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Id: biblio-1147092
Autor: Oliveira, Ligia Petrolini de.
Título: Investigação da diversidade proteica, transcricional e genômica de TP53 e seu impacto em adenocarcinomas colorretais / Investigation of protein, transcriptional and genomic diversity of TP53 and its impact on colorectal adenocarcinomas.
Fonte: São Paulo; s.n; 2012. 139 p. ilust, tabelas, quadros.
Idioma: pt.
Tese: Apresentada a Fundação Antônio Prudente para obtenção do grau de Doutor.
Resumo: O câncer colorretal (CCR) é resultado da interação de fatores ambientais com múltiplos fatores genéticos. O gene TP53 regula muitas funções celulares e apresenta-se mutado na maioria dos casos de CCR. Mutações, polimorfismos e variações de expressão gênica fornecem a base genética para a diversidade humana e podem ter um papel crucial na variabilidade fenotípica e susceptibilidade às doenças. O estudo analisou as alterações em TP53 encontradas e buscou associações entre os achados com a expressão imunoistoquímica e os dados clinicopatológicos. Foram realizadas análises da proteína, do cDNA e gDNA de TP53 em 101 pacientes com CCR submetidos à cirurgia no Hospital AC Camargo, no período de 2000-2006. Foram encontradas mutações em TP53 em 54,5% dos tumores. As mutações foram mais frequentes no grupo de pacientes que apresentaram reação imunoistoquímica positiva para p53 (48,5%) do que no grupo negativo (51,5%) (p < 0,001). Foram encontradas três (3%) mutações sinônimas, o que corresponde a 8,8% das mutações pontuais; uma (33,4%) delas levando à ruptura do sítio de splicing. Foram encontradas oito inserções/deleções (7,9%), quatro (50%) delas descritas pela primeira vez e três (37,5%) delas levando à ruptura do sítio de splicing. O polimorfismo PIN2 (c.74+38C>G) foi encontrado em 89,1% dos pacientes. A frequência do alelo G foi de 0,72. O polimorfismo PIN3 (c.96+41_96+56del16) foi encontrado em 21,8% dos pacientes. A frequência do alelo A2 foi de 0,12. O polimorfismo 72Pro>Arg foi encontrado em 85,4% dos pacientes. A frequência do alelo Pro72 foi de 0,26 para o cDNA e 0,23 para o gDNA, diferença encontrada devido a expressão preferencial de um dos alelos em 40,7% dos heterozigotos. A expressão de p53, a mutação de TP53, a presença do alelo A2 e expressão do alelo Pro72 foram associadas significativamente às características clinicopatológicas que conferem pior comportamento tumoral e prognóstico adverso. Assim, a análise do cDNA de TP53 foi importante para determinar seu padrão de alteração e a contribuição específica do alelo expresso. Os dados obtidos foram congruentes com a forte associação que existe entre a mutação de TP53 e o seu acúmulo proteico, ainda que este acúmulo tenha sido verificado na minoria das amostras. Existe envolvimento de mutação sinônima com o mecanismo de splicing. As associações com os dados clinicopatológicos indicam que os polimorfismos em TP53 podem ter um papel na agressividade do CCR

Colorectal cancer (CRC) is the result of the interaction of environmental factors with multiple genetic factors. The TP53 gene regulates many cellular functions and is presented mutated in the majority of CRC cases. The mutations, polymorphisms and variations in gene expression provide the genetic basis for human diversity and may have a crucial role in the phenotypic variability and disease susceptibility. The study examined the TP53 alterations and sought associations between the findings with the immunohistochemical expression and clinicopathological data. We studied 101 patients, who underwent surgery at AC Camargo Hospital in the 2000-2006 period, through analysis of the protein, cDNA and gDNA of TP53. We found 54.5% of tumors with mutations in TP53. The mutations were significantly more frequent in the group of patients with positive immunohistochemistry reactions for p53 than in the negative group (p < 0.001). Synonymous mutations were found in three tumors, one of them leading to disruption of the splicing site. We found eight insertions/deletions, four of them described for the first time and three of them leading to the rupture of the splicing site. The PIN2 (c.74+38C>G) polymorphism was found in 89.1% of patients. The frequency of the G allele was 0.72. PIN3 (c.96+41_96+56del16) polymorphism was found in 21.8% of patients. The frequency of the A2 allele was 0.12. The polymorphism 72Pro>Arg was found in 85.4% of patients. The frequency of allele Pro72 was 0.26 for the cDNA and 0.23 for the gDNA. This difference was found because it was noticed the preferential expression of one allele in 40.7% of heterozygotes.The expression of p53, the TP53 mutation, the presence of the A2 allele and the allele Pro72 expression were significantly associated with tumor characteristics that confer worse tumor behavior and unfavorable prognosis. The analysis of TP53 cDNA is important to determine the pattern of alteration and the specific contribution of the allele expressed. This approach is consistent with the strong association that exists between TP53 mutation and its protein accumulation. Synonymous mutations are involved with splicing. The associations with linocophatological characteristics indicate that TP53 polymorphisms may play a role in the aggressiveness of CRC.
Descritores: Neoplasias Colorretais
Splicing de RNA
Genes p53
Proteína Supressora de Tumor p53
Mutação
Responsável: BR30.1 - Biblioteca
BR30.1


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Id: biblio-839288
Autor: Wang, Q; Shi, CJ; Lv, SH.
Título: Benchmarking pathway interaction network for colorectal cancer to identify dysregulated pathways
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;50(5):e5981, 2017. tab, graf.
Idioma: en.
Resumo: Different pathways act synergistically to participate in many biological processes. Thus, the purpose of our study was to extract dysregulated pathways to investigate the pathogenesis of colorectal cancer (CRC) based on the functional dependency among pathways. Protein-protein interaction (PPI) information and pathway data were retrieved from STRING and Reactome databases, respectively. After genes were aligned to the pathways, each pathway activity was calculated using the principal component analysis (PCA) method, and the seed pathway was discovered. Subsequently, we constructed the pathway interaction network (PIN), where each node represented a biological pathway based on gene expression profile, PPI data, as well as pathways. Dysregulated pathways were then selected from the PIN according to classification performance and seed pathway. A PIN including 11,960 interactions was constructed to identify dysregulated pathways. Interestingly, the interaction of mRNA splicing and mRNA splicing-major pathway had the highest score of 719.8167. Maximum change of the activity score between CRC and normal samples appeared in the pathway of DNA replication, which was selected as the seed pathway. Starting with this seed pathway, a pathway set containing 30 dysregulated pathways was obtained with an area under the curve score of 0.8598. The pathway of mRNA splicing, mRNA splicing-major pathway, and RNA polymerase I had the maximum genes of 107. Moreover, we found that these 30 pathways had crosstalks with each other. The results suggest that these dysregulated pathways might be used as biomarkers to diagnose CRC.
Descritores: Adenoma/genética
Adenoma/metabolismo
Neoplasias Colorretais/genética
Neoplasias Colorretais/metabolismo
Mapas de Interação de Proteínas/genética
-Área Sob a Curva
Biomarcadores Tumorais/genética
Estudos de Casos e Controles
Perfilação da Expressão Gênica/métodos
Regulação da Expressão Gênica
Análise de Componente Principal
Análise Serial de Proteínas
Valores de Referência
Splicing de RNA
Transdução de Sinais
Transcriptoma
Limites: Humanos
Responsável: BR1.1 - BIREME


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Id: biblio-829951
Autor: Donaires, Flávia Sacilotto; Martelli, Felipe; Alves-Paiva, Raquel de Melo; Magalhães, Silvia Maria Meira; Pinheiro, Ronald Feitosa; Calado, Rodrigo Tocantins.
Título: Splicing factor SF3B1 mutations and ring sideroblasts in myelodysplastic syndromes: a Brazilian cohort screening study
Fonte: Rev. bras. hematol. hemoter;38(4):320-324, Oct.-Dec. 2016. tab, graf.
Idioma: en.
Projeto: FAPESP.
Resumo: ABSTRACT Background: Myelodysplastic syndromes (MDS) comprise a group of malignant clonal hematologic disorders characterized by ineffective hematopoiesis and propensity for progression to acute myeloid leukemia. Acquired mutations in the gene encoding RNA splicing factor 3B subunit 1 (SF3B1) are highly associated with the MDS subtypes presenting ring sideroblasts, and represent a specific nosological entity. The effects of these mutations on clinical outcomes are diverse and contrasting. Methods: A cohort of 91 Brazilian MDS patients, including patients with ring sideroblasts in the bone marrow, were screened for mutations in the SF3B1 hotspots (exons 12-15) by direct Sanger sequencing. Results: SF3B1 heterozygous mutations were identified in six patients (7%), all of them with ring sideroblasts, thus confirming the association between SF3B1 mutations and myelodysplastic syndrome subtypes bearing this morphologic feature (frequency of 6/13, p-value < 0.0001). Conclusion: This is the first screening of SF3B1 mutations in a cohort of Brazilian myelodysplastic syndrome patients. Our findings confirm that mutations in this splicing gene correlate with bone marrow ringed sideroblasts.
Descritores: Anemia Sideroblástica
Mutação
Síndromes Mielodisplásicas
Splicing de RNA
Fatores de Processamento de RNA
Limites: Humanos
Feminino
Responsável: BR1.1 - BIREME


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Id: lil-783530
Autor: Gómez, Vanessa; Wasserman, Moisés.
Título: Inhibición parcial de dos genes que codifican para proteínas del empalmosoma en Giardia intestinalis / Partial inhibition of two genes that encode spliceosomal proteins in Giardia intestinalis
Fonte: Biomédica (Bogotá);36(supl.1):128-136, dic. 2016. ilus, graf.
Idioma: es.
Resumo: Introducción. Giardia intestinalis es un organismo tempranamente divergente en el que recientemente se demostró la presencia de intrones. La maquinaria responsable de la remoción de intrones en organismos eucariotas superiores es el empalmosoma, el cual está conformado por cinco ribonucleoproteínas, cada una de las cuales tiene un ARN pequeño nuclear, un set de siete proteínas Sm (B, D1, D2, D3, E, F y G) y varias proteínas específicas. En G. intestinalis se han identificado los genes de algunas proteínas del empalmosoma por bioinformática. Aunque se asume que este es el responsable del empalme en el parásito, su caracterización bioquímica no se ha hecho. Objetivo. Inhibir dos genes que codifican para proteínas del empalmosoma de G. intestinalis con el fin de determinar si esta inhibición afecta el crecimiento o el enquistamiento del parásito. Materiales y métodos. En un vector específico para G. intestinalis se clonaron secuencias antisentido de los genes que codifican para las proteínas SmB y SmD3 del empalmosoma del parásito. Posteriormente, se transfectó G. intestinalis con los vectores recombinantes y se seleccionaron aquellos parásitos que lo incorporaron. Se confirmó la disminución del mensajero mediante reacción en cadena de la polimerasa (PCR) en tiempo real, y se evaluaron el crecimiento y el enquistamiento en parásitos silvestres y transfectados. Resultados. Se observó una disminución de 40 y 70 % en el ARNm de SmB y SmD3, respectivamente. El crecimiento y el enquistamiento no se vieron afectados en estos parásitos. Conclusión. La disminución de SmB y SmD3 no afectó al parásito, lo que indica que el empalmosoma sigue siendo funcional, o que el empalme no es una función vital del parásito.

Introduction. Giardia intestinalis is an early divergent organism that was recently shown to have introns. The machinery responsible for the removal of introns in higher eukaryotes is the spliceosome, which consists of five ribonucleoproteins. Each of these ribonucleoproteins has a small nuclear RNA, a set of seven Sm proteins (B, D1, D2, D3, E, F and G) and several specific proteins. Some genes that encode spliceosome proteins have been bioinformatically identified in the parasite genome. Although it is assumed that the spliceosome is responsible for splicing in this parasite, biochemical characterization is lacking. Objective. To inhibit two G. intestinalis spliceosome protein genes in order to determine whether this inhibition affects parasite growth or encystation. Materials and methods. Antisense sequences of the genes encoding the spliceosomal parasite proteins SmB and SmD3 were cloned into a specific G. intestinalis vector. G. intestinalis individuals were subsequently transfected with the recombinant vectors and those parasites that incorporated the vector were selected. A decrease in mRNA levels by real-time PCR was confirmed and the growth and encystation in wild and transfected parasites was assessed. Results. A decrease of 40% and 70% of SmB and SmD3 mRNA levels, respectively, was observed. Growth and encystation in these parasites were not affected. Conclusion. Decrease of SmB and SmD3 mRNA levels does not affect the parasite, indicating that the spliceosome remains functional or that splicing is not essential for parasite viability.
Descritores: Giardia lamblia
Spliceossomos
-Parasitos
Splicing de RNA
Transfecção
Organismos Eucariotos Unicelulares
Responsável: CO332 - Facultad de Medicina


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Id: lil-750520
Autor: Laurito, Sergio; Di Pierri, José; Roqué, María.
Título: Neurofibromatosis tipo I: Mutación de splicing detectada por MLPA y secuenciación en la Argentina
Fonte: Medicina (B.Aires);75(2):91-94, abr. 2015. graf.
Idioma: es.
Resumo: La neurofibromatosis tipo 1 (NF1) es un desorden genético autosómico dominante, con una prevalencia de 1 en 2500-3000 nacidos vivos. La dificultad diagnóstica se debe al tamaño extenso del gen NF1 con pocos sitios hot-spot, la ausencia de una clara relación genotipo-fenotipo y rasgos clínicos con un espectro muy heterogéneo. Un caso sospechoso de NF1 procedente de la provincia de Jujuy fue analizado por MLPA (multiplex ligation-dependent probe amplification) en nuestro laboratorio. Mujer, adolescente mestiza (Amerindia/Europea), con un osteoma maxilar, lordosis lumbar, neurofibromas cutáneos y manchas café con leche. Por MLPA se detectó una alteración en el exón 13 del gen NF1. Por secuenciación del exón 13 se identificó una mutación "missense" en la posición 1466 del ARNm (NM_000267.3:c.1466A>G) que introduce un sitio de splicing aberrante. La patogenicidad de la mutación fue corroborada en la base de datos de variantes clínicas del National Center for Biotechnology Information. En nuestro conocimiento, este es el primer registro de una mutación NF1 en un paciente proveniente de poblaciones mestizas del Noroeste Argentino. La alteración ha sido reportada en individuos de otras poblaciones de origen muy disímil al del caso presentado, como la europea, sugiriendo que el sitio podría considerarse un sitio hot-spot del gen. Donde exista baja disponibilidad de diagnósticos moleculares, como en nuestro caso, se puede aplicar un algoritmo que comience por el estudio del gen NF1 por MLPA, metodología relativamente sencilla y de costo accesible. Con ella se evita enviar muestras al extranjero para análisis genéticos.

Neurofibromatosis type 1 (NF1) is a dominant autosomic genetic disorder, with a birth incidence of 1 in 2500-3000. Diagnosis is difficult because of the size of gene NF1 that has few hot-spots sites, the absence of a clear genotype-phenotype relation, and a heterogeneous clinical manifestation. A NF1 suspected case from Jujuy province was analyzed by multiplex ligation-dependent probe amplification (MLPA). Mestizo female teenage (Amerindian/European), with a maxilar osteoma, lumbar lordosis, cutaneous neurofibromas and café au lait spots. MLPA detected an alteration in exon 13 of the NF1 gene. By sequencing of exon 13, a missense mutation (NM_000267.3:c.1466A>G) was found which introduces an aberrant splicing site and is registered as pathogenic in the clinical variants database of NCBI. As far as we are aware, this is the first report of a NF1 mutation in mestizo population of Northwest Argentina. 1466A>G has been described before in patients of European origin, suggesting that the affected site could be a hot-spot site of the gene. For countries as Argentina, with limited availability of molecular diagnostic methods, we propose a diagnosis algorithm by starting the mutational analysis of NF1 with MLPA. This methodology is relatively simple and of low cost, avoiding to send samples abroad for genetic analyses.
Descritores: Reação em Cadeia da Polimerase Multiplex
Mutação de Sentido Incorreto
Neurofibromatose 1/genética
Splicing de RNA
Análise de Sequência de DNA
-Algoritmos
Argentina
Grupo com Ancestrais do Continente Europeu
Índios Sul-Americanos
Limites: Adolescente
Feminino
Humanos
Tipo de Publ: Relatos de Casos
Responsável: AR1.2 - Instituto de Investigaciónes Epidemiológicas


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Id: lil-742741
Autor: RETES, Felipe Alves; MARTINS, Bruno da Costa; SORBELLO, Mauricio Paulin; SATO, Cezar Fabiano Manabu; KAWAGUTI, Fabio Shiguehissa; MALUF-FILHO, Fauze; RIBEIRO-JUNIOR, Ulysses.
Título: Endoscopic hemostasis of a bleeding gastric gastrointestinal stromal tumor (GIST) with endoloop placement / Hemostasia endoscópica de tumor estromal gastrointestinal (GIST) gástrico com colocação de "endoloop"
Fonte: ABCD arq. bras. cir. dig;28(1):89-90, 2015. graf.
Idioma: en.
Descritores: Anticolesterolemiantes/uso terapêutico
Apolipoproteínas B/genética
Atrofia Muscular Espinal/tratamento farmacológico
Oligonucleotídeos Antissenso/uso terapêutico
Splicing de RNA/genética
Proteínas do Complexo SMN/genética
-Éxons/genética
Modelos Biológicos
Atrofia Muscular Espinal/genética
Oligonucleotídeos Antissenso/genética
SURVIVAL OF MOTOR NEURON TEMEFOS PROTEIN
Limites: Humanos
Tipo de Publ: Revisão
Responsável: BR1.1 - BIREME


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Id: lil-711583
Autor: López Q., Juan A; Vélez T., Gabriel J; Mendivil P., Miguel Á.
Título: Caracterización clínica y genético-molecular de un paciente con enfermedad granulomatosa crónica ligada al X: reporte de una nueva mutación asociada al splicing: caso clínico / Clinical, genetic and molecular characterization of the X-linked chronic granulomatous disease: a case report of a new splicing mutation
Fonte: Rev. chil. pediatr;85(2):213-221, abr. 2014. ilus, tab.
Idioma: es.
Resumo: Introducción: La Enfermedad Granulomatosa Crónica (EGC) se presenta como consecuencia de mutaciones en los genes que codifican 5 de las subunidades del sistema NADPH oxidasa humano. Su forma más común es causada por cambios en el gen CYBB que codifica gp91 phox. Objetivo: Identificar el defecto molecular que lleva a la presentación de la EGC. Caso clínico: Paciente de sexo masculino con antecedentes de enfermedad diarreica aguda y abscesos perianales recurrentes desde los 2 meses. A los 6 meses, presentó una inflamación crónica del colon y colitis bacteriana. A los 3 años tenía infecciones en las vías respiratorias inferiores y perianales. Estudio compatible con EGC. El análisis del ADNc identificó expresión anormal del ARNm, lo cual se confirmó al realizar la secuenciación. Específicamente se observó la ausencia del exón 2. Adicionalmente, los datos de la secuenciación del ADNg identificaron una alteración en el sitio aceptor de "splicing" del intrón 1, que incluye una deleción seguida de la inserción de 3 nucleótidos (c.46-14_-11delTTCT insGAA). Conclusiones: Se presenta el primer estudio molecular de un paciente con EGC por defecto de "splicing" reportado en Colombia. La definición de la mutación y su correlación con el fenotipo es importante para proveer una apropiada consejería genética al paciente y su familia.

Chronic granulomatous disease (CGD) is caused by mutations in the genes that encode five of the subunits of the human NADPH oxidase. The most common form is caused by mutations in CYBB, the human gene encoding gp 91 phox. Objective: To identify the molecular defects causing CGD. Case report: A male patient with a history of acute diarrhea and recurrent perianal abscess since two months old. At 6 months, the patient presented a chronic inflammatory disease of the colon and bacterial colitis. After three years, he developed infections in the lower and perianal respiratory tract. The cDNA analysis identified abnormal mRNA expression, which was confirmed by sequencing. Specifically the exclusion of exon 2 was observed. Additionally, gDNA sequencing identified an alteration in the acceptor splice site of intron 1, including a deletion followed by insertion of three nucleotides (c.46-14_-11delTTCT insGAA). Conclusions: The first molecular study of a patient with CGD due to splicing pattern change, reported in Colombia, is presented. The definition of the mutation and its correlation with the phenotype is essential to provide appropriate genetic counseling to patients and their families.
Descritores: Cromossomos Humanos X
Doença Granulomatosa Crônica/genética
Mutação
NADPH Oxidases/genética
-DNA Complementar/genética
RNA Mensageiro/genética
Sequência de Bases
Separação Celular
Éxons
Doença Granulomatosa Crônica/diagnóstico
Citometria de Fluxo
Fenótipo
Reação em Cadeia da Polimerase
Polimorfismo Conformacional de Fita Simples
Splicing de RNA
Limites: Humanos
Masculino
Lactente
Tipo de Publ: Relatos de Casos
Responsável: CL1.1 - Biblioteca Central


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Id: lil-698570
Autor: Oliveira, Ingrid; Girão, Manoel João Batista Castello; Sampaio, Misako Uemura; Oliva, Maria Luiza Vilela; Andrade, Sheila Siqueira.
Título: Plaquetas: papéis tradicionais e não tradicionais na hemostasia, na inflamação e no câncer / Platelets: traditional and nontraditional roles in hemostasis, inflammation and cancer
Fonte: ABCS health sci;38(3), set.-dez. 2013.
Idioma: pt.
Resumo: A principal e mais conhecida função plaquetária ainda está relacionada à parada de sangramento após um dano vascular. No entanto, plaquetas estão envolvidas em diversos processos, tais como iniciar e amplificar a inflamação, interagir com células da resposta imune, além de participar na progressão tumoral, angiogênese e metástase. Neste sentido, está claro que plaquetas apresentam funções no processo inflamatório e podem influenciar respostas imune, além de desordens plaquetárias autoimune erelacionadas a presença de auto-anticorpos após transfusões, comopor exemplo, na lesão pulmonar aguda associada à transfusão. Após muita especulação, recentes observações têm estabelecido novos paradigmas relacionando plaquetas à biologia molecular. Plaquetas humanas contêm fatores de spliceossomo, incluindo pequenos RNAs nucleares, proteínas de splicing e pre-mRNA endógenos. Outro ponto importante é o controle do número de plaquetas circulantes, resultado do equilíbrio entre a produção e destruição dessas células. Assim, é proposto um processo de morte programada da célula anucleada que determina seu tempo de vida. Esse processo é alvo de especulações desde a década de 60 e ainda permanece em discussão. A noção geral de que plaquetas funcionais são importantes para o sucesso de processos hematogênicos corroboram com inovações experimentais e também ligam a processos de interação plaquetas-células tumorais e seu microambiente que regula a progressão maligna. Plaquetas contribuem na sobrevivência e disseminação de células tumorais. Desta forma, discutimos aqui os mecanismos pelos quais as plaquetas atuam na imunidade, na inflamação e no câncer, uma vez que estas pequenas células são mais versáteis do que se pensava.

The principal and the most known function of platelets still remains stopping hemorrhage following vascular injury. However, platelets are involved in diverse processes such as triggering inflammation, participating in the immune response, besides tumor progression, angiogenesis, and metastasis. In this sense, it is becoming increasingly clear that platelets display inflammatory functions and can influence both innate and adaptive immune responses, such as autoimmune and alloimmune platelet disorders, and transfusion-related acute lung injury (TRALI). Despite much speculation recent observations have established new paradigms relevant to influence of platelets on molecular biology. Primary human platelets contain essential spliceosome factors including small nuclear RNAs, splicing proteins, and endogenous pre-mRNAs. Other point is, like all lineages of blood cells, the steady state number of mature platelets is the result of a balance between their production and destruction. Thus, it isproposed a programmed anuclear cell death delimits platelet lifespan is subject of speculation since the 1960s and has remainedelusive. The general notion that functional platelets are importantfor successful hematogenous tumor metastasis dates more than 4 decades and has been corroborated in numerous experimentalsettings. The dynamic crosstalk between tumors and their microenvironment is increasingly recognized as a key regulator ofmalignant progression. These contributions of platelets to tumorcell survival and spread suggest platelets as a new avenue forresearch. Here, we discuss the mechanisms by which plateletscontribute to immunity, inflammation, and cancer, since thesesmall cells are more versatile than we once thought.
Descritores: Plaquetas
Transfusão de Sangue
Hemostasia
Inflamação
Neoplasias
Splicing de RNA
-Biologia Molecular
Limites: Humanos
Masculino
Feminino
Tipo de Publ: Revisão
Responsável: BR1342.1 - Biblioteca da Escola de Enfermagem BENF


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Id: lil-602989
Autor: Cui, Yihong; Zhu, Guangqin; Chen, Qiuju; Wang, Yunfei; Yang, Mingming; Song, Yuxuan; Wang, Jiangang; Cao, Binyun.
Título: A preferable approach to clone hLIF cDNA from the genomic DNA
Fonte: Electron. j. biotechnol;14(3):12-12, May 2011. ilus, tab.
Idioma: en.
Projeto: National 863 Program of China.
Resumo: Complementary DNA (cDNA) is valuable for investigating protein structure and function in the research of life science, but it is difficult to obtain by traditional reverse transcription. In this study, we employed a novel strategy to clone the human leukemia inhibitory factor (hLIF) gene cDNA from genomic DNA directly isolated from the mucous membrane of mouth. The hLIF sequence can be acquired within a few hours by means of amplification of each exon and splicing using overlap-PCR. Thus, the new approach developed in this study is simple, time- and cost-effective, and it is not limited to particular gene expression levels of each tissue.
Descritores: DNA Complementar/genética
Fator Inibidor de Leucemia/genética
Mucosa Bucal
-Sequência de Bases
Clonagem Molecular
Splicing de RNA/genética
Éxons/genética
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Limites: Humanos
Responsável: CL1.1 - Biblioteca Central


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Valentini, Sandro R
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Id: lil-583935
Autor: Silva, Marco Túlio A da; Ambrósio, Daniela L; Trevelin, Caroline C; Watanabe, Tatiana F; Laure, Helen J; Greene, Lewis J; Rosa, José C; Valentini, Sandro R; Cicarelli, Regina MB.
Título: New insights into trypanosomatid U5 small nuclear ribonucleoproteins
Fonte: Mem. Inst. Oswaldo Cruz;106(2):130-138, Mar. 2011. ilus.
Idioma: en.
Projeto: FAPESP; . CAPES.
Resumo: Several protozoan parasites exist in the Trypanosomatidae family, including various agents of human diseases. Multiple lines of evidence suggest that important differences are present between the translational and mRNA processing (trans splicing) systems of trypanosomatids and other eukaryotes. In this context, certain small complexes of RNA and protein, which are named small nuclear ribonucleoproteins (U snRNPs), have an essential role in pre-mRNA processing, mainly during splicing. Even though they are well defined in mammals, snRNPs are still not well characterized in trypanosomatids. This study shows that a U5-15K protein is highly conserved among various trypanosomatid species. Tandem affinity pull-down assays revealed that this protein interacts with a novel U5-102K protein, which suggests the presence of a sub-complex that is potentially involved in the assembly of U4/U6-U5 tri-snRNPs. Functional analyses showed that U5-15K is essential for cell viability and is somehow involved with the trans and cis splicing machinery. Similar tandem affinity experiments with a trypanonosomatid U5-Cwc21 protein led to the purification of four U5 snRNP specific proteins and a Sm core, suggesting U5-Cwc-21 participation in the 35S U5 snRNP particle. Of these proteins, U5-200K was molecularly characterized. U5-200K has conserved domains, such as the DEAD/DEAH box helicase and Sec63 domains and displays a strong interaction with U5 snRNA.
Descritores: DNA de Protozoário
Precursores de RNA
Splicing de RNA
RIBONUCLEOPROTEIN, UABDOMEN SMALL NUCLEAR/EEET
Trypanosoma
-Sequência de Aminoácidos
Dados de Sequência Molecular
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME



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