Junb
Mostrando 1-12 de 142 artigos, teses e dissertações.
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1. A phthalide derivative isolated from endophytic fungiPestalotiopsis photiniae induces G1 cell cycle arrest and apoptosis in human HeLa cells
MP [4-(3′,3′-dimethylallyloxy)-5-methyl-6-methoxyphthalide] was obtained from liquid culture of Pestalotiopsis photiniaeisolated from the Chinese Podocarpaceae plant Podocarpus macrophyllus. MP significantly inhibited the proliferation of HeLa tumor cell lines. After treatment with MP, characteristic apoptotic features such as DNA fragmentation and chrom
Braz J Med Biol Res. Publicado em: 30/07/2013
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2. Expressão das proteinas c-jun, junb, JNK e pc-jun no carcinoma adenóide cístico e carcinoma epidermóide da cavidade bucal / c-jun, junB, JNK and pc-jun protein expression in adenoid cystic carcinoma and squamous cell carcinoma of the oral cavity
O carcinoma adenóide cístico e o carcinoma epidermóide são neoplasmas de origem epitelial que afetam a cavidade oral. O carcinoma adenóide cístico pode apresentar-se em glândulas salivares maiores e menores, possue alta propensão de invasão perineural e o padrão de infiltracão: sólido, tubular e cribriforme. O carcinoma epidermóide foi descrito
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 06/12/2011
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3. Padrão de metilação dos genes SOCS 1 e JUNB em pacientes com leucemia mieloide crônica
Alteração no padrão de metilação gênica pode contribuir para a progressão da leucemia mielóide crônica (LMC). Neste estudo, o padrão de metilação no exon 2 do gene SOCS- 1 e região promotora de ambos SOCS- 1 e JUNB foram avaliadas em pacientes com LMC. O padrão de metilação desses genes foi analisado usando a técnica " methylation- specific
Revista Brasileira de Hematologia e Hemoterapia. Publicado em: 26/06/2009
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4. Metilação e expressão do gene JUNB na leucemia mieloide crônica
Revista Brasileira de Hematologia e Hemoterapia. Publicado em: 2009
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5. c-Jun and junB immunoprofile in adenoid cystic carcinoma and polymorphous low-grade adenocarcinoma of salivary glands / Estudo da imunoexpressão das proteínas C-JUN e JUNB em carcinoma adenóide cístico e adenocarcinoma polimorfo de baixo grau de malignidade de glândulas salivares
Adenoid cystic carcinoma and polymorphous low grade are salivary gland neoplasms. ACC can arise in both, major or minor salivary glands. However, Polymorphous lowgrade adenocarcinoma, occurs specifically in minor salivary glands dispersed in the oral cavity. They share many common histologic features, as infiltrating solid, tubular and cribiform patterns and
Publicado em: 2008
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6. The expression of early primary gene proteins, fos and jun family proteins, in rat adrenal primary cultures treated with ACTH and FGF2. / Análise da expressão das proteínas dos genes de resposta primária, proteínas da família Fos e Jun, em culturas primárias de supra-renal de rato tratadas com ACTH e FGF2.
There are evidences that in vivo the adrenocorticotropic hormone (ACTH) displays an important role in the balance of proliferation and cellular death in the adrenal gland. The early response gene proteins, Fos and Jun family, are components of the transcription factor AP-1 that, depending on its composition, could be related with proliferation, differentiati
Publicado em: 2008
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7. Expressão genica global e estudo do gene JUNB em policitemia vera / Global gene expression and study of the JUNB gene in polycythemia
Polycythemia vera (PV) is a chronic myeloproliferative disorder that arises through clonal proliferation of multipotent hematopoietic progenitors. PV patients present bone marrow trilineage expansion, leading to increased production of mature red cells, granulocytes and platelets. Important PV features are elevated red cell mass, despite normal or subnormal
Publicado em: 2007
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8. Effects of ACTH, PMA and dcAMP on fos, jun and c-myc gene expression and AP-1 transcription factor activity control in Y-1 adrenocortical cells / Efeitos de ACTH, PMA e dcAMP na expressão de genes das famílias FOS e JUN do gene C-MYC e na atividade do fator de transcrição AP-1 em células adrenocorticais Y-1.
As células Y-1 pertencem a uma linhagem clonal de células funcionais de córtex adrenal de camundongo, que respondem a ACTH. Em células Y-1, ACTH promove a esteroidogênese (função) e tem efeitos regulatórios complexos na transição G0→G1→S do ciclo celular. ACTH promove a transição G0→G1, mas inibe a transição G1→S. É pos
Publicado em: 1996
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9. JunB suppresses cell proliferation by transcriptional activation of p16INK4a expression
A role for the transcription factor JunB in proliferation control was investigated in genetically modified mouse fibroblasts. Increased JunB expression induced high levels of the cyclin-dependent kinase inhibitor p16INK4a, leading to premature senescence in primary cells and reduced proliferation in 3T3 cells, whereas lack of JunB expression results in decre
Oxford University Press.
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10. Morphine induces c-fos and junB in striatum and nucleus accumbens via D1 and N-methyl-D-aspartate receptors.
Morphine induced the c-fos and junB immediate early genes in neurons of the medial and ventral striatum and nucleus accumbens. Induction of c-fos and junB mRNA and Fos protein was blocked by naloxone, the D1 dopamine (DA) receptor antagonists SCH23390 and SCH39166, and the N-methyl-D-aspartate (NMDA) glutamate receptor antagonist MK801. SCH23390 attenuated m
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11. Regulation of the junB gene by v-src.
The proteins encoded by cellular and viral src genes are believed to be involved in the transmission of mitogenic signals, the nuclear recipients of which are largely unknown. In this work, we report that four different v-src-transformed cell lines from three different species possess elevated levels of junB transcripts. Transient expression of junB promoter
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12. Activation of junB by PKC and PKA signal transduction through a novel cis-acting element.
The product of the junB gene, a gene homologous to the proto-oncogene c-jun, is a component of transcription factor AP-1. JunB expression is modulated by a wide variety of extracellular stimuli, such as serum, growth factors, phorbol esters (TPA) and activators of protein kinase A (PKA). In order to study the molecular basis of this complex regulation, we ha