emphasis on correlation with tissue damage in drug-induced hypersensitivity syndrome and drug reaction with eosinophilia and systemic symptoms.
[So] Source:Br J Dermatol;175(5):944-952, 2016 Nov.
[Is] ISSN:1365-2133
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: The evidence for severe drug eruption as a trigger for autoimmune disease has recently increased. No information is available on how tissue damage in severe drug eruptions can induce autoimmune responses. OBJECTIVES: To investigate whether the generation of autoantibodies (autoAbs) against plakin family proteins could be the cause or result of tissue damage in patients with severe drug eruptions and whether the generation of autoAbs could be prevented by systemic corticosteroids during the acute stage. METHODS: We retrospectively analysed alterations of serum levels of autoAbs against plakin family proteins in patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) and drug-induced hypersensitivity syndrome (DiHS)/drug reaction with eosinophilia and systemic symptoms (DRESS) during the acute stage and long after resolution over a period of more than 10 years. RESULTS: AutoAbs against plakin family proteins were detected in patients with either SJS/TEN or DiHS/DRESS regardless of the epidermal damage in the acute stage, and were sustained even long after resolution in DiHS/DRESS, indicating that those autoAbs are neither the cause nor the consequence of epidermal damage, at least in DiHS/DRESS. Severe liver damage and noncorticosteroid therapy during the early and acute stages of DiHS/DRESS were associated with the subsequent generation of these autoAbs. CONCLUSIONS: These autoAbs are neither necessarily the cause nor the result of epidermal damage in DiHS/DRESS, because the presence of these autoAbs was not restricted to patients with SJS/TEN but was also observed in those with DiHS/DRESS, which is characterized by lack of epidermal damage. Severe liver damage and/or immune responses that could be prevented by corticosteroids in the acute stage of DiHS/DRESS are among the causal factors contributing to the generation of autoimmune responses.
[Mh] Termos MeSH primário: Autoanticorpos/metabolismo
Erupção por Droga/imunologia
Plaquinas/imunologia
[Mh] Termos MeSH secundário: Doença Aguda
Corticosteroides/uso terapêutico
Estudos de Casos e Controles
Síndrome de Hipersensibilidade a Medicamentos/imunologia
Eosinofilia/imunologia
Feminino
Seres Humanos
Hepatopatias/imunologia
Masculino
Meia-Idade
Proteínas Recombinantes
Estudos Retrospectivos
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); 0 (Autoantibodies); 0 (Plakins); 0 (Recombinant Proteins)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:171006
[Lr] Data última revisão:
171006
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160419
[St] Status:MEDLINE
[do] DOI:10.1111/bjd.14677


  8 / 131 MEDLINE  
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[PMID]:26940098
[Au] Autor:Salih M; Demmers JA; Bezstarosti K; Leonhard WN; Losekoot M; van Kooten C; Gansevoort RT; Peters DJ; Zietse R; Hoorn EJ; DIPAK Consortium
[Ad] Endereço:Department of Internal Medicine, Division of Nephrology & Transplantation, and.
[Ti] Título:Proteomics of Urinary Vesicles Links Plakins and Complement to Polycystic Kidney Disease.
[So] Source:J Am Soc Nephrol;27(10):3079-3092, 2016 Oct.
[Is] ISSN:1533-3450
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Novel therapies in autosomal dominant polycystic kidney disease (ADPKD) signal the need for markers of disease progression or response to therapy. This study aimed to identify disease-associated proteins in urinary extracellular vesicles (uEVs), which include exosomes, in patients with ADPKD. We performed quantitative proteomics on uEVs from healthy controls and patients with ADPKD using a labeled approach and then used a label-free approach with uEVs of different subjects (healthy controls versus patients with ADPKD versus patients with non-ADPKD CKD). In both experiments, 30 proteins were consistently more abundant (by two-fold or greater) in ADPKD-uEVs than in healthy- and CKD-uEVs. Of these proteins, we selected periplakin, envoplakin, villin-1, and complement C3 and C9 for confirmation because they were also significantly overrepresented in pathway analysis and were previously implicated in ADPKD pathogenesis. Immunoblotting confirmed higher abundances of the selected proteins in uEVs from three independent groups of patients with ADPKD. Whereas uEVs of young patients with ADPKD and preserved kidney function already had higher levels of complement, only uEVs of patients with advanced stages of ADPKD had increased levels of villin-1, periplakin, and envoplakin. Furthermore, all five proteins correlated positively with total kidney volume. Analysis in kidney tissue from mice with kidney-specific, tamoxifen-inducible Pkd1 deletion demonstrated higher expression in more severe stages of the disease and correlation with kidney weight for each protein of interest. In summary, proteomic analysis of uEVs identified plakins and complement as disease-associated proteins in ADPKD. These proteins are new candidates for evaluation as biomarkers or targets for therapy in ADPKD.
[Mh] Termos MeSH primário: Complemento C3/fisiologia
Complemento C9/fisiologia
Vesículas Extracelulares
Plaquinas/fisiologia
Rim Policístico Autossômico Dominante/etiologia
Proteômica
Urina/química
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Complement C3); 0 (Complement C9); 0 (Plakins)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171001
[Lr] Data última revisão:
171001
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160305
[St] Status:MEDLINE


  9 / 131 MEDLINE  
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[PMID]:26778565
[Au] Autor:Boczonadi V; Määttä A
[Ad] Endereço:Institute of Genetic Medicine, Newcastle University, Newcastle-upon-Tyne, United Kingdom.
[Ti] Título:Functional Analysis of Periplakin and Envoplakin, Cytoskeletal Linkers, and Cornified Envelope Precursor Proteins.
[So] Source:Methods Enzymol;569:309-29, 2016.
[Is] ISSN:1557-7988
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Envoplakin and periplakin are the two smallest plakin family cytoskeletal linker proteins that connect intermediate filaments to cellular junctions and other membrane locations. These two plakins have a structural role in the assembly of the cornified envelope (CE), the terminal stage of epidermal differentiation. Analysis of gene-targeted mice lacking both these plakins and the third initial CE scaffold protein, involucrin, demonstrate the importance of the structural integrity of CE for a proper epidermal barrier function. It has emerged that periplakin, which also has a wider tissue distribution than envoplakin, has additional, independent roles. Periplakin participates in the cytoskeletal organization also in other tissues and interacts with a wide range of membrane-associated proteins such as kazrin and butyrophilin BTN3A1. This review covers methods used to understand periplakin and envoplakin functions in cell culture models, including siRNA ablation of periplakin expression and the use of tagged protein domain constructs to study localization and interactions. In addition, assays that can be used to analyze CEs and epidermal barrier function in gene-targeted mice are described and discussed.
[Mh] Termos MeSH primário: Proteínas Ricas em Prolina do Estrato Córneo/fisiologia
Proteínas de Membrana/fisiologia
Plaquinas/fisiologia
Precursores de Proteínas/fisiologia
[Mh] Termos MeSH secundário: Animais
Fracionamento Celular
Linhagem Celular Tumoral
Proteínas Ricas em Prolina do Estrato Córneo/isolamento & purificação
Técnicas de Silenciamento de Genes
Seres Humanos
Queratinócitos/metabolismo
Proteínas de Membrana/isolamento & purificação
Plaquinas/isolamento & purificação
Precursores de Proteínas/isolamento & purificação
Técnicas do Sistema de Duplo-Híbrido
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Cornified Envelope Proline-Rich Proteins); 0 (Membrane Proteins); 0 (Plakins); 0 (Protein Precursors); 0 (envoplakin)
[Em] Mês de entrada:1610
[Cu] Atualização por classe:161230
[Lr] Data última revisão:
161230
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160119
[St] Status:MEDLINE


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[PMID]:26740080
[Au] Autor:Has C
[Ad] Endereço:Department of Dermatology, Medical Center - University of Freiburg, Freiburg, Germany.
[Ti] Título:Hemidesmosomes: how much plakins do they need?
[So] Source:Exp Dermatol;25(4):263-4, 2016 Apr.
[Is] ISSN:1600-0625
[Cp] País de publicação:Denmark
[La] Idioma:eng
[Mh] Termos MeSH primário: Hemidesmossomos/metabolismo
Queratinócitos/metabolismo
Plaquinas/metabolismo
[Mh] Termos MeSH secundário: Animais
Colágeno/metabolismo
Distonina/metabolismo
Epidermólise Bolhosa Simples/metabolismo
Neuropatias Hereditárias Sensoriais e Autônomas/metabolismo
Seres Humanos
Integrina beta4/metabolismo
Camundongos
Mutação
Isoformas de Proteínas/metabolismo
Transdução de Sinais
Biologia de Sistemas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DST protein, human); 0 (Dystonin); 0 (ITGB4 protein, human); 0 (Integrin beta4); 0 (Plakins); 0 (Protein Isoforms); 9007-34-5 (Collagen)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:170207
[Lr] Data última revisão:
170207
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160108
[St] Status:MEDLINE
[do] DOI:10.1111/exd.12939



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