5 Aza 2 Deoxycytidine
Mostrando 1-12 de 59 artigos, teses e dissertações.
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1. Effects of 5-aza-2′deoxycytidine on RECK gene expression and tumor invasion in salivary adenoid cystic carcinoma
Reversion-inducing cysteine-rich protein with kazal motifs (RECK), a novel tumor suppressor gene that negatively regulates matrix metalloproteinases (MMPs), is expressed in various normal human tissues but downregulated in several types of human tumors. The molecular mechanism for this downregulation and its biological significance in salivary adenoid cystic
Braz J Med Biol Res. Publicado em: 12/12/2014
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2. Stability of XIST repression in relation to genomic imprinting following global genome demethylation in a human cell line
DNA methylation is essential in X chromosome inactivation and genomic imprinting, maintaining repression of XIST in the active X chromosome and monoallelic repression of imprinted genes. Disruption of the DNA methyltransferase genes DNMT1 and DNMT3B in the HCT116 cell line (DKO cells) leads to global DNA hypomethylation and biallelic expression of the imprin
Braz J Med Biol Res. Publicado em: 17/10/2014
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3. The epigenetic modifiers 5-aza-2'-deoxycytidine and trichostatin A influence adipocyte differentiation in human mesenchymal stem cells
Epigenetic mechanisms such as DNA methylation and histone modification are important in stem cell differentiation. Methylation is principally associated with transcriptional repression, and histone acetylation is correlated with an active chromatin state. We determined the effects of these epigenetic mechanisms on adipocyte differentiation in mesenchymal ste
Braz J Med Biol Res. Publicado em: 2013-05
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4. Use of chromatin modifying agents in bovine somatic cell nuclear transfer / Uso de agentes modificadores de cromatina na transferência nuclear de células somáticas em bovinos
Embora a transferência nuclear de células somáticas (TNCS) seja uma ferramenta promissora, seu amplo uso é impedido devido às altas taxas de mortalidade durante o desenvolvimento dos animais clonados. Acredita-se que a reprogramação epigenética anormal seja a principal causa desta baixa eficiência. Nós hipotetizamos que agentes modificadores de cro
IBICT - Instituto Brasileiro de Informação em Ciência e Tecnologia. Publicado em: 13/12/2011
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5. Mecanismos associados à perda de expressão do gene de galectina-3 em um modelo de progressão de melanoma murino / Mechanisms associated to the loss of galectin-3 gene expression in a model of murine melanoma progression
Galectin-3 is a b-galactoside-binding animal lectin, shown to be involved in tumor progression and metastasis. Galectin-3 expression has been found altered along tumor progression of different tumors. In some types of cancers such as thyroid carcinoma and bladder carcinoma, galectin-3 expression has been found increased, whereas in tumors such as breast carc
Publicado em: 2007
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6. Mutagenicity of 5-aza-2′-deoxycytidine is mediated by the mammalian DNA methyltransferase
The cytosine analog 5-aza-2′-deoxycytidine has been used clinically to reactivate genes silenced by DNA methylation. In particular, patients with β-thalassemia show fetal globin expression after administration of this hypomethylating drug. In addition, silencing of tumor suppressor gene expression by aberrant DNA methylation in tumor cells may potentially
The National Academy of Sciences of the USA.
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7. DNA methylation in 5-aza-2'-deoxycytidine-resistant variants of C3H 10T1/2 C18 cells.
A cell line (T17) was derived from C3H 10T1/2 C18 cells after 17 treatments with increasing concentrations of 5-aza-2'-deoxycytidine. The T17 cell line was very resistant to the cytotoxic effects of 5-aza-2'-deoxycytidine, and the 50% lethal dose for 5-aza-2'-deoxycytidine was ca. 3 microM, which was 30-fold greater than that of the parental C3H 10T1/2 C18 c
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8. Differential nuclear protein binding to 5-azacytosine-containing DNA as a potential mechanism for 5-aza-2'-deoxycytidine resistance.
A clonal cell line (56-42) that was stably and exclusively resistant to the toxic effects of the antileukemic agent 5-aza-2'-deoxycytidine (5-aza-CdR) was derived from C3H 10T1/2 C18 cells after multiple treatments with 5-aza-CdR. The 50% lethal dose of 5-aza-CdR for these cells was 1.3 microM, which was 15-fold greater than that for the parental cells. Cell
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9. Silencing of Mouse Aprt Is a Gradual Process in Differentiated Cells
Mouse Aprt constructs that are highly susceptible to DNA methylation-associated inactivation in embryonal carcinoma cells were transfected into differentiated cells, where they were expressed. Construct silencing was induced by either whole-cell fusion of the expressing differentiated cells with embryonal carcinoma cells or by treatment of the differentiated
American Society for Microbiology.
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10. Inhibition of DNA methyltransferase stimulates the expression of signal transducer and activator of transcription 1, 2, and 3 genes in colon tumor cells
Inhibitors of DNA methyltransferase, typified by 5-aza-2′-deoxycytidine (5-Aza-CdR), induce the expression of genes transcriptionally down-regulated by de novo methylation in tumor cells. We utilized gene expression microarrays to examine the effects of 5-Aza-CdR treatment in HT29 colon adenocarcinoma cells. This analysis revealed the induction of a set of
The National Academy of Sciences.
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11. Propynyl groups in duplex DNA: stability of base pairs incorporating 7-substituted 8-aza-7-deazapurines or 5-substituted pyrimidines
Oligonucleotides incorporating the 7-propynyl derivatives of 8-aza-7-deaza-2′-deoxyguanosine (3b) and 8-aza-7-deaza-2′-deoxyadenosine (4b) were synthesized and their duplex stability was compared with those containing the 5-propynyl derivatives of 2′-deoxycytidine (1) and 2′-deoxyuridine (2). For this purpose phosphoramidites of the 8-aza- 7-deazapur
Oxford University Press.
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12. Cell cycle-specific reactivation of an inactive X-chromosome locus by 5-azadeoxycytidine.
Three cytidine analogs containing modifications in the 5-position of the cytosine ring (5-azacytidine, 5-aza-2'-deoxycytidine and pseudoisocytidine) induced the expression of human hypoxanthine/guanine phosphoribosyltransferase (IMP; pyrophosphate phosphoribosyltransferase, EC 2.4.2.8) gene (HPRT) from a structurally normal inactive human X chromosome retai