Base de dados : MEDLINE
Pesquisa : D12.776.220.150 [Categoria DeCS]
Referências encontradas : 254 [refinar]
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[PMID]:29055413
[Au] Autor:Archer NK; Dilolli MN; Miller LS
[Ad] Endereço:Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
[Ti] Título:Pushing the Envelope in Psoriasis: Late Cornified Envelope Proteins Possess Antimicrobial Activity.
[So] Source:J Invest Dermatol;137(11):2257-2259, 2017 Nov.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Deletion of late cornified envelope (LCE) genes LCE3B and LCE3C (LCE3B/C-del) is a psoriasis risk factor linked to the major psoriasis risk gene HLA-C*06. Niehues et al. demonstrate that LCE3B/C-del leads to increased keratinocyte LCE3A expression. They also show that LCE3A/B/C possess antimicrobial activity but do not obviously regulate epidermal barrier integrity. These findings implicate LCE proteins in psoriasis pathogenesis via a new functional role.
[Mh] Termos MeSH primário: Proteínas Ricas em Prolina do Estrato Córneo/genética
Regulação da Expressão Gênica
Predisposição Genética para Doença
Polimorfismo de Nucleotídeo Único
Psoríase/tratamento farmacológico
Psoríase/genética
[Mh] Termos MeSH secundário: Anti-Infecciosos/uso terapêutico
Estudos de Casos e Controles
Feminino
Genótipo
Seres Humanos
Masculino
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Infective Agents); 0 (Cornified Envelope Proline-Rich Proteins); 0 (LCE3A protein, human); 0 (LCE3B protein, human); 0 (LCE3C protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171023
[St] Status:MEDLINE


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[PMID]:28886156
[Au] Autor:Lietman CD; Segedy AK; Li B; Fazio S; Atkinson JB; Linton MF; Young PP
[Ad] Endereço:Department of Pathology Microbiology and Immunology; Vanderbilt University Medical Center; Nashville, TN, United States of America.
[Ti] Título:Loss of SPRR3 in ApoE-/- mice leads to atheroma vulnerability through Akt dependent and independent effects in VSMCs.
[So] Source:PLoS One;12(9):e0184620, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Vascular smooth muscle cells (VSMCs) represent important modulators of plaque stability in advanced lesions. We previously reported that loss of small proline-rich repeat protein 3 (Sprr3), leads to VSMC apoptosis in a PI3K/Akt-dependent manner and accelerates lesion progression. Here, we investigated the role of Sprr3 in modulating plaque stability in hyperlipidemic ApoE-/- mice. We show that loss of Sprr3 increased necrotic core size and reduced cap collagen content of atheromas in brachiocephalic arteries with evidence of plaque rupture and development of intraluminal thrombi. Moreover, Sprr3-/-ApoE-/- mice developed advanced coronary artery lesions accompanied by intraplaque hemorrhage and left ventricle microinfarcts. SPRR3 is known to reduce VSMC survival in lesions by promoting their apoptosis. In addition, we demonstrated that Sprr3-/- VSMCs displayed reduced expression of procollagen in a PI3K/Akt dependent manner. SPRR3 loss also increased MMP gelatinase activity in lesions, and increased MMP2 expression, migration and contraction of VSMCs independently of PI3K/Akt. Consequently, Sprr3 represents the first described VSMC modulator of each of the critical features of cap stability, including VSMC numbers, collagen type I synthesis, and protease activity through Akt dependent and independent pathways.
[Mh] Termos MeSH primário: Apolipoproteínas E/metabolismo
Proteínas Ricas em Prolina do Estrato Córneo/metabolismo
Miócitos de Músculo Liso/metabolismo
[Mh] Termos MeSH secundário: Animais
Apolipoproteínas E/genética
Proteínas Ricas em Prolina do Estrato Córneo/genética
Feminino
Fibronectinas/metabolismo
Immunoblotting
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Músculo Liso Vascular/citologia
Fosfatidilinositol 3-Quinases/genética
Fosfatidilinositol 3-Quinases/metabolismo
Proteínas Proto-Oncogênicas c-akt/genética
Proteínas Proto-Oncogênicas c-akt/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Transdução de Sinais/genética
Transdução de Sinais/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Apolipoproteins E); 0 (Cornified Envelope Proline-Rich Proteins); 0 (Fibronectins); EC 2.7.1.- (Phosphatidylinositol 3-Kinases); EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171016
[Lr] Data última revisão:
171016
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170909
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0184620


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[PMID]:28634035
[Au] Autor:Niehues H; Tsoi LC; van der Krieken DA; Jansen PAM; Oortveld MAW; Rodijk-Olthuis D; van Vlijmen IMJJ; Hendriks WJAJ; Helder RW; Bouwstra JA; van den Bogaard EH; Stuart PE; Nair RP; Elder JT; Zeeuwen PLJM; Schalkwijk J
[Ad] Endereço:Department of Dermatology, Radboud University Medical Center, Radboud Institute for Molecular Life Sciences, Nijmegen, The Netherlands.
[Ti] Título:Psoriasis-Associated Late Cornified Envelope (LCE) Proteins Have Antibacterial Activity.
[So] Source:J Invest Dermatol;137(11):2380-2388, 2017 Nov.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Terminally differentiating epidermal keratinocytes express a large number of structural and antimicrobial proteins that are involved in the physical barrier function of the stratum corneum and provide innate cutaneous host defense. Late cornified envelope (LCE) genes, located in the epidermal differentiation complex on chromosome 1, encode a family of 18 proteins of unknown function, whose expression is largely restricted to epidermis. Deletion of two members, LCE3B and LCE3C (LCE3B/C-del), is a widely-replicated psoriasis risk factor that interacts with the major psoriasis-psoriasis risk gene HLA-C*06. Here we performed quantitative trait locus analysis, utilizing RNA-seq data from human skin and found that LCE3B/C-del was associated with a markedly increased expression of LCE3A, a gene directly adjacent to LCE3B/C-del. We confirmed these findings in a 3-dimensional skin model using primary keratinocytes from LCE3B/C-del genotyped donors. Functional analysis revealed that LCE3 proteins, and LCE3A in particular, have defensin-like antimicrobial activity against a variety of bacterial taxa at low micromolar concentrations. No genotype-dependent effect was observed for the inside-out or outside-in physical skin barrier function. Our findings identify an unknown biological function for LCE3 proteins and suggest a role in epidermal host defense and LCE3B/C-del-mediated psoriasis risk.
[Mh] Termos MeSH primário: Proteínas Ricas em Prolina do Estrato Córneo/genética
Regulação da Expressão Gênica/imunologia
Imunidade Inata/genética
Psoríase/genética
Psoríase/imunologia
[Mh] Termos MeSH secundário: Antibacterianos/imunologia
Biópsia por Agulha
Células Cultivadas/citologia
Células Cultivadas/metabolismo
Feminino
Predisposição Genética para Doença
Genótipo
Seres Humanos
Imuno-Histoquímica
Queratinócitos
Desequilíbrio de Ligação
Masculino
Polimorfismo de Nucleotídeo Único
Psoríase/patologia
Reação em Cadeia da Polimerase em Tempo Real/métodos
Papel (Figurativo)
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Cornified Envelope Proline-Rich Proteins); 0 (LCE3B protein, human); 0 (LCE3C protein, human)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170622
[St] Status:MEDLINE


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[PMID]:27463736
[Au] Autor:Yoshida S; Yamamoto N; Wada N; Tomokiyo A; Hasegawa D; Hamano S; Mitarai H; Monnouchi S; Yuda A; Maeda H
[Ad] Endereço:Department of Endodontology, Kyushu University Hospital, Maidashi, Higashi-ku, Fukuoka, Japan.
[Ti] Título:GDNF From Human Periodontal Ligament Cells Treated With Pro-Inflammatory Cytokines Promotes Neurocytic Differentiation of PC12 Cells.
[So] Source:J Cell Biochem;118(4):699-708, 2017 Apr.
[Is] ISSN:1097-4644
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Glial cell line-derived neurotrophic factor (GDNF) is known to mediate multiple biological activities such as promotion of cell motility and proliferation, and morphogenesis. However, little is known about its effects on periodontal ligament (PDL) cells. Recently, we reported that GDNF expression is increased in wounded rat PDL tissue and human PDL cells (HPDLCs) treated with pro-inflammatory cytokines. Here, we investigated the associated expression of GDNF and the pro-inflammatory cytokine interleukin-1 beta (IL-1ß) in wounded PDL tissue, and whether HPDLCs secrete GDNF which affects neurocytic differentiation. Rat PDL cells near the wounded area showed intense immunoreactions against an anti-GDNF antibody, where immunoreactivity was also increased against an anti-IL-1ß antibody. Compared with untreated cells, HPDLCs treated with IL-1ß or tumor necrosis factor-alpha showed an increase in the secretion of GDNF protein. Conditioned medium of IL-1ß-treated HPDLCs (IL-1ß-CM) increased neurite outgrowth of PC12 rat adrenal pheochromocytoma cells. The expression levels of two neural regeneration-associated genes, growth-associated protein-43 (Gap-43), and small proline-rich repeat protein 1A (Sprr1A), were also upregulated in IL-1ß-CM-treated PC12 cells. These stimulatory effects of IL-1ß-CM were significantly inhibited by a neutralizing antibody against GDNF. In addition, U0126, a MEK inhibitor, inhibited GDNF-induced neurite outgrowth of PC12 cells. These findings suggest that an increase of GDNF in wounded PDL tissue might play an important role in neural regeneration probably via the MEK/ERK signaling pathway. J. Cell. Biochem. 118: 699-708, 2017. © 2016 Wiley Periodicals, Inc.
[Mh] Termos MeSH primário: Citocinas/fisiologia
Fator Neurotrófico Derivado de Linhagem de Célula Glial/fisiologia
Neurônios/citologia
Neurônios/fisiologia
Ligamento Periodontal/fisiologia
[Mh] Termos MeSH secundário: Animais
Diferenciação Celular/fisiologia
Células Cultivadas
Proteínas Ricas em Prolina do Estrato Córneo/genética
Citocinas/farmacologia
Proteína GAP-43/genética
Expressão Gênica/efeitos dos fármacos
Fator Neurotrófico Derivado de Linhagem de Célula Glial/farmacologia
Seres Humanos
Interleucina-1beta/farmacologia
Interleucina-1beta/fisiologia
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Masculino
Regeneração Nervosa/efeitos dos fármacos
Regeneração Nervosa/fisiologia
Neuritos/efeitos dos fármacos
Neuritos/fisiologia
Neurônios/efeitos dos fármacos
Células PC12
Ligamento Periodontal/citologia
Ligamento Periodontal/lesões
RNA Mensageiro/genética
RNA Mensageiro/metabolismo
Ratos
Ratos Sprague-Dawley
Proteínas Recombinantes/farmacologia
Fator de Necrose Tumoral alfa/farmacologia
Fator de Necrose Tumoral alfa/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cornified Envelope Proline-Rich Proteins); 0 (Cytokines); 0 (GAP-43 Protein); 0 (GDNF protein, human); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Interleukin-1beta); 0 (RNA, Messenger); 0 (Recombinant Proteins); 0 (Tumor Necrosis Factor-alpha)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160728
[St] Status:MEDLINE
[do] DOI:10.1002/jcb.25662


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[PMID]:27304082
[Au] Autor:Trzeciak M; Sakowicz-Burkiewicz M; Wesserling M; Dobaczewska D; Glen J; Nowicki R; Pawelczyk T
[Ad] Endereço:Department of Dermatology, Venereology and Allergology, Medical University of Gdansk, 80-211 Gdansk, Poland. mtrzeciak@gumed.edu.pl.
[Ti] Título:Expression of Cornified Envelope Proteins in Skin and Its Relationship with Atopic Dermatitis Phenotype.
[So] Source:Acta Derm Venereol;97(1):36-41, 2017 01 04.
[Is] ISSN:1651-2057
[Cp] País de publicação:Sweden
[La] Idioma:eng
[Ab] Resumo:Changes in the expression of cornified envelope (CE) proteins are thought to affect the development and course of atopic dermatitis (AD). The aim of this study was to examine the expression level of CE proteins in order to identify new molecular markers of the AD phenotype. Expression levels of CE proteins were evaluated in the skin of patients with AD (38 biopsies) and healthy subjects (26 biopsies). Levels of FLG, FLG2 and SPRR3 mRNAs and proteins were reduced in AD skin. Levels of LELP-1 and SPRR1A transcripts and proteins were significantly increased in AD skin. SPRR3v2 mRNA level in non-lesional AD skin correlated with severity of AD, and SPRR3 protein level in non-lesional AD skin correlated inversely with pruritus. FLG protein level in AD skin correlated inversely with severity of AD. These results point to SPRR3 as an important factor in AD and itch.
[Mh] Termos MeSH primário: Proteínas Ricas em Prolina do Estrato Córneo/genética
Dermatite Atópica/genética
Expressão Gênica
[Mh] Termos MeSH secundário: Adolescente
Adulto
Biomarcadores/metabolismo
Biópsia
Estudos de Casos e Controles
Proteínas Ricas em Prolina do Estrato Córneo/metabolismo
Dermatite Atópica/metabolismo
Ensaio de Imunoadsorção Enzimática
Feminino
Seres Humanos
Imunoglobulina E/sangue
Proteínas de Filamentos Intermediários/genética
Masculino
Meia-Idade
Fenótipo
Reação em Cadeia da Polimerase em Tempo Real
Proteínas S100/genética
Índice de Gravidade de Doença
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cornified Envelope Proline-Rich Proteins); 0 (Intermediate Filament Proteins); 0 (LELP1 protein, human); 0 (S100 Proteins); 0 (SPRR1A protein, human); 0 (SPRR3 protein, human); 0 (filaggrin); 0 (filaggrin-2 protein, human); 149686-82-8 (SPRR1B protein, human); 37341-29-0 (Immunoglobulin E)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170309
[Lr] Data última revisão:
170309
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160616
[St] Status:MEDLINE
[do] DOI:10.2340/00015555-2482


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[PMID]:27919236
[Au] Autor:Pajic P; Lin YL; Xu D; Gokcumen O
[Ad] Endereço:Department of Biological Sciences, University at Buffalo, Cooke 639, Buffalo, NY, 14260, USA.
[Ti] Título:The psoriasis-associated deletion of late cornified envelope genes LCE3B and LCE3C has been maintained under balancing selection since Human Denisovan divergence.
[So] Source:BMC Evol Biol;16(1):265, 2016 Dec 05.
[Is] ISSN:1471-2148
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: A common, 32kb deletion of LCE3B and LCE3C genes is strongly associated with psoriasis. We recently found that this deletion is ancient, predating Human-Denisovan divergence. However, it was not clear why negative selection has not removed this deletion from the population. RESULTS: Here, we show that the haplotype block that harbors the deletion (i) retains high allele frequency among extant and ancient human populations; (ii) harbors unusually high nucleotide variation (π, P < 4.1 × 10 ); (iii) contains an excess of intermediate frequency variants (Tajima's D, P < 3.9 × 10 ); and (iv) has an unusually long time to coalescence to the most recent common ancestor (TSel, 0.1 quantile). CONCLUSIONS: Our results are most parsimonious with the scenario where the LCE3BC deletion has evolved under balancing selection in humans. More broadly, this is consistent with the hypothesis that a balance between autoimmunity and natural vaccination through increased exposure to pathogens maintains this deletion in humans.
[Mh] Termos MeSH primário: Proteínas Ricas em Prolina do Estrato Córneo/genética
Evolução Molecular
Deleção de Genes
Psoríase/genética
[Mh] Termos MeSH secundário: Alelos
Frequência do Gene
Predisposição Genética para Doença
Seres Humanos
Polimorfismo de Nucleotídeo Único
Deleção de Sequência
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cornified Envelope Proline-Rich Proteins); 0 (LCE3B protein, human); 0 (LCE3C protein, human)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170801
[Lr] Data última revisão:
170801
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161207
[St] Status:MEDLINE


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[PMID]:27736988
[Au] Autor:Moriyama M; Moriyama H; Uda J; Kubo H; Nakajima Y; Goto A; Akaki J; Yoshida I; Matsuoka N; Hayakawa T
[Ad] Endereço:Pharmaceutical Research and Technology Institute, Kindai University, Higashi-Osaka, Osaka, Japan.
[Ti] Título:Beneficial Effects of the Genus Aloe on Wound Healing, Cell Proliferation, and Differentiation of Epidermal Keratinocytes.
[So] Source:PLoS One;11(10):e0164799, 2016.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Aloe has been used as a folk medicine because it has several important therapeutic properties. These include wound and burn healing, and Aloe is now used in a variety of commercially available topical medications for wound healing and skin care. However, its effects on epidermal keratinocytes remain largely unclear. Our data indicated that both Aloe vera gel (AVG) and Cape aloe extract (CAE) significantly improved wound healing in human primary epidermal keratinocytes (HPEKs) and a human skin equivalent model. In addition, flow cytometry analysis revealed that cell surface expressions of ß1-, α6-, ß4-integrin, and E-cadherin increased in HPEKs treated with AVG and CAE. These increases may contribute to cell migration and wound healing. Treatment with Aloe also resulted in significant changes in cell-cycle progression and in increases in cell number. Aloe increased gene expression of differentiation markers in HPEKs, suggesting roles for AVG and CAE in the improvement of keratinocyte function. Furthermore, human skin epidermal equivalents developed from HPEKs with medium containing Aloe were thicker than control equivalents, indicating the effectiveness of Aloe on enhancing epidermal development. Based on these results, both AVG and CAE have benefits in wound healing and in treatment of rough skin.
[Mh] Termos MeSH primário: Aloe/química
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Extratos Vegetais/farmacologia
[Mh] Termos MeSH secundário: Aloe/metabolismo
Caderinas/genética
Caderinas/metabolismo
Linhagem Celular
Movimento Celular/efeitos dos fármacos
Proteínas Ricas em Prolina do Estrato Córneo/genética
Proteínas Ricas em Prolina do Estrato Córneo/metabolismo
Seres Humanos
Integrina alfa6/genética
Integrina alfa6/metabolismo
Integrina beta1/genética
Integrina beta1/metabolismo
Integrina beta4/genética
Integrina beta4/metabolismo
Queratinócitos/citologia
Queratinócitos/efeitos dos fármacos
Queratinócitos/metabolismo
Microscopia de Fluorescência
Modelos Biológicos
Extratos Vegetais/química
Cicatrização
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cadherins); 0 (Cornified Envelope Proline-Rich Proteins); 0 (Integrin alpha6); 0 (Integrin beta1); 0 (Integrin beta4); 0 (Plant Extracts); 0 (SPRR2A protein, human); 149686-82-8 (SPRR1B protein, human)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161014
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0164799


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[PMID]:27667567
[Au] Autor:Scholz GM; Sulaiman NS; Al Baiiaty S; Kwa MQ; Reynolds EC
[Ad] Endereço:Oral Health Cooperative Research Centre, Melbourne Dental School, Bio21 Molecular Science and Biotechnology Institute, University of Melbourne, Victoria 3010, Australia.
[Ti] Título:A novel regulatory relationship between RIPK4 and ELF3 in keratinocytes.
[So] Source:Cell Signal;28(12):1916-1922, 2016 Dec.
[Is] ISSN:1873-3913
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Keratinocytes are central to the barrier functions of surface epithelia, such as the gingiva and epidermis. RIPK4 is a key regulator of keratinocyte differentiation; however, the signalling pathways in which it functions remain poorly defined. In this study, we identified a regulatory relationship between RIPK4 and ELF3, an ETS family transcription factor. RIPK4 was shown to be important for the upregulation of ELF3 gene expression by the PKC agonist PMA in both oral and epidermal keratinocytes. RIPK4 promotes keratinocyte differentiation in part by phosphorylating and thereby activating the IRF6 transcription factor. Significantly, silencing of IRF6 inhibited the PMA-inducible expression of ELF3. A role for the GRHL3 transcription factor, a downstream target gene of IRF6, in the regulation of ELF3 expression was similarly demonstrated. ELF3 has previously been shown to regulate the expression of SPPR1A and SPRR1B, small proline-rich proteins that contribute to the cornification of keratinocytes. Consistently, RIPK4 and IRF6 were important for the PMA-inducible expression of SPRR1A and SPRR1B. They were also important for the upregulation of TGM1, a transglutaminase that catalyses the cross-linking of proteins, including small proline-rich proteins, during keratinocyte cornification. RIPK4 was also shown to upregulate the expression of TGM2 independently of IRF6. Collectively, our findings position RIPK4 upstream of a hierarchal IRF6-GRHL3-ELF3 transcription factor pathway in keratinocytes, as well as provide insight into a potential role for RIPK4 in the regulation of keratinocyte cornification.
[Mh] Termos MeSH primário: Proteínas de Ligação a DNA/metabolismo
Queratinócitos/metabolismo
Proteínas Serina-Treonina Quinases/metabolismo
Proteínas Proto-Oncogênicas c-ets/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Proteínas Ricas em Prolina do Estrato Córneo/genética
Proteínas Ricas em Prolina do Estrato Córneo/metabolismo
Proteínas de Ligação a DNA/genética
Proteínas de Ligação ao GTP/genética
Proteínas de Ligação ao GTP/metabolismo
Regulação da Expressão Gênica/efeitos dos fármacos
Seres Humanos
Fatores Reguladores de Interferon/metabolismo
Modelos Biológicos
Biossíntese de Proteínas/efeitos dos fármacos
Inibidores da Síntese de Proteínas/farmacologia
Proteínas Proto-Oncogênicas c-ets/genética
Fatores de Transcrição/genética
Transglutaminases/genética
Transglutaminases/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cornified Envelope Proline-Rich Proteins); 0 (DNA-Binding Proteins); 0 (ELF3 protein, human); 0 (GRHL3 protein, human); 0 (IRF6 protein, human); 0 (Interferon Regulatory Factors); 0 (Protein Synthesis Inhibitors); 0 (Proto-Oncogene Proteins c-ets); 0 (Transcription Factors); EC 2.3.2.- (transglutaminase 2); EC 2.3.2.13 (Transglutaminases); EC 2.3.2.13 (transglutaminase 1); EC 2.7.1.- (ANKRD3 protein, human); EC 2.7.11.1 (Protein-Serine-Threonine Kinases); EC 3.6.1.- (GTP-Binding Proteins)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170929
[Lr] Data última revisão:
170929
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160927
[St] Status:MEDLINE


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[PMID]:27167730
[Au] Autor:Ishitsuka Y; Huebner AJ; Rice RH; Koch PJ; Speransky VV; Steven AC; Roop DR
[Ad] Endereço:Department of Dermatology and Charles C. Gates Center for Regenerative Medicine, University of Colorado Anschutz Medical Campus, Aurora, Colorado, USA.
[Ti] Título:Lce1 Family Members Are Nrf2-Target Genes that Are Induced to Compensate for the Loss of Loricrin.
[So] Source:J Invest Dermatol;136(8):1656-63, 2016 Aug.
[Is] ISSN:1523-1747
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Loricrin is a major component of the cornified cell envelope, a highly insoluble structure composed of covalently cross-linked proteins. Although loricrin knockout mice only exhibit a mild transient phenotype at birth, they show a marked delay in the formation of an epidermal barrier in utero. We recently discovered that induction of a compensatory response to repair the defective barrier is initiated by amniotic fluid via activation of NF-E2-related factor 2 and identified Sprr2d and Sprr2h as direct transcriptional targets. Proteomic analysis suggested that other proteins were also incorporated into the loricrin knockout cell envelope, in addition to the small proline rich proteins. Here we present evidence suggesting that the late cornified envelope 1 proteins are also compensatory components as determined by their localization within the loricrin knockout cell envelope via immunoelectron microscopy. We also demonstrate that late cornified envelope 1 genes are upregulated at the transcriptional level in loricrin knockout mouse skin and confirm that late cornified envelope 1 genes are transcriptional targets of NRF2. Our present study further highlights the complexity and importance of a compensatory mechanism that evolved in terrestrial animals to ensure the formation of a functional epidermal barrier.
[Mh] Termos MeSH primário: Proteínas Ricas em Prolina do Estrato Córneo/metabolismo
Epiderme/metabolismo
Proteínas de Membrana/metabolismo
Fator 2 Relacionado a NF-E2/metabolismo
[Mh] Termos MeSH secundário: Motivos de Aminoácidos
Animais
Proteínas Ricas em Prolina do Estrato Córneo/genética
Proteína 1 Associada a ECH Semelhante a Kelch/genética
Proteína 1 Associada a ECH Semelhante a Kelch/metabolismo
Proteínas de Membrana/genética
Camundongos
Camundongos Knockout
Microscopia Imunoeletrônica
Fator 2 Relacionado a NF-E2/genética
Regiões Promotoras Genéticas
Proteômica
Transgenes
Regulação para Cima
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cornified Envelope Proline-Rich Proteins); 0 (Keap1 protein, mouse); 0 (Kelch-Like ECH-Associated Protein 1); 0 (Membrane Proteins); 0 (NF-E2-Related Factor 2); 0 (Nfe2l2 protein, mouse); 0 (Sprr2d protein, mouse); 0 (Sprr2h protein, mouse); 0 (loricrin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170717
[Lr] Data última revisão:
170717
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160512
[St] Status:MEDLINE


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[PMID]:27048876
[Au] Autor:Chandra A; Lahiri A; Senapati S; Basu B; Ghosh S; Mukhopadhyay I; Behra A; Sarkar S; Chatterjee G; Chatterjee R
[Ad] Endereço:Human Genetics Unit, Indian Statistical Institute, 203 B. T. Road, Kolkata, India 700108.
[Ti] Título:Increased Risk of Psoriasis due to combined effect of HLA-Cw6 and LCE3 risk alleles in Indian population.
[So] Source:Sci Rep;6:24059, 2016 Apr 06.
[Is] ISSN:2045-2322
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:HLA-Cw6 is one of the most associated alleles in psoriasis. Recently, Late Cornified Envelop 3 (LCE3) genes were identified as a susceptibility factor for psoriasis. Some population showed epistatic interaction of LCE3 risk variants with HLA-Cw6, while some population failed to show any association. We determined the associations of a 32.2 kb deletion comprising LCE3C-3B genes and three SNPs (rs1886734, rs4112788; rs7516108) at the LCE3 gene cluster among the psoriasis patients in India. All three SNPs at the LCE3 gene cluster failed to show any association. In contrary, for patients with HLA-Cw6 allele, all three SNPs and the LCE3C-3B deletion showed significant associations. While, all five LCE3 genes were upregulated in psoriatic skin, only LCE3A showed significant overexpression with homozygous risk genotype compared to the non-risk genotype. LCE3B also showed significant overexpression in patients with HLA-Cw6 allele. Moreover, LCE3A showed significantly higher expression in patients bearing homozygous risk genotype in presence of HLA-Cw6 allele but not in those having non-risk genotype, demonstrating the combined effect of HLA-Cw6 allele and risk associated genotype near LCE3A gene. Integration of genetic and gene expression data thus allowed us to identify the actual disease variants at the LCE3 cluster among the psoriasis patients in India.
[Mh] Termos MeSH primário: Proteínas Ricas em Prolina do Estrato Córneo/genética
Antígenos HLA-C/genética
Psoríase/genética
[Mh] Termos MeSH secundário: Adulto
Alelos
Estudos de Casos e Controles
Epistasia Genética
Feminino
Deleção de Genes
Genótipo
Homozigoto
Seres Humanos
Índia
Masculino
Meia-Idade
Polimorfismo de Nucleotídeo Único
Risco
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cornified Envelope Proline-Rich Proteins); 0 (HLA-C Antigens); 0 (HLA-C*06 antigen); 0 (LCE3A protein, human); 0 (LCE3B protein, human); 0 (LCE3C protein, human)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170331
[Lr] Data última revisão:
170331
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160407
[St] Status:MEDLINE
[do] DOI:10.1038/srep24059



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