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Pesquisa : D05.750.078.593.450.600.200 [Categoria DeCS]
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[PMID]:28026086
[Au] Autor:Buragohain L; Nanda T; Ghosh A; Ghosh M; Kumar R; Kumar S; Gupta SS; Bharali A; Mohanty AK; Singh I; Balhara AK
[Ad] Endereço:Indian Veterinary Research Institute, Bareilly, Uttar Pradesh, India.
[Ti] Título:Identification of serum protein markers for early diagnosis of pregnancy in buffalo.
[So] Source:Anim Sci J;88(8):1189-1197, 2017 Aug.
[Is] ISSN:1740-0929
[Cp] País de publicação:Australia
[La] Idioma:eng
[Ab] Resumo:Improper or delayed pregnancy diagnosis has significant impact over animal production, particularly in buffaloes which inherently suffer from several reproductive inefficiencies. Thus the present study has undertaken to identify serum protein markers pertaining to early pregnancy diagnosis in buffaloes. Serum samples were collected from 10 pregnant Murrah Buffalo heifers at weekly intervals from days 0-35 post-artificial insemination and from 12 inseminated non-pregnant cyclic buffalo heifers on days 0, 7, 14 and 21. Two-dimensional gel electrophoresis and densitometric analysis revealed the presence of five protein spots showing average density fold change of ≥4 during early pregnancy. Mass spectrometry analysis identified these up-regulated proteins as anti-testosterone antibody light chain, apolipoprotein A-II precursor, serum amyloid A, cytokeratin type II, component IV isoform 1, which are have established roles in embryogenesis, but over-expression of the fifth identified protein immunoglobulin lambda light chain in pregnancy has been elucidated as a novel finding in the current study. Further, with bioinformatics analysis, potential antigenic B-cell epitopes were predicted for all these five proteins. An antibody cocktail-based approach involving antibodies against all these five up-regulated entire proteins or their epitopes could be developed for early detection of pregnancy in buffaloes. © 2016 Japanese Society of Animal Science.
[Mh] Termos MeSH primário: Anticorpos/sangue
Búfalos
Testes de Gravidez/veterinária
Prenhez
[Mh] Termos MeSH secundário: Animais
Apolipoproteína A-II/sangue
Biomarcadores/sangue
Complemento C4
Eletroforese em Gel Bidimensional
Epitopos de Linfócito B/sangue
Feminino
Queratina-2/sangue
Espectrometria de Massas
Gravidez
Testes de Gravidez/métodos
Precursores de Proteínas/sangue
Proteína Amiloide A Sérica
Testosterona/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antibodies); 0 (Apolipoprotein A-II); 0 (Biomarkers); 0 (Complement C4); 0 (Epitopes, B-Lymphocyte); 0 (Keratin-2); 0 (Protein Precursors); 0 (Serum Amyloid A Protein); 3XMK78S47O (Testosterone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170921
[Lr] Data última revisão:
170921
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161228
[St] Status:MEDLINE
[do] DOI:10.1111/asj.12754


  2 / 37 MEDLINE  
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[PMID]:27324070
[Au] Autor:Aktug H; Acikgoz E; Uysal A; Oltulu F; Oktem G; Yigitturk G; Demir K; Yavasoglu A; Bozok Cetintas V
[Ad] Endereço:Department of Histology and Embryology, Faculty of Medicine, Ege University, Izmir, Turkey.
[Ti] Título:Comparison of cell cycle components, apoptosis and cytoskeleton-related molecules and therapeutic effects of flavopiridol and geldanamycin on the mouse fibroblast, lung cancer and embryonic stem cells.
[So] Source:Tumour Biol;37(9):12423-12440, 2016 Sep.
[Is] ISSN:1423-0380
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Similarities and differences in the cell cycle components, apoptosis and cytoskeleton-related molecules among mouse skin fibroblast cells (MSFs), mouse squamous cell lung carcinomas (SqCLCs) and mouse embryonic stem cells (mESCs) are important determinants of the behaviour and differentiation capacity of these cells. To reveal apoptotic pathways and to examine the distribution and the role of cell cycle-cell skeleton comparatively would necessitate tumour biology and stem cell biology to be assessed together in terms of oncogenesis and embryogenesis. The primary objectives of this study are to investigate the effects of flavopiridol, a cell cycle inhibitor, and geldanamycin, a heat shock protein inhibitor on mouse somatic, tumour and embryonic stem cells, by specifically focusing on alterations in cytoskeletal proteins, cell polarity and motility as well as cell cycle regulators. To meet these objectives, expression of several genes, cell cycle analysis and immunofluorescence staining of intracellular cytoskeletal molecules were performed in untreated and flavopiridol- or geldanamycin-treated cell lines. Cytotoxicity assays showed that SqCLCs are more sensitive to flavopiridol than MSFs and mESCs. Keratin-9 and keratin-2 expressions increased dramatically whereas cell cycle regulatory genes decreased significantly in the flavopiridol-treated MSFs. Flavopiridol-treated SqCLCs displayed a slight increase in several cell cytoskeleton regulatory genes as well as cell cycle regulatory genes. However, gene expression profiles of mESCs were not affected after flavopiridol treatment except the Cdc2a. Cytotoxic concentrations of geldanamycin were close to each other for all cell lines. Cdkn1a was the most increased gene in the geldanamycin-treated MSFs. However, expression levels of cell cytoskeleton-associated genes were increased dramatically in the geldanamycin-treated SqCLCs. Our results revealing differences in molecular mechanisms between embryogenesis and carcinogenesis may prove crucial in developing novel therapeutics that specifically target cancer cells.
[Mh] Termos MeSH primário: Apoptose/efeitos dos fármacos
Benzoquinonas/farmacologia
Células-Tronco Embrionárias/efeitos dos fármacos
Flavonoides/farmacologia
Lactamas Macrocíclicas/farmacologia
Neoplasias Pulmonares/tratamento farmacológico
Piperidinas/farmacologia
[Mh] Termos MeSH secundário: Actinas/análise
Animais
Ciclo Celular/efeitos dos fármacos
Linhagem Celular Tumoral
Transição Epitelial-Mesenquimal
Fibroblastos/efeitos dos fármacos
Flavonoides/uso terapêutico
Queratina-2/análise
Neoplasias Pulmonares/patologia
Camundongos
Piperidinas/uso terapêutico
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Actins); 0 (Benzoquinones); 0 (Flavonoids); 0 (Keratin-2); 0 (Lactams, Macrocyclic); 0 (Piperidines); 45AD6X575G (alvocidib); Z3K3VJ16KU (geldanamycin)
[Em] Mês de entrada:1702
[Cu] Atualização por classe:171111
[Lr] Data última revisão:
171111
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160622
[St] Status:MEDLINE


  3 / 37 MEDLINE  
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[PMID]:27265811
[Au] Autor:Cui Y; Song Y; Geng Q; Ding Z; Qin Y; Fan R; Dong C; Geng J
[Ad] Endereço:College of Animal Science and Veterinary Medicine, Shanxi Agricultural University, Taigu, 030801, PR China.
[Ti] Título:The expression of KRT2 and its effect on melanogenesis in alpaca skins.
[So] Source:Acta Histochem;118(5):505-12, 2016 Jun.
[Is] ISSN:1618-0372
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:In order to investigate the effects of the keratin 2 (KRT2) on alpaca melanocyte in vivo and vitro, the immunohistochemistry (IHC), quantitative real-time PCR (qPCR), Western blot, and alpaca melanocytes transfection methods were used. The results showed that mRNA and protein expression of KRT2 was highly expressed in brown skin in comparison with that in white skin. Moreover, we found that KRT2 was expressed in alpaca melanocytes in vitro by immunocytochemistry. After transfection with KRT2 in alpaca melanocytes, the relative mRNA and protein expression of KRT2, microphthalmia-associtated transcription factor (MITF), tyrosinase (TYR) and tyrosinase-related protein 1 (TYRP1) in alpaca skin melanocytes was increased with significant differences; a further result was the increase of melanin production. The results suggested that KRT2 functions in alpaca hair color formation, which offered an essential theoretical basis for further exploration of the role of melanogenesis.
[Mh] Termos MeSH primário: Queratina-2/metabolismo
Melaninas/biossíntese
Pele/metabolismo
[Mh] Termos MeSH secundário: Animais
Camelídeos Americanos
Expressão Gênica
Cor de Cabelo
Queratina-2/genética
Melanócitos/metabolismo
Pele/citologia
Pigmentação da Pele
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Keratin-2); 0 (Melanins)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170116
[Lr] Data última revisão:
170116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160607
[St] Status:MEDLINE


  4 / 37 MEDLINE  
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[PMID]:26603179
[Au] Autor:Fischer H; Langbein L; Reichelt J; Buchberger M; Tschachler E; Eckhart L
[Ad] Endereço:Department of Dermatology, Medical University of Vienna, 1090 Vienna, Austria. Electronic address: heinz.fischer@meduniwien.ac.at.
[Ti] Título:Keratins K2 and K10 are essential for the epidermal integrity of plantar skin.
[So] Source:J Dermatol Sci;81(1):10-6, 2016 Jan.
[Is] ISSN:1873-569X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: K1 and K2 are the main type II keratins in the suprabasal epidermis where each of them heterodimerizes with the type I keratin K10 to form intermediate filaments. In regions of the ears, tail, and soles of the mouse, only K2 is co-expressed with K10, suggesting that these keratins suffice to form a mechanically resilient cytoskeleton. OBJECTIVE: To determine the effects of the suppression of both main keratins, K2 and K10, in the suprabasal plantar epidermis of the mouse. METHODS: Krt2(-/-) Krt10(-/-) mice were generated by crossing Krt2(-/-) and Krt10(-/-) mice. Epidermal morphology of soles of hind-paws was examined macroscopically and histologically. Immunofluorescence analysis and quantitative PCR analysis were performed to analyze the expression of keratins in sole skin of wildtype and Krt2(-/-) Krt10(-/-) mice. Highly abundant proteins of the sole stratum corneum were determined by electrophoretic and chromatographic separation and subsequent mass spectrometry. RESULTS: K2 and K10 are the most prominent suprabasal keratins in normal mouse soles with the exception of the footpads where K1, K9 and K10 predominate. Mice lacking both K2 and K10 were viable and developed epidermal acanthosis and hyperkeratosis in inter-footpad epidermis of the soles. The expression of keratins K1, K9 and K16 was massively increased at the RNA and protein levels in the soles of Krt2(-/-) Krt10(-/-) mice. CONCLUSIONS: This study demonstrates that the loss of the main cytoskeletal components of plantar epidermis, i.e. K2 and K10, can be only partly compensated by the upregulation of other keratins. The thickening of the epidermis in the soles of Krt2(-/-) Krt10(-/-) mice may serve as a model for pathomechanistic aspects of palmoplantar keratoderma.
[Mh] Termos MeSH primário: Epiderme/fisiologia
Queratina-10/fisiologia
Queratina-2/fisiologia
[Mh] Termos MeSH secundário: Animais
Fenômenos Biomecânicos
Modelos Animais de Doenças
Epiderme/anatomia & histologia
Extremidades
Seres Humanos
Queratina-1/genética
Queratina-1/metabolismo
Queratina-10/genética
Queratina-16/genética
Queratina-16/metabolismo
Queratina-2/deficiência
Queratina-2/genética
Queratina-9/genética
Queratina-9/metabolismo
Ceratodermia Palmar e Plantar/genética
Ceratodermia Palmar e Plantar/metabolismo
Ceratodermia Palmar e Plantar/patologia
Ceratose/genética
Ceratose/metabolismo
Ceratose/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Knockout
Fenótipo
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Keratin-1); 0 (Keratin-16); 0 (Keratin-2); 0 (Keratin-9); 0 (Krt1-10 protein, mouse); 0 (Krt1-9 protein, mouse); 0 (RNA, Messenger); 147785-83-9 (Keratin-10)
[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:151126
[St] Status:MEDLINE


  5 / 37 MEDLINE  
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[PMID]:26581228
[Au] Autor:Hotz A; Oji V; Bourrat E; Jonca N; Mazereeuw-Hautier J; Betz RC; Blume-Peytavi U; Stieler K; Morice-Picard F; Schönbuchner I; Markus S; Schlipf N; Fischer J
[Ad] Endereço:Institute of Human Genetics, , University Medical Center Freiburg,, Freiburg, Germany.
[Ti] Título:Expanding the Clinical and Genetic Spectrum of KRT1, KRT2 and KRT10 Mutations in Keratinopathic Ichthyosis.
[So] Source:Acta Derm Venereol;96(4):473-8, 2016 May.
[Is] ISSN:1651-2057
[Cp] País de publicação:Sweden
[La] Idioma:eng
[Ab] Resumo:Twenty-six families with keratinopathic ichthyoses (epidermolytic ichthyosis, superficial epidermolytic ichthyosis or congenital reticular ichthyosiform erythroderma) were studied. Epidermolytic ichthyosis is caused by mutations in the genes KRT1 or KRT10, mutations in the gene KRT2 lead to superficial epidermolytic ichthyosis, and congenital reticular ichthyosiform erythroderma is caused by frameshift mutations in the genes KRT10 or KRT1, which lead to the phenomenon of revertant mosaicism. In this study mutations were found in KRT1, KRT2 and KRT10, including 8 mutations that are novel pathogenic variants. We report here the first case of a patient with congenital reticular ichthyosiform erythroderma carrying a mutation in KRT10 that does not lead to an arginine-rich reading frame. Novel clinical features found in patients with congenital reticular ichthyosiform erythroderma are described, such as mental retardation, spasticity, facial dysmorphisms, symblepharon and malposition of the 4th toe.
[Mh] Termos MeSH primário: Hiperceratose Epidermolítica/genética
Ictiose Lamelar/genética
Queratina-10/genética
Queratina-1/genética
Queratina-2/genética
Mutação
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Criança
Pré-Escolar
Análise Mutacional de DNA
Feminino
Estudos de Associação Genética
Predisposição Genética para Doença
Hereditariedade
Seres Humanos
Hiperceratose Epidermolítica/diagnóstico
Ictiose Lamelar/diagnóstico
Lactente
Recém-Nascido
Masculino
Meia-Idade
Linhagem
Fenótipo
Fatores de Risco
Índice de Gravidade de Doença
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (KRT1 protein, human); 0 (KRT10 protein, human); 0 (KRT2 protein, human); 0 (Keratin-1); 0 (Keratin-2); 147785-83-9 (Keratin-10)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170117
[Lr] Data última revisão:
170117
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:151120
[St] Status:MEDLINE
[do] DOI:10.2340/00015555-2299


  6 / 37 MEDLINE  
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[PMID]:26391144
[Au] Autor:Rauhala L; Hämäläinen L; Dunlop TW; Pehkonen P; Bart G; Kokkonen M; Tammi M; Tammi R; Pasonen-Seppänen S
[Ad] Endereço:Institute of Biomedicine, University of Eastern Finland, P.O. Box 1627, FI-70211 Kuopio, Finland. Electronic address: leena.rauhala@uef.fi.
[Ti] Título:The organic osmolyte betaine induces keratin 2 expression in rat epidermal keratinocytes - A genome-wide study in UVB irradiated organotypic 3D cultures.
[So] Source:Toxicol In Vitro;30(1 Pt B):462-75, 2015 Dec 25.
[Is] ISSN:1879-3177
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The moisturizing and potentially protective properties of the organic osmolyte betaine (trimethylglycine) have made it an attractive component for skin care products. Its wide use despite the lack of comprehensive studies addressing its specific effects in skin led us to characterize the molecular targets of betaine in keratinocytes and to explore, whether it modifies the effects of acute UVB exposure. Genome-wide expression analysis was performed on organotypic cultures of rat epidermal keratinocytes, treated either with betaine (10mM), UVB (30 mJ/cm(2)) or their combination. Results were verified with qRT-PCR, western blotting and immunohistochemistry. Additionally, cell proliferation and differentiation were analyzed. Among the 89 genes influenced by betaine, the differentiation marker keratin 2 showed the highest upregulation, which was also confirmed at protein level. Expression of Egr1, a transcription factor, and Purkinje cell protein 4, a regulator of Ca(2+)/calmodulin metabolism, also increased, while downregulated genes included several ion-channel components, such as Fxyd2. Bioinformatics analyses suggest that genes modulated by betaine are involved in DNA replication, might counteract UV-induced processes, and include many targets of transcription factors associated with cell proliferation and differentiation. Our results indicate that betaine controls unique gene expression pathways in keratinocytes, including some involved in differentiation.
[Mh] Termos MeSH primário: Betaína/farmacologia
Queratina-2/genética
Queratinócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Estudo de Associação Genômica Ampla
Queratinócitos/metabolismo
Queratinócitos/efeitos da radiação
RNA Mensageiro/análise
Ratos
Raios Ultravioleta
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Keratin-2); 0 (RNA, Messenger); 3SCV180C9W (Betaine)
[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:150923
[St] Status:MEDLINE


  7 / 37 MEDLINE  
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[PMID]:25979451
[Au] Autor:Akasaka E; Minakawa S; Rokunohe D; Toyomaki Y; Matsuzaki Y; Sawamura D; Nakano H
[Ad] Endereço:Department of Dermatology, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
[Ti] Título:Superficial epidermolytic ichthyosis caused by a novel KRT2 mutation.
[So] Source:J Dermatol Sci;79(1):86-8, 2015 Jul.
[Is] ISSN:1873-569X
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Mh] Termos MeSH primário: Hiperceratose Epidermolítica/genética
Queratina-2/genética
Mutação
[Mh] Termos MeSH secundário: Criança
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; LETTER
[Nm] Nome de substância:
0 (KRT2 protein, human); 0 (Keratin-2)
[Em] Mês de entrada:1603
[Cu] Atualização por classe:150530
[Lr] Data última revisão:
150530
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150517
[St] Status:MEDLINE


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[PMID]:24838180
[Au] Autor:Kawasaki H; Tominaga M; Shigenaga A; Kamo A; Kamata Y; Iizumi K; Kimura U; Ogawa H; Takamori K; Yamakura F
[Ad] Endereço:The Institute for Environmental and Gender-Specific Medicine, Juntendo University Graduate School of Medicine, Inzai, Chiba 270-1695, Japan.
[Ti] Título:Importance of tryptophan nitration of carbonic anhydrase III for the morbidity of atopic dermatitis.
[So] Source:Free Radic Biol Med;73:75-83, 2014 Aug.
[Is] ISSN:1873-4596
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The nitration of proteins results from the vigorous production of reactive nitrogen species in inflammatory disease. We previously reported the proteomic analysis of nitrated tryptophan residues in in vitro model cells for inflammatory diseases using a 6-nitrotryptophan-specific antibody. In this paper, we applied this method to the analysis of a disease model animal and identified the 6-nitrotryptophan-containing proteins in the skin of atopic dermatitis model mice (AD-NC/Nga mice). We found three nitrotryptophan-containing proteins, namely, carbonic anhydrase III (CAIII), α-enolase (α-ENO), and cytoskeletal keratin type II (KTII), and identified the positions of the nitrotryptophan residues in their amino acid sequences: Trp47 and Trp123 in CAIII, Trp365 in α-ENO, and Trp221 in KTII. Among these, the nitration of CAIII was increased not only in the lesional skin of AD-NC/Nga mice but also in the mice that did not present any symptoms. The in vitro nitration of purified CAIII by peroxynitrite reduced its CO2 hydratase activity in a dose-dependent manner. In addition, we found that CAIII was induced during the differentiation of normal human epidermal keratinocytes. Furthermore, we found the presence of CAIII and the formation of 6-nitrotryptophan-containing proteins in both the lesional and the nonlesional sections of the skin of patients with atopic dermatitis through immunohistochemical staining. This study provides the first demonstration of the formation of 6-nitrotryptophan in human tissues and disease.
[Mh] Termos MeSH primário: Anidrase Carbônica III/metabolismo
Dermatite Atópica/patologia
Queratina-2/metabolismo
Fosfopiruvato Hidratase/metabolismo
Triptofano/análogos & derivados
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Modelos Animais de Doenças
Seres Humanos
Imuno-Histoquímica
Inflamação/imunologia
Inflamação/patologia
Queratinócitos/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos ICR
Ácido Peroxinitroso/química
Ratos
Espécies Reativas de Nitrogênio/química
Pele/patologia
Triptofano/química
Triptofano/imunologia
Triptofano/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Keratin-2); 0 (Reactive Nitrogen Species); 14691-52-2 (Peroxynitrous Acid); 46885-76-1 (6-nitrotryptophan); 8DUH1N11BX (Tryptophan); EC 4.2.1.- (Carbonic Anhydrase III); EC 4.2.1.11 (Phosphopyruvate Hydratase)
[Em] Mês de entrada:1505
[Cu] Atualização por classe:140726
[Lr] Data última revisão:
140726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140520
[St] Status:MEDLINE


  9 / 37 MEDLINE  
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[PMID]:24751727
[Au] Autor:Fischer H; Langbein L; Reichelt J; Praetzel-Wunder S; Buchberger M; Ghannadan M; Tschachler E; Eckhart L
[Ad] Endereço:Department of Dermatology, Medical University of Vienna, Vienna, Austria.
[Ti] Título:Loss of keratin K2 expression causes aberrant aggregation of K10, hyperkeratosis, and inflammation.
[So] Source:J Invest Dermatol;134(10):2579-2588, 2014 Oct.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Keratin K2 is one of the most abundant structural proteins of the epidermis; however, its biological significance has remained elusive. Here we show that suprabasal type II keratins, K1 and K2, are expressed in a mutually exclusive manner at different body sites of the mouse, with K2 being confined to the ear, sole, and tail skin. Deletion of K2 caused acanthosis and hyperkeratosis of the ear and the tail epidermis, corneocyte fragility, increased transepidermal water loss, and local inflammation in the ear skin. The loss of K2 was partially compensated by upregulation of K1 expression. However, a significant portion of K2-deficient suprabasal keratinocytes lacked a regular cytoskeleton and developed massive aggregates of the type I keratin, K10. Aggregate formation, but not hyperkeratosis, was suppressed by the deletion of both K2 and K10, whereas deletion of K10 alone caused clumping of K2 in ear skin. Taken together, this study demonstrates that K2 is a necessary and sufficient binding partner of K10 at distinct body sites of the mouse and that unbalanced expression of these keratins results in aggregate formation.
[Mh] Termos MeSH primário: Dermatite/metabolismo
Hiperceratose Epidermolítica/metabolismo
Queratina-10/metabolismo
Queratina-2/deficiência
Queratina-2/metabolismo
Dermatopatias/metabolismo
[Mh] Termos MeSH secundário: Animais
Dermatite/genética
Dermatite/patologia
Modelos Animais de Doenças
Orelha

Hiperceratose Epidermolítica/genética
Hiperceratose Epidermolítica/patologia
Queratina-1/metabolismo
Queratina-10/genética
Queratina-2/genética
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Pele/metabolismo
Pele/patologia
Dermatopatias/genética
Dermatopatias/patologia
Cauda
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Keratin-1); 0 (Keratin-2); 147785-83-9 (Keratin-10)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:170903
[Lr] Data última revisão:
170903
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140423
[St] Status:MEDLINE


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[PMID]:24254769
[Au] Autor:Lee HR; Shin HK; Park SY; Kim HY; Lee WS; Rhim BY; Hong KW; Kim CD
[Ad] Endereço:Medical Research Center for Ischemic Tissue Regeneration, Pusan National University, Yangsan-si, Gyeongsangnam-do, Republic of Korea.
[Ti] Título:Attenuation of ß-amyloid-induced tauopathy via activation of CK2α/SIRT1: targeting for cilostazol.
[So] Source:J Neurosci Res;92(2):206-17, 2014 Feb.
[Is] ISSN:1097-4547
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:ß-Amyloid (Aß) deposits and hyperphosphorylated tau aggregates are the chief hallmarks in the Alzheimer's disease (AD) brains, but the strategies for controlling these pathological events remain elusive. We hypothesized that CK2-coupled SIRT1 activation stimulated by cilostazol suppresses tau acetylation (Ac-tau) and tau phosphorylation (P-tau) by inhibiting activation of P300 and GSK3ß. Aß was endogenously overproduced in N2a cells expressing human APP Swedish mutation (N2aSwe) by exposure to medium containing 1% fetal bovine serum for 24 hr. Increased Aß accumulation was accompanied by increased Ac-tau and P-tau levels. Concomitantly, these cells showed increased P300 and GSK3ß P-Tyr216 expression; their expressions were significantly reduced by treatment with cilostazol (3-30 µM) and resveratrol (20 µM). Moreover, decreased expression of SIRT1 and its activity by Aß were significantly reversed by cilostazol as by resveratrol. In addition, cilostazol strongly stimulated CK2α phosphorylation and its activity, and then stimulated SIRT1 phosphorylation. These effects were confirmed by using the pharmacological inhibitors KT5720 (1 µM, PKA inhibitor), TBCA (20 µM, inhibitor of CK2), and sirtinol (20 µM, SIRT1 inhibitor) as well as by SIRT1 gene silencing and overexpression techniques. In conclusion, increased cAMP-dependent protein kinase-linked CK2/SIRT1 expression by cilostazol can be a therapeutic strategy to suppress the tau-related neurodegeneration in the AD brain.
[Mh] Termos MeSH primário: Queratina-2/metabolismo
Neurônios/efeitos dos fármacos
Fármacos Neuroprotetores/farmacologia
Sirtuína 1/biossíntese
Tauopatias/metabolismo
Tetrazóis/farmacologia
[Mh] Termos MeSH secundário: Doença de Alzheimer/metabolismo
Peptídeos beta-Amiloides/metabolismo
Precursor de Proteína beta-Amiloide/genética
Animais
Western Blotting
Linhagem Celular
Imunofluorescência
Seres Humanos
Camundongos
Neurônios/metabolismo
Transfecção
Proteínas tau/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Amyloid beta-Protein Precursor); 0 (Keratin-2); 0 (Neuroprotective Agents); 0 (Tetrazoles); 0 (tau Proteins); EC 3.5.1.- (Sirt1 protein, mouse); EC 3.5.1.- (Sirtuin 1); N7Z035406B (cilostazol)
[Em] Mês de entrada:1408
[Cu] Atualização por classe:131211
[Lr] Data última revisão:
131211
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:131121
[St] Status:MEDLINE
[do] DOI:10.1002/jnr.23310



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