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Pesquisa : G05.360.340.024.340.375.500.791.552 [Categoria DeCS]
Referências encontradas : 87 [refinar]
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[PMID]:28095352
[Au] Autor:Hu X; Baytak E; Li J; Akman B; Okay K; Hu G; Scuto A; Zhang W; Küçük C
[Ad] Endereço:Izmir International Biomedicine and Genome Institute (iBG-izmir), Dokuz Eylul University, Izmir, Turkey.
[Ti] Título:The relationship of REL proto-oncogene to pathobiology and chemoresistance in follicular and transformed follicular lymphoma.
[So] Source:Leuk Res;54:30-38, 2017 Mar.
[Is] ISSN:1873-5835
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Follicular lymphoma (FL) is a common type of indolent lymphoma that occasionally transforms to more aggressive B-cell lymphomas. These transformed follicular lymphomas (tFL) are often associated with chemoresistance whose mechanisms are currently unknown. REL, a proto-oncogene located on frequently amplified 2p16.1-p15 locus, promotes tumorigenesis in many cancer types through deregulation of the NF-κB pathway; however, its role in FL pathobiology or chemoresistance has not been addressed. Here, we evaluated REL gene copy number by q-PCR on FFPE FL tumor samples, and observed REL amplification in 30.4% of FL cases that was associated with weak elevation of transcript levels. PCR-Sanger analysis did not show any somatic mutation in FL tumors. In support of a marginal oncogenic role, a REL-transduced FL cell line was positively selected under limiting serum conditions. Interestingly, reanalysis of previously reported gene expression profiles revealed significant enrichment of DNA damage-induced repair and cell cycle arrest pathways in tFL tumors with high REL expression compared to those with low REL expression consistent with the critical role of c-REL in genotoxicity-induced NF-κB signaling, which was reported to lead to drug resistance. In addition to DNA damage repair genes such as ATM and BRCA1, anti-apoptotic BCL2 was significantly elevated in REL-high FL and tFL tumors. Altogether these data suggest that other genes located in amplified 2p16.1-p15 locus may have more oncogenic role in FL etiology; however, high REL expression may be useful as a predictive biomarker of response to immunochemotherapy, and inhibition of c-REL may potentially sensitize resistant FL or tFL cells to chemotherapy.
[Mh] Termos MeSH primário: Genes rel/fisiologia
Linfoma Folicular/genética
[Mh] Termos MeSH secundário: Biópsia
Pontos de Checagem do Ciclo Celular/genética
Reparo do DNA/genética
Resistência a Medicamentos Antineoplásicos/genética
Dosagem de Genes
Perfilação da Expressão Gênica
Seres Humanos
Linfoma Folicular/etiologia
Linfoma Folicular/patologia
NF-kappa B/metabolismo
Prognóstico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (NF-kappa B)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170731
[Lr] Data última revisão:
170731
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170118
[St] Status:MEDLINE


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[PMID]:26993753
[Au] Autor:Fan T; Wang S; Yu L; Yi H; Liu R; Geng W; Wan X; Ma Y; Cai L; Chen YH; Ruan Q
[Ad] Endereço:Shenzhen Laboratory of Fully Human Antibody Engineering, Institute of Biomedicine and Biotechnology, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen 518055, People's Republic of China.
[Ti] Título:Treating psoriasis by targeting its susceptibility gene Rel.
[So] Source:Clin Immunol;165:47-54, 2016 Apr.
[Is] ISSN:1521-7035
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Psoriasis is a chronic inflammatory disorder of the skin. Accumulating evidence indicates that the Rel gene, a member of the NF-κB family, is a risk factor for the disease. We sought to investigate whether psoriasis can be prevented by directly targeting the Rel gene transcript, i.e., the c-Rel mRNA. Using chemically-modified c-Rel specific siRNA (siRel) and poly(ethylene glycol)-b-poly(l-lysine)-b-poly(l-leucine) (PEG-PLL-PLLeu) micelles, we successfully knocked down the expression of c-Rel, and showed that the expression of cytokine IL-23, a direct target of c-Rel that can drive the development of IL-17-producing T cells, was markedly inhibited. More importantly, treating mice with siRel not only prevented but also ameliorated imiquimod (IMQ)-induced psoriasis. Mechanistic studies showed that siRel treatment down-regulated the expression of multiple inflammatory cytokines. Taken together, these results indicate that the susceptibility gene Rel can be targeted to treat and prevent psoriasis.
[Mh] Termos MeSH primário: Sistemas de Liberação de Medicamentos
Genes rel/genética
Predisposição Genética para Doença
Psoríase/tratamento farmacológico
Psoríase/genética
RNA Interferente Pequeno/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Camundongos
Camundongos Endogâmicos BALB C
Complexo de Inativação Induzido por RNA/uso terapêutico
Reação em Cadeia da Polimerase em Tempo Real
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Small Interfering); 0 (RNA-Induced Silencing Complex)
[Em] Mês de entrada:1608
[Cu] Atualização por classe:160419
[Lr] Data última revisão:
160419
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160320
[St] Status:MEDLINE


  3 / 87 MEDLINE  
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[PMID]:26757421
[Au] Autor:Hunter JE; Leslie J; Perkins ND
[Ad] Endereço:Institute for Cell and Molecular Biosciences, Faculty of Medical Sciences, Newcastle University, Newcastle Upon Tyne NE2 4HH, UK.
[Ti] Título:c-Rel and its many roles in cancer: an old story with new twists.
[So] Source:Br J Cancer;114(1):1-6, 2016 Jan 12.
[Is] ISSN:1532-1827
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:When the genes encoding NF-κB subunits were first isolated, their homology to the previously identified c-Rel proto-oncogene and its viral homologue v-Rel was clear. This provided the first indication that these transcription factors also had a role in cancer. Because of its homology to v-Rel, which transforms chicken B cells together with the important role c-Rel can have as a regulator of B- and T-cell proliferation, most attention has focussed on its role in B-cell lymphomas, where the REL gene is frequently amplified. However, a growing number of reports now indicate that c-Rel has important functions in many solid tumours, although studies in mice suggest it may not always function as an oncogene. Moreover, c-Rel is a critical regulator of fibrosis, which provides an environment for tumour development in many settings. Overall, c-Rel is emerging as a complex regulator of tumorigenesis, and there is still much to learn about its functions in human malignancies and the response to cancer therapies.
[Mh] Termos MeSH primário: Neoplasias/etiologia
Proteínas Proto-Oncogênicas c-rel/fisiologia
[Mh] Termos MeSH secundário: Animais
Fibrose
Genes p53/fisiologia
Genes rel/fisiologia
Seres Humanos
Linfoma de Células B/etiologia
Camundongos
Neoplasias/terapia
Proteínas Proto-Oncogênicas c-rel/química
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T; REVIEW
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-rel)
[Em] Mês de entrada:1605
[Cu] Atualização por classe:170922
[Lr] Data última revisão:
170922
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160113
[St] Status:MEDLINE
[do] DOI:10.1038/bjc.2015.410


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[PMID]:25912249
[Au] Autor:Savli H; Akkoyunlu RU; Çine N; Gluzman DF; Zavelevich MP; Sklyarenko LM; Koval SV; Sünnetçi D
[Ti] Título:Deregulated Levels of the NF-κB1, NF-κB2, and Rel Genes in Ukrainian Patients with Leukemia and Lymphoma in the Post-Chernobyl Period.
[So] Source:Turk J Haematol;33(1):8-14, 2016 Mar 05.
[Is] ISSN:1308-5263
[Cp] País de publicação:Turkey
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: Nuclear factor kappa B (NF-κB) is an important transcription factor in cancer and NF-κB activation has been seen in angiogenesis, tumor progression, and metastasis. Relationships between specific NF-κB gene networks, leukemogenesis, and radiation exposure are still unknown. Our aim was to study the expression levels of the NF-κB1, NF-κB2, and Rel genes in hematological malignancies in the post-Chernobyl period. MATERIALS AND METHODS: We analyzed gene expression levels of NF-κB1, NF-κB2, and Rel in 49 B-cell chronic lymphocytic leukemia, 8 B-cell non-Hodgkin's lymphoma, 3 acute myeloid leukemia, 3 chronic myeloid leukemia, 2 hairy cell leukemia, 2 myelodysplastic syndrome, and 2 T-cell large granular lymphocytic leukemia patients using real-time polymerase chain reaction. RESULTS: Expression levels of NF-κB1, NF-κB2, and Rel genes were found to be deregulated. CONCLUSION: These results could be accepted as specific gene traces to radiation-induced leukemia or as potential candidates for new diagnostic biomarker studies. Larger experiments and non-exposed control malignant cell populations are needed to clarify these suggestions.
[Mh] Termos MeSH primário: Acidente Nuclear de Chernobyl
Genes rel
Leucemia Induzida por Radiação/genética
Linfoma/genética
Subunidade p50 de NF-kappa B/genética
Subunidade p52 de NF-kappa B/genética
NF-kappa B/genética
Neoplasias Induzidas por Radiação/genética
Fator de Transcrição RelA/genética
[Mh] Termos MeSH secundário: Adulto
Idoso
Feminino
Seres Humanos
Leucemia Induzida por Radiação/epidemiologia
Leucemia Induzida por Radiação/etiologia
Linfoma/epidemiologia
Linfoma/etiologia
Linfoma/metabolismo
Masculino
Meia-Idade
Síndromes Mielodisplásicas/epidemiologia
Síndromes Mielodisplásicas/etiologia
Síndromes Mielodisplásicas/genética
Síndromes Mielodisplásicas/metabolismo
NF-kappa B/biossíntese
Subunidade p50 de NF-kappa B/biossíntese
Subunidade p52 de NF-kappa B/biossíntese
Neoplasias Induzidas por Radiação/epidemiologia
Neoplasias Induzidas por Radiação/etiologia
Neoplasias Induzidas por Radiação/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Fator de Transcrição RelA/biossíntese
Ucrânia/epidemiologia
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (NF-kappa B); 0 (NF-kappa B p50 Subunit); 0 (NF-kappa B p52 Subunit); 0 (Transcription Factor RelA)
[Em] Mês de entrada:1701
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150428
[St] Status:MEDLINE
[do] DOI:10.4274/tjh.2014.0190


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[PMID]:25912355
[Au] Autor:Liu T; Gao Y; Xu T
[Ad] Endereço:Laboratory of Fish Biogenetics & Immune Evolution, College of Marine Science, Zhejiang Ocean University, Zhoushan 316022, China.
[Ti] Título:Evolution of akirin family in gene and genome levels and coexpressed patterns among family members and rel gene in croaker.
[So] Source:Dev Comp Immunol;52(1):17-25, 2015 Sep.
[Is] ISSN:1879-0089
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Akirins, which are highly conserved nuclear proteins, are present throughout the metazoan and regulate innate immunity, embryogenesis, myogenesis, and carcinogenesis. This study reports all akirin genes from miiuy croaker and analyzes comprehensively the akirin gene family combined with akirin genes from other species. A second nuclear localization signal (NLS) is observed in akirin2 homologues, which is not in akirin1 homologues in all teleosts and most other vertebrates. Thus, we deduced that the loss of second NLS in akirin1 homologues in teleosts likely occurred in an ancestor to all Osteichthyes after splitting with cartilaginous fish. Significantly, the akirin2(2) gene included six exons interrupted by five introns in the miiuy croaker, which may be caused by the intron insertion event as a novel evidence for the variation of akirin gene structure in some species. In addition, comparison of the genomic neighborhood genes of akirin1, akirin2(1), and akirin2(2) demonstrates a strong level of conserved synteny across the teleost classes, which further proved the deduction of Macqueen and Johnston 2009 that the produce of akirin paralogues can be attributed to whole-genome duplications and the loss of some akirin paralogues after genome duplications. Furthermore, akirin gene family members and relish gene are ubiquitously expressed across all tissues, and their expression levels are increased in three immune tissues after infection with Vibrio anguillarum. Combined with the expression patterns of LEAP-1 and LEAP-2 from miiuy croaker, an intricate network of co-regulation among family members is established. Thus, it is further proved that akirins acted in concert with the relish protein to induce the expression of a subset of downstream pathway elements in the NF-kB dependent signaling pathway.
[Mh] Termos MeSH primário: Proteínas de Peixes/metabolismo
Genes rel
NF-kappa B/metabolismo
Perciformes/fisiologia
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Sequência de Aminoácidos
Animais
Biologia Computacional
Evolução Molecular
Proteínas de Peixes/genética
Genoma
Seres Humanos
Camundongos
Dados de Sequência Molecular
Proteínas Nucleares/genética
Filogenia
Homologia de Sequência de Aminoácidos
Transdução de Sinais
Fatores de Transcrição/genética
Transcriptoma
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Akirin1 protein, mouse); 0 (Fish Proteins); 0 (NF-kappa B); 0 (Nuclear Proteins); 0 (Transcription Factors)
[Em] Mês de entrada:1609
[Cu] Atualização por classe:150606
[Lr] Data última revisão:
150606
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150428
[St] Status:MEDLINE


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[PMID]:25842178
[Au] Autor:Li R; Zhang R; Zhang L; Zou J; Xing Q; Dou H; Hu X; Zhang L; Wang R; Bao Z
[Ad] Endereço:Key Laboratory of Marine Genetics and Breeding, College of Marine Life Sciences, Ocean University of China, 5 Yushan Road, Qingdao 266003, China.
[Ti] Título:Characterizations and expression analyses of NF-κB and Rel genes in the Yesso scallop (Patinopecten yessoensis) suggest specific response patterns against Gram-negative infection in bivalves.
[So] Source:Fish Shellfish Immunol;44(2):611-21, 2015 Jun.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Rel/NF-κB (nuclear factor kappa-light-chain-enhancer of activated B cells) genes are evolutionarily conserved and play a pivotal role in several physiological events. They have been extensively studied from various species, including both vertebrates and invertebrates. However, the Rel/NF-κB genes have not been systematically characterized in bivalves. In this study, we identified and characterized PyNF-κB and PyRel in the Yesso scallop (Patinopecten yessoensis). Phylogenetic and protein structural analyses were conducted to determine the identities and evolutionary relationships of Rel/NF-κB genes in Yesso scallop. Compared with the Rel/NF-κB genes from vertebrate species, the PyNF-κB and PyRel are relatively conserved in their structural features, but there were no paralogs found in P. yessoensis or other invertebrates. To gain insights into the roles of Rel/NF-κB genes during the innate immune response in scallop, quantitative real-time PCR was used to investigate the expression profiles of these genes at different developmental stages, in healthy adult tissues and in the hemolymph after bacterial infection with Micrococcus luteus and Vibrio anguillarum. The real-time PCR results indicated the abundance of PyNF-κB in the first four embryonic stages, including oocytes, fertilized eggs, morulae and blastulae. By contrast, PyRel was abundantly expressed in blastulae, trochophores and D-shaped larvae. In adult scallops, PyNF-κB and PyRel were ubiquitously expressed in most healthy tissues and highly expressed in most of the immune related tissues. Both genes were significantly up-regulated during the acute phase (3 h) after infection with Gram-positive (M. luteus) and negative (V. anguillarum) bacteria, while the much higher expression level of PyNF-κB suggested the involvement of the extra immune deficiency (IMD)-like pathway against the Gram-negative bacterial infection. The complex pattern of Rel/NF-κB induced expression suggested that PyNF-κB and PyRel both have specific and cooperative roles in the acute immune responses to bacterial infection.
[Mh] Termos MeSH primário: Regulação da Expressão Gênica/imunologia
Genes rel/genética
Bactérias Gram-Negativas/imunologia
NF-kappa B/genética
Pectinidae/genética
Pectinidae/imunologia
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
Análise por Conglomerados
Primers do DNA/genética
Mineração de Dados
Genes rel/imunologia
Modelos Genéticos
Dados de Sequência Molecular
NF-kappa B/imunologia
Pectinidae/microbiologia
Filogenia
Reação em Cadeia da Polimerase em Tempo Real
Análise de Sequência de DNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA Primers); 0 (NF-kappa B)
[Em] Mês de entrada:1601
[Cu] Atualização por classe:150429
[Lr] Data última revisão:
150429
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150406
[St] Status:MEDLINE


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[PMID]:25842167
[Au] Autor:Lorenz VN; Schön MP; Seitz CS
[Ad] Endereço:Department of Dermatology, Venereology and Allergology, University Medical Center Göttingen, Robert-Koch-Str. 40, 37075, Göttingen, Germany, verena.lorenz@med.uni-goettingen.de.
[Ti] Título:The c-Rel subunit of NF-κB is a crucial regulator of phenotype and motility of HaCaT keratinocytes.
[So] Source:Arch Dermatol Res;307(6):523-30, 2015 Aug.
[Is] ISSN:1432-069X
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:The transcription factor NF-κB exerts key functions in epidermal homeostasis and carcinogenesis. Its c-Rel subunit is expressed in squamous cell carcinoma, and c-Rel down-regulation results in increased apoptosis, G2/M cell cycle delay with reduced proliferation and aberrant mitotic spindle formation. To further study the impact of c-Rel on essential keratinocyte features such as migration and epithelial morphology, c-Rel was down-regulated in HaCaT keratinocytes by a siRNA approach. This inhibition of c-Rel impaired the keratinocyte-typical clustered growth leading to a more scattered appearance of the cultures. The cells were more spindle-shaped and elongated, albeit without expression changes of markers characteristic for epithelial mesenchymal transition. In addition, wound healing-related migration and adhesion to type I collagen, fibronectin, laminin and vitronectin were significantly impaired. On the sub-cellular level, these functional features were not associated with quantitatively altered adhesion receptor or Rho-GTPase expression, but rather with a significantly reduced length of cell-matrix adhesion complexes and altered appearance of filamentous actin. Thus, our studies support a role for c-Rel in processes crucial for keratinocyte integrity and malignant transformation such as adhesion and migration.
[Mh] Termos MeSH primário: Movimento Celular/fisiologia
Genes rel/fisiologia
Queratinócitos/metabolismo
NF-kappa B/metabolismo
[Mh] Termos MeSH secundário: Western Blotting
Adesão Celular/fisiologia
Células Cultivadas
Colágeno Tipo I/metabolismo
Regulação para Baixo/fisiologia
Fibronectinas/metabolismo
Imunofluorescência
Seres Humanos
Laminina/metabolismo
Fenótipo
RNA Interferente Pequeno/genética
Transfecção
Vitronectina/metabolismo
Proteínas rho de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Collagen Type I); 0 (Fibronectins); 0 (Laminin); 0 (NF-kappa B); 0 (RNA, Small Interfering); 0 (Vitronectin); EC 3.6.5.2 (rho GTP-Binding Proteins)
[Em] Mês de entrada:1604
[Cu] Atualização por classe:150720
[Lr] Data última revisão:
150720
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:150406
[St] Status:MEDLINE
[do] DOI:10.1007/s00403-015-1562-2


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[PMID]:25544748
[Au] Autor:Raymond A; Liu B; Liang H; Wei C; Guindani M; Lu Y; Liang S; St John LS; Molldrem J; Nagarajan L
[Ad] Endereço:Department of Genetics, the University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA. Graduate Program in Genes and Development, the University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
[Ti] Título:A role for BMP-induced homeobox gene MIXL1 in acute myelogenous leukemia and identification of type I BMP receptor as a potential target for therapy.
[So] Source:Oncotarget;5(24):12675-93, 2014 Dec 30.
[Is] ISSN:1949-2553
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mesoderm Inducer in Xenopus Like1 (MIXL1), a paired-type homeobox transcription factor induced by TGF-ß family of ligands is required for early embryonic specification of mesoderm and endoderm. Retrovirally transduced Mixl1 is reported to induce acute myelogenous leukemia (AML) with a high penetrance. But the mechanistic underpinnings of MIXL1 mediated leukemogenesis are unknown. Here, we establish the protooncogene c-REL to be a transcriptional target of MIXL1 by genome wide chromatin immune precipitation. Accordingly, expression of c-REL and its downstream targets BCL2L1 and BCL2A2 are elevated in MIXL1 expressing cells. Notably, MIXL1 regulates c-REL through a zinc finger binding motif, potentially by a MIXL1-Zinc finger protein transcriptional complex. Furthermore, MIXL1 expression is detected in the cancer genome atlas (TCGA) AML samples in a pattern mutually exclusive from that of HOXA9, CDX2 and HLX suggesting the existence of a core, yet distinct HOX transcriptional program. Finally, we demonstrate MIXL1 to be induced by BMP4 and not TGF-ß in primary human hematopoietic stem and progenitor cells. Consequently, MIXL1 expressing AML cells are preferentially sensitive to the BMPR1 kinase inhibitor LDN-193189. These findings support the existence of a novel MIXL1-c REL mediated survival axis in AML that can be targeted by BMPR1 inhibitors. (MIXL1- human gene, Mixl1- mouse ortholog, MIXL1- protein).
[Mh] Termos MeSH primário: Proteína Morfogenética Óssea 4/genética
Proteínas de Homeodomínio/genética
Leucemia Mieloide Aguda/genética
[Mh] Termos MeSH secundário: Animais
Receptores de Proteínas Morfogenéticas Ósseas Tipo I/antagonistas & inibidores
Diferenciação Celular/fisiologia
Linhagem Celular Tumoral
Genes Homeobox
Genes rel
Células HEK293
Células HL-60
Proteínas de Homeodomínio/biossíntese
Seres Humanos
Células K562
Leucemia Mieloide Aguda/tratamento farmacológico
Leucemia Mieloide Aguda/metabolismo
Camundongos
Terapia de Alvo Molecular
Células U937
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (BMP4 protein, human); 0 (Bone Morphogenetic Protein 4); 0 (Homeodomain Proteins); 0 (MIXL1 protein, human); EC 2.7.11.30 (Bone Morphogenetic Protein Receptors, Type I)
[Em] Mês de entrada:1511
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141230
[St] Status:MEDLINE


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[PMID]:25282160
[Au] Autor:Jeltsch KM; Hu D; Brenner S; Zöller J; Heinz GA; Nagel D; Vogel KU; Rehage N; Warth SC; Edelmann SL; Gloury R; Martin N; Lohs C; Lech M; Stehklein JE; Geerlof A; Kremmer E; Weber A; Anders HJ; Schmitz I; Schmidt-Supprian M; Fu M; Holtmann H; Krappmann D; Ruland J; Kallies A; Heikenwalder M; Heissmeyer V
[Ad] Endereço:1] Institute for Immunology, Ludwig-Maximilians-Universität München, Munich, Germany. [2] Institute of Molecular Immunology, Helmholtz Zentrum München, Munich, Germany.
[Ti] Título:Cleavage of roquin and regnase-1 by the paracaspase MALT1 releases their cooperatively repressed targets to promote T(H)17 differentiation.
[So] Source:Nat Immunol;15(11):1079-89, 2014 Nov.
[Is] ISSN:1529-2916
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Humoral autoimmunity paralleled by the accumulation of follicular helper T cells (T(FH) cells) is linked to mutation of the gene encoding the RNA-binding protein roquin-1. Here we found that T cells lacking roquin caused pathology in the lung and accumulated as cells of the T(H)17 subset of helper T cells in the lungs. Roquin inhibited T(H)17 cell differentiation and acted together with the endoribonuclease regnase-1 to repress target mRNA encoding the T(H)17 cell-promoting factors IL-6, ICOS, c-Rel, IRF4, IκBNS and IκBζ. This cooperation required binding of RNA by roquin and the nuclease activity of regnase-1. Upon recognition of antigen by the T cell antigen receptor (TCR), roquin and regnase-1 proteins were cleaved by the paracaspase MALT1. Thus, this pathway acts as a 'rheostat' by translating TCR signal strength via graded inactivation of post-transcriptional repressors and differential derepression of targets to enhance T(H)17 differentiation.
[Mh] Termos MeSH primário: Caspases/metabolismo
Proteínas de Neoplasias/metabolismo
Receptores de Antígenos de Linfócitos T/imunologia
Ribonucleases/metabolismo
Células Th17/citologia
Ubiquitina-Proteína Ligases/metabolismo
[Mh] Termos MeSH secundário: Proteínas Adaptadoras de Transdução de Sinal/genética
Sequência de Aminoácidos
Animais
Sítios de Ligação/imunologia
Diferenciação Celular/imunologia
Linhagem Celular
Genes rel/genética
Células HEK293
Seres Humanos
Proteína Coestimuladora de Linfócitos T Induzíveis/genética
Fatores Reguladores de Interferon/genética
Interleucina-6/genética
Pulmão/imunologia
Pulmão/patologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Camundongos Endogâmicos NOD
Camundongos Knockout
Proteína de Translocação 1 do Linfoma de Tecido Linfoide Associado à Mucosa
Proteínas Nucleares/genética
Proteínas/genética
RNA Mensageiro/genética
Proteínas de Ligação a RNA/metabolismo
Alinhamento de Sequência
Células Th17/imunologia
Ubiquitina-Proteína Ligases/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Adaptor Proteins, Signal Transducing); 0 (Icos protein, mouse); 0 (IkappaBNS protein, mouse); 0 (Inducible T-Cell Co-Stimulator Protein); 0 (Interferon Regulatory Factors); 0 (Interleukin-6); 0 (Neoplasm Proteins); 0 (Nfkbiz protein, mouse); 0 (Nuclear Proteins); 0 (Proteins); 0 (RNA, Messenger); 0 (RNA-Binding Proteins); 0 (Receptors, Antigen, T-Cell); 0 (interferon regulatory factor-4); EC 2.3.2.27 (Rc3h1 protein, mouse); EC 2.3.2.27 (Ubiquitin-Protein Ligases); EC 3.1.- (Ribonucleases); EC 3.1.- (regnase-1, mouse); EC 3.4.22.- (Caspases); EC 3.4.22.- (Malt1 protein, mouse); EC 3.4.22.- (Mucosa-Associated Lymphoid Tissue Lymphoma Translocation 1 Protein)
[Em] Mês de entrada:1501
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:141006
[St] Status:MEDLINE
[do] DOI:10.1038/ni.3008


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[PMID]:25158315
[Au] Autor:Zhang X; Huang Y; Cai X; Zou Z; Wang G; Wang S; Wang Y; Zhang Z
[Ad] Endereço:Key Laboratory of Healthy Mariculture for the East China Sea, Ministry of Agriculture, Fisheries College, Jimei University, Xiamen 361021, China.
[Ti] Título:Identification and expression analysis of immune-related genes linked to Rel/NF-κB signaling pathway under stresses and bacterial challenge from the small abalone Haliotis diversicolor.
[So] Source:Fish Shellfish Immunol;41(2):200-8, 2014 Dec.
[Is] ISSN:1095-9947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Inhibitor of NF-κB (IκB), nuclear factor-κB (NF-κB), and Akirin2 are all important members of Rel/NF-κB signaling pathway, which plays a pivotal role in regulating the innate immune response of vertebrates and invertebrates. In this study, the IκB (SaIκB) and Akirin2 (SaAkirin2) cDNAs of small abalone Haliotis diversicolor were cloned and characterized. The full length cDNA of SaIκB and SaAkirin2 were 1748 bp and 1452 bp respectively, encoding a protein of 401 aa and 187 aa respectively. A conserved degradation motif (DS56GIYS60) and six ankyrin repeats were identified in the SaIκB by SMART analysis. Meanwhile, a typical nuclear localization signal (NLS) was found at the N-terminal region of the SaAkirin2 protein. Also, the mRNA expression level of SaIκB, SaAkirin2, and AbNF-κB were detected by quantitative real-time PCR. The results revealed that all these three genes were ubiquitously expressed in 7 selected tissues. The expression level of SaIκB in gills was higher than that in other tissues (P < 0.05) while the expression level of AbNF-κB was significantly higher in hepatopancreas and haemocytes. The highest expression level of SaAkirin2 was detected in hepatopancreas, followed by mantle. The mRNA expression levels in either gills or haemocytes of SaIκB, SaAkirin2, and AbNF-κB were significantly up-regulated (P < 0.05) post thermal stress, hypoxia exposure, thermal plus hypoxia stress and the injection of Vibrio parahaemolyticus. These results indicated that these three NF-κB signaling pathway-related genes are involved in response to bacterial infection and play essential roles in response to thermal and hypoxia stress.
[Mh] Termos MeSH primário: Gastrópodes/genética
Gastrópodes/imunologia
Regulação da Expressão Gênica/imunologia
Transdução de Sinais/imunologia
Estresse Fisiológico/imunologia
[Mh] Termos MeSH secundário: Animais
Sequência de Bases
China
Clonagem Molecular
DNA Complementar/genética
Gastrópodes/microbiologia
Genes rel/genética
Genes rel/imunologia
Brânquias/metabolismo
Hepatopâncreas/metabolismo
Dados de Sequência Molecular
NF-kappa B/genética
NF-kappa B/imunologia
Oxigênio/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Análise de Sequência de DNA
Transdução de Sinais/genética
Temperatura Ambiente
Vibrio parahaemolyticus/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (DNA, Complementary); 0 (NF-kappa B); S88TT14065 (Oxygen)
[Em] Mês de entrada:1507
[Cu] Atualização por classe:141203
[Lr] Data última revisão:
141203
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:140827
[St] Status:MEDLINE



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