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Pesquisa : A11.118.637.555.567.569.360.800 [Categoria DeCS]
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  1 / 922 MEDLINE  
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[PMID]:29335408
[Au] Autor:Ju JM; Jung MH; Nam G; Kim W; Oh S; Kim HD; Kim JY; Chang J; Lee SH; Park GS; Min CK; Lee DS; Kim MG; Choi K; Choi EY
[Ad] Endereço:Department of Biomedical Sciences, Seoul National University College of Medicine, Seoul, 03080, Korea.
[Ti] Título:Escape from thymic deletion and anti-leukemic effects of T cells specific for hematopoietic cell-restricted antigen.
[So] Source:Nat Commun;9(1):225, 2018 01 15.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Whether hematopoietic cell-restricted distribution of antigens affects the degree of thymic negative selection has not been investigated in detail. Here, we show that T cells specific for hematopoietic cell-restricted antigens (HRA) are not completely deleted in the thymus, using the mouse minor histocompatibility antigen H60, the expression of which is restricted to hematopoietic cells. As a result, low avidity T cells escape from thymic deletion. This incomplete thymic deletion occurs to the T cells developing de novo in the thymus of H60-positive recipients in H60-mismatched bone marrow transplantation (BMT). H60-specific thymic deletion escapee CD8 T cells exhibit effector differentiation potentials in the periphery and contribute to graft-versus-leukemia effects in the recipients of H60-mismatched BMT, regressing H60 hematological tumors. These results provide information essential for understanding thymic negative selection and developing a strategy to treat hematological tumors.
[Mh] Termos MeSH primário: Linfócitos T CD8-Positivos/imunologia
Células-Tronco Hematopoéticas/imunologia
Antígenos de Histocompatibilidade Menor/imunologia
Timo/imunologia
[Mh] Termos MeSH secundário: Animais
Células Apresentadoras de Antígenos/imunologia
Células Apresentadoras de Antígenos/metabolismo
Transplante de Medula Óssea/métodos
Linfócitos T CD8-Positivos/metabolismo
Citometria de Fluxo
Células-Tronco Hematopoéticas/metabolismo
Camundongos Knockout
Camundongos Transgênicos
Antígenos de Histocompatibilidade Menor/genética
Antígenos de Histocompatibilidade Menor/metabolismo
Timócitos/imunologia
Timócitos/metabolismo
Timo/metabolismo
Imunologia de Transplantes/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Minor Histocompatibility Antigens); 0 (minor H antigen H60)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180117
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02665-z


  2 / 922 MEDLINE  
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[PMID]:29427588
[Au] Autor:Nishimura-Danjobara Y; Oyama K; Yokoigawa K; Oyama Y
[Ad] Endereço:Department of Food Science, Faculty of Bioscience and Bioindustry, Tokushima University, Tokushima 770-8513, Japan.
[Ti] Título:Hyperpolarization by N-(3-oxododecanoyl)-l-homoserine-lactone, a quorum sensing molecule, in rat thymic lymphocytes.
[So] Source:Chem Biol Interact;283:91-96, 2018 Mar 01.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:To study the adverse effects of N-(3-oxododecanoyl)-l-homoserine-lactone (ODHL), a quorum sensing molecule, on mammalian host cells, its effect on membrane potential was examined in rat thymic lymphocytes using flow cytometric techniques with a voltage-sensitive fluorescent probe. As 3-300 µM ODHL elicited hyperpolarization, it is likely that it increases membrane K permeability because hyperpolarization is directly linked to changing K gradient across membranes, but not Na and Cl gradients. ODHL did not increase intracellular Ca concentration. ODHL also produced a response in the presence of an intracellular Zn chelator. Thus, it is unlikely that intracellular Ca and Zn are attributed to the response. Quinine, a non-specific K channel blocker, greatly reduced hyperpolarization. However, because charybdotoxin, tetraethylammonium chloride, 4-aminopyridine, and glibenclamide did not affect it, it is pharmacologically hypothesized that Ca -activated K channels, voltage-gated K channels, and ATP-sensitive K channels are not involved in ODHL-induced hyperpolarization. Although the K channels responsible for ODHL-induced hyperpolarization have not been identified, it is suggested that ODHL can elicit hyperpolarization in mammalian host cells, disturbing cellular functions.
[Mh] Termos MeSH primário: 4-Butirolactona/análogos & derivados
Polaridade Celular/efeitos dos fármacos
Homosserina/análogos & derivados
Percepção de Quorum/efeitos dos fármacos
[Mh] Termos MeSH secundário: 4-Butirolactona/farmacologia
Animais
Cálcio/metabolismo
Charibdotoxina/farmacologia
Citometria de Fluxo
Glibureto/farmacologia
Homosserina/farmacologia
Canais KATP/metabolismo
Linfócitos/citologia
Linfócitos/efeitos dos fármacos
Linfócitos/metabolismo
Permeabilidade/efeitos dos fármacos
Potássio/metabolismo
Canais de Potássio de Abertura Dependente da Tensão da Membrana/metabolismo
Quinina/farmacologia
Ratos
Ratos Wistar
Timócitos/citologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KATP Channels); 0 (N-(3-oxododecanoyl)homoserine lactone); 0 (Potassium Channels, Voltage-Gated); 115422-61-2 (Charybdotoxin); 6KA95X0IVO (Homoserine); A7V27PHC7A (Quinine); OL659KIY4X (4-Butyrolactone); RWP5GA015D (Potassium); SX6K58TVWC (Glyburide); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180211
[St] Status:MEDLINE


  3 / 922 MEDLINE  
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[PMID]:28462532
[Au] Autor:Daley SR; Teh C; Hu DY; Strasser A; Gray DHD
[Ad] Endereço:Infection and Immunity Program, Biomedicine Discovery Institute and Department of Biochemistry and Molecular Biology, Monash University, Melbourne, VIC, Australia.
[Ti] Título:Cell death and thymic tolerance.
[So] Source:Immunol Rev;277(1):9-20, 2017 05.
[Is] ISSN:1600-065X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The differentiation of hematopoietic precursors into the many functionally distinct T-cell types produced by the thymus is a complex process. It proceeds through a series of stages orchestrated by a variety of thymic microenvironments that shape the T-cell developmental processes. Numerous cytokine and cell surface receptors direct thymocyte differentiation but the primary determinant of cell fate is the engagement of the T-cell antigen receptor (TCR). The strength of the TCR signal and the maturation stage of the thymocyte receiving it can direct the various differentiation programs or, alternatively, end the process by inducing cell death. The regulation of thymocyte death is critical for the efficiency of thymic T-cell differentiation and the preservation of immune tolerance. A detailed knowledge of mechanisms that eliminate thymocytes from the T-cell repertoire is essential to understand the "logic" of T-cell selection in the thymus. This review focuses on the central role of the BCL-2 family of proteins in the apoptotic checkpoints that punctuate thymocyte differentiation and the consequences of defects in these processes.
[Mh] Termos MeSH primário: Proteínas Proto-Oncogênicas c-bcl-2/metabolismo
Linfócitos T/fisiologia
Timócitos/fisiologia
Timo/imunologia
[Mh] Termos MeSH secundário: Animais
Morte Celular
Diferenciação Celular
Microambiente Celular
Tolerância Central
Hematopoese
Seres Humanos
Receptores de Antígenos de Linfócitos T/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Proto-Oncogene Proteins c-bcl-2); 0 (Receptors, Antigen, T-Cell)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180220
[Lr] Data última revisão:
180220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170503
[St] Status:MEDLINE
[do] DOI:10.1111/imr.12532


  4 / 922 MEDLINE  
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[PMID]:29326336
[Au] Autor:Leong WZ; Tan SH; Ngoc PCT; Amanda S; Yam AWY; Liau WS; Gong Z; Lawton LN; Tenen DG; Sanda T
[Ad] Endereço:Cancer Science Institute of Singapore, National University of Singapore, 117599 Singapore.
[Ti] Título:ARID5B as a critical downstream target of the TAL1 complex that activates the oncogenic transcriptional program and promotes T-cell leukemogenesis.
[So] Source:Genes Dev;31(23-24):2343-2360, 2017 12 01.
[Is] ISSN:1549-5477
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The oncogenic transcription factor induces an aberrant transcriptional program in T-cell acute lymphoblastic leukemia (T-ALL) cells. However, the critical factors that are directly activated by TAL1 and contribute to T-ALL pathogenesis are largely unknown. Here, we identified ( ) as a collaborating oncogenic factor involved in the transcriptional program in T-ALL. expression is down-regulated at the double-negative 2-4 stages in normal thymocytes, while it is induced by the TAL1 complex in human T-ALL cells. The enhancer located 135 kb upstream of the gene locus is activated under a superenhancer in T-ALL cells but not in normal T cells. Notably, ARID5B-bound regions are associated predominantly with active transcription. ARID5B and TAL1 frequently co-occupy target genes and coordinately control their expression. ARID5B positively regulates the expression of TAL1 and its regulatory partners. ARID5B also activates the expression of the oncogene Importantly, ARID5B is required for the survival and growth of T-ALL cells and forced expression of ARID5B in immature thymocytes results in thymus retention, differentiation arrest, radioresistance, and tumor formation in zebrafish. Our results indicate that ARID5B reinforces the oncogenic transcriptional program by positively regulating the TAL1-induced regulatory circuit and in T-ALL, thereby contributing to T-cell leukemogenesis.
[Mh] Termos MeSH primário: Carcinogênese/genética
Proteínas de Ligação a DNA/metabolismo
Regulação Neoplásica da Expressão Gênica
Proteína 1 de Leucemia Linfocítica Aguda de Células T/metabolismo
Fatores de Transcrição/metabolismo
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Sobrevivência Celular/genética
Proteínas de Ligação a DNA/genética
Elementos Facilitadores Genéticos/genética
Perfilação da Expressão Gênica
Genes myc/genética
Células HEK293
Seres Humanos
Leucemia-Linfoma Linfoblástico de Células T Precursoras
Ligação Proteica
Domínios Proteicos/genética
Timócitos/metabolismo
Timo/crescimento & desenvolvimento
Fatores de Transcrição/genética
Ativação Transcricional/genética
Peixe-Zebra
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (ARID5B protein, human); 0 (DNA-Binding Proteins); 0 (T-Cell Acute Lymphocytic Leukemia Protein 1); 0 (Transcription Factors); 135471-20-4 (TAL1 protein, human)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180208
[Lr] Data última revisão:
180208
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180113
[St] Status:MEDLINE
[do] DOI:10.1101/gad.302646.117


  5 / 922 MEDLINE  
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[PMID]:28747348
[Au] Autor:Ghosh MK; Muller HK; Walker AM
[Ad] Endereço:Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, CA 92521; and.
[Ti] Título:Lactation-Based Maternal Educational Immunity Crosses MHC Class I Barriers and Can Impart Th1 Immunity to Th2-Biased Recipients.
[So] Source:J Immunol;199(5):1729-1736, 2017 09 01.
[Is] ISSN:1550-6606
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:We have previously demonstrated lactational transfer of T cell-based immunity from dam to foster pup. In the short term, a significant part of transferred immunity is passive cellular immunity. However, as time progresses, this is replaced by what we have described as maternal educational immunity such that by young adulthood, all immune cells responding to a foster dam immunogen are the product of the foster pup's thymus. To reduce confounding factors, this original demonstration used congenic/syngeneic dam and foster pup pairs. In this study, we investigated lactational transfer of immunity to in MHC class I-mismatched animals, as well as from Th1-biased dams to Th2-biased foster pups. Using immunized C57BL/6J dams, lactational transfer to nonimmunized BALB/cJ foster pups resulted in much greater immunity than direct immunization in 5-wk-old pups (ex vivo assay of pup splenocytes). At this age, 82% of immunogen-responding cells in the pup spleen were produced through maternal educational immunity. FVB/NJ nonimmunized foster recipients had a greater number of maternal cells in the spleen and thymus but a much larger percentage was Foxp3 , resulting in equivalent immunity to direct immunization. Depletion of maternal Foxp3 cells from pup splenocytes illustrated a substantial role for lactationally transferred dam regulatory T cells in suppression of the ex vivo response in FVB/NJ, but not BALB/cJ, recipients. We conclude that lactational transfer of immunity can cross MHC class I barriers and that Th1 immunity can be imparted to Th2-biased offspring; in some instances, it can be greater than that achieved by direct immunization.
[Mh] Termos MeSH primário: Imunidade Materno-Adquirida
Lactação/imunologia
Mycobacterium tuberculosis/imunologia
Linfócitos T Reguladores/imunologia
Células Th1/imunologia
Células Th2/imunologia
Timócitos/imunologia
Tuberculose/imunologia
[Mh] Termos MeSH secundário: Animais
Feminino
Fatores de Transcrição Forkhead/metabolismo
Antígenos de Histocompatibilidade Classe I/imunologia
Isoantígenos/imunologia
Camundongos
Camundongos Endogâmicos BALB C
Camundongos Endogâmicos C57BL
Gravidez
Equilíbrio Th1-Th2
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Forkhead Transcription Factors); 0 (Foxp3 protein, mouse); 0 (Histocompatibility Antigens Class I); 0 (Isoantigens)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:180128
[Lr] Data última revisão:
180128
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:170728
[St] Status:MEDLINE
[do] DOI:10.4049/jimmunol.1601375


  6 / 922 MEDLINE  
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[PMID]:28741728
[Au] Autor:Ki S; Thyagarajan HM; Hu Z; Lancaster JN; Ehrlich LIR
[Ad] Endereço:Department of Molecular Biosciences, Institute for Cellular and Molecular Biology, The University of Texas at Austin, Austin, TX, USA.
[Ti] Título:EBI2 contributes to the induction of thymic central tolerance in mice by promoting rapid motility of medullary thymocytes.
[So] Source:Eur J Immunol;47(11):1906-1917, 2017 11.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Maturing thymocytes enter the thymic medulla, where they encounter numerous self-antigens presented by antigen presenting cells (APCs). Those thymocytes that are strongly self-reactive undergo either negative selection or diversion into the regulatory T-cell lineage. Although the majority of the proteome is expressed in the medulla, many self-antigens are expressed by only a minor fraction of medullary APCs; thus, thymocytes must efficiently enter the medulla and scan APCs to ensure central tolerance. Chemokine receptors promote lymphocyte migration, organization within tissues, and interactions with APCs in lymphoid organs. The chemokine receptor EBI2 governs localization of T cells, B cells, and dendritic cells (DCs) during immune responses in secondary lymphoid organs. However, the role of EBI2 in thymocyte development has not been elucidated. Here, we demonstrate that EBI2 is expressed by murine CD4 single positive (CD4SP) thymocytes and thymic DCs. EBI2 deficiency alters the TCR repertoire, but does not grossly impact thymocyte cellularity or subset distribution. EBI2 deficiency also impairs negative selection of OT-II TCR transgenic thymocytes responding to an endogenous self-antigen. Two-photon imaging revealed that EBI2 deficiency results in reduced migration and impaired medullary accumulation of CD4SP thymocytes. These data identify a role for EBI2 in promoting efficient thymic central tolerance.
[Mh] Termos MeSH primário: Diferenciação Celular/imunologia
Tolerância Central/imunologia
Receptores Acoplados a Proteínas-G/imunologia
Timócitos/imunologia
Timo/imunologia
[Mh] Termos MeSH secundário: Animais
Quimiotaxia de Leucócito/imunologia
Camundongos
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Gpr183 protein, mouse); 0 (Receptors, G-Protein-Coupled)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:180124
[Lr] Data última revisão:
180124
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170726
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201747020


  7 / 922 MEDLINE  
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[PMID]:29217698
[Au] Autor:Tai X
[Ad] Endereço:NATIONAL CANCER INSTITUTE.
[Ti] Título:MCL-1 keeps a charming home for thymocytes.
[So] Source:Blood;130(23):2448-2450, 2017 12 07.
[Is] ISSN:1528-0020
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Proteína de Sequência 1 de Leucemia de Células Mieloides
Timócitos
[Mh] Termos MeSH secundário: Apoptose
Seres Humanos
Proteínas Proto-Oncogênicas c-bcl-2
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Myeloid Cell Leukemia Sequence 1 Protein); 0 (Proto-Oncogene Proteins c-bcl-2)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE
[do] DOI:10.1182/blood-2017-10-809665


  8 / 922 MEDLINE  
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[PMID]:29283520
[Au] Autor:Tishevskaya NV; Gevorkyan NM; Kozlova NI
[Ti] Título:Sensitivity of T-Lymphocytes to Hormones of the Anterior Pituitary Gland.
[So] Source:Usp Fiziol Nauk;48(1):80-90, 2017 Jan-Mar.
[Is] ISSN:0301-1798
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:The review provides information about the features of the sensitivity of thymocytes, lymphoid organs' cells and T-lymphocytes of peripheral blood to the hormones secreted by anterior pituitary gland's cells: growth hormone, thyrotropin, adrenocorticotropic hormone, prolactin and ß-endorphin. Some aspects of the T-lymphocytes's response to humoral signals from the hypophysis are shown in the article. Also the pituitary hormones' role in the regulation of proliferation, differentiation, and cytokine production of T-lymphocytes in normal and pathological conditions of the organism being discussed.
[Mh] Termos MeSH primário: Hormônio Adrenocorticotrópico/farmacologia
Hormônio do Crescimento/farmacologia
Adeno-Hipófise/secreção
Prolactina/farmacologia
Timócitos/efeitos dos fármacos
Tireotropina/farmacologia
beta-Endorfina/farmacologia
[Mh] Termos MeSH secundário: Hormônio Adrenocorticotrópico/genética
Hormônio Adrenocorticotrópico/imunologia
Animais
Diferenciação Celular/efeitos dos fármacos
Proliferação Celular/efeitos dos fármacos
Regulação da Expressão Gênica
Hormônio do Crescimento/genética
Hormônio do Crescimento/imunologia
Seres Humanos
Leucócitos Mononucleares/citologia
Leucócitos Mononucleares/efeitos dos fármacos
Leucócitos Mononucleares/imunologia
Cultura Primária de Células
Prolactina/genética
Prolactina/imunologia
Transdução de Sinais
Timócitos/citologia
Timócitos/imunologia
Tireotropina/genética
Tireotropina/imunologia
beta-Endorfina/genética
beta-Endorfina/imunologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
60617-12-1 (beta-Endorphin); 9002-60-2 (Adrenocorticotropic Hormone); 9002-62-4 (Prolactin); 9002-71-5 (Thyrotropin); 9002-72-6 (Growth Hormone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171229
[St] Status:MEDLINE


  9 / 922 MEDLINE  
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[PMID]:29227077
[Au] Autor:Franskevych DV; Grynyuk II; Prylutska SV; Matyshevs ka OP
[Ti] Título:Modulation of cisplatin-induced reactive oxygen species production by fullerene C(60) in normal and transformed lymphoid cells
[So] Source:Ukr Biochem J;88(1):44-50, 2016 Jan-Feb.
[Is] ISSN:2409-4943
[Cp] País de publicação:Ukraine
[La] Idioma:eng
[Ab] Resumo:The early response of normal (Wistar rat thymocytes) and transformed (mice lymphoid leukemia L1210) cells to treatment with anticancer drug cisplatin or to combined treatment with cisplatin and carbon nanostructure fullerene C60 was studied. We demonstrated with fluorescent probes DCFH-DA and TMRE that cisplatin at concentration 1 µg/ml induced reactive oxygen species (ROS) production and decreased the value of mitochondrial membrane potential in both cell types. The combined treatment with cisplatin (1 µg/ml) and fullerene C60 (7.2 µg/ml) was shown to be followed by oppositely directed modulation of ROS production in thymocytes and L1210 cells. Cisplatin-induced ROS production was intensified in L1210 cells, while in thymocytes it was decreased. It is supposed that the different effects of combined treatment are associated with peculiarities of fullerene C60 accumulation and localization in normal and cancer cells.
[Mh] Termos MeSH primário: Antineoplásicos/farmacologia
Cisplatino/farmacologia
Fulerenos/farmacologia
Linfócitos/efeitos dos fármacos
Espécies Reativas de Oxigênio/metabolismo
Timócitos/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Linhagem Celular Tumoral
Combinação de Medicamentos
Interações Medicamentosas
Fluoresceínas/química
Corantes Fluorescentes/química
Linfócitos/metabolismo
Linfócitos/patologia
Potencial da Membrana Mitocondrial/efeitos dos fármacos
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Especificidade de Órgãos
Compostos Organometálicos/química
Cultura Primária de Células
Ratos
Ratos Wistar
Espécies Reativas de Oxigênio/agonistas
Espécies Reativas de Oxigênio/antagonistas & inibidores
Timócitos/citologia
Timócitos/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antineoplastic Agents); 0 (Drug Combinations); 0 (Fluoresceins); 0 (Fluorescent Dyes); 0 (Fullerenes); 0 (Organometallic Compounds); 0 (Reactive Oxygen Species); 0 (tetramethyl rhodamine ethyl ester); 2044-85-1 (diacetyldichlorofluorescein); NP9U26B839 (fullerene C60); Q20Q21Q62J (Cisplatin)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171212
[St] Status:MEDLINE
[do] DOI:10.15407/ubj88.01.044


  10 / 922 MEDLINE  
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[PMID]:28471480
[Au] Autor:Mildner A; Chapnik E; Varol D; Aychek T; Lampl N; Rivkin N; Bringmann A; Paul F; Boura-Halfon S; Hayoun YS; Barnett-Itzhaki Z; Amit I; Hornstein E; Jung S
[Ad] Endereço:Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.
[Ti] Título:MicroRNA-142 controls thymocyte proliferation.
[So] Source:Eur J Immunol;47(7):1142-1152, 2017 07.
[Is] ISSN:1521-4141
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:T-cell development is a spatially and temporally regulated process, orchestrated by well-defined contributions of transcription factors and cytokines. Here, we identify the noncoding RNA miR-142 as an additional regulatory layer within murine thymocyte development and proliferation. MiR-142 deficiency impairs the expression of cell cycle-promoting genes in mature mouse thymocytes and early progenitors, accompanied with increased levels of cyclin-dependent kinase inhibitor 1B (Cdkn1b, also known as p27 ). By using CRISPR/Cas9 technology to delete the miR-142-3p recognition element in the 3'UTR of cdkn1b, we confirm that this gene is a novel target of miR-142-3p in vivo. Increased Cdkn1b protein expression alone however was insufficient to cause proliferation defects in thymocytes, indicating the existence of additional critical miR-142 targets. Collectively, we establish a key role for miR-142 in the control of early and mature thymocyte proliferation, demonstrating the multifaceted role of a single miRNA on several target genes.
[Mh] Termos MeSH primário: Inibidor de Quinase Dependente de Ciclina p27/genética
MicroRNAs/metabolismo
Timócitos/fisiologia
[Mh] Termos MeSH secundário: Regiões 3' não Traduzidas
Animais
Sistemas CRISPR-Cas
Diferenciação Celular
Linhagem Celular Tumoral
Proliferação Celular
Inibidor de Quinase Dependente de Ciclina p27/deficiência
Inibidor de Quinase Dependente de Ciclina p27/metabolismo
Regulação Neoplásica da Expressão Gênica
Camundongos
MicroRNAs/genética
Processamento Pós-Transcricional do RNA
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3' Untranslated Regions); 0 (Cdkn1b protein, mouse); 0 (MicroRNAs); 0 (Mirn142 microRNA, mouse); 147604-94-2 (Cyclin-Dependent Kinase Inhibitor p27)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171202
[Lr] Data última revisão:
171202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170505
[St] Status:MEDLINE
[do] DOI:10.1002/eji.201746987



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