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1.
Yi Chuan ; 37(8): 756-64, 2015 08.
Artigo em Chinês | MEDLINE | ID: mdl-26266779

RESUMO

Recent studies demonstrate that RNA species could regulate each other by competing for shared microRNA response elements (MREs). This regulatory model is called competing endogenous RNA (ceRNA). Currently, the identified ceRNAs cover coding and non-coding RNAs. The latter includes pseudogene transcripts, long non-coding RNAs (lncRNAs), circular RNAs (circRNAs) and so on. In this review, we summarize the biological functions of regulatory networks consisting of various types of ceRNAs and their roles in the pathological and physiological processes. Additionally, several factors that may regulate ceRNAs were discussed.


Assuntos
Pseudogenes/fisiologia , RNA Longo não Codificante/fisiologia , RNA/fisiologia , Animais , Redes Reguladoras de Genes , Humanos , MicroRNAs/fisiologia , RNA Circular , RNA Mensageiro/fisiologia
2.
BMB Rep ; 43(4): 291-6, 2010 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-20423616

RESUMO

Cyclin-dependent kinase 2 (CDK2) is a member of serine/ threonine protein kinases, which initiates the principal transitions of the eukaryotic cell cycle and is a promising target for cancer therapy. The present study was designed to inhibit cdk2 gene expression to induce cell cycle arrest and cell proliferation suppression. Here, we constructed a series of RNA interference (RNAi) plasmids which can successfully express small interference RNA (siRNA) in the transfected human cells. The results showed that the RNAi plasmids containing the coding sequences for siRNAs down-regulated the cdk2 gene expression in human cancer cells at the mRNA and the protein levels. Furthermore, we found that the cell cycle was arrested at G0G1 phases and the cell proliferation was inhibited by different siRNAs. These results demonstrate that suppression of CDK2 activity by RNAi may be an effective strategy for gene therapy in human cancers.


Assuntos
Quinase 2 Dependente de Ciclina/antagonistas & inibidores , Neoplasias/enzimologia , Interferência de RNA , Proliferação de Células , Quinase 2 Dependente de Ciclina/genética , Quinase 2 Dependente de Ciclina/metabolismo , Regulação para Baixo , Fase G1 , Células HeLa , Humanos , RNA Interferente Pequeno/metabolismo , Fase de Repouso do Ciclo Celular , Células Tumorais Cultivadas
3.
J Cell Mol Med ; 9(4): 961-5, 2005.
Artigo em Inglês | MEDLINE | ID: mdl-16364203

RESUMO

Stargardt disease-3 (STGD3) is an autosomal dominant juvenile-onset macular dystrophy characterized by progressive decreasing visual acuity, bilateral atrophic changes in the macula and absence of characteristic dark choroids. We identified a STGD3-like macular dystrophy pedigree by clinical examination. To explore whether the STGD3-like phenotype in the kindred is linked to ELOVL4 gene or associated with any other identified STGD gene, we extracted genomic DNA from leukocytes of peripheral blood from the available family members and 50 normal controls for mutation analysis. Then the exons of ELOVL4, RDS and the three exons of ABCR were amplified by polymerase chain reaction (PCR). All PCR products were screened for mutations by combination of denaturing high-performance liquid chromatography (DHPLC) analysis and DNA sequencing. No mutation was found in the exons of three candidate genes, but we obtained three non-pathogenic polymorphisms, IVS5-2533T-->A in ELOVL4, 558C-->T (Val106Val) and 1150G-->C (Glu304Gln) in RDS. And IVS5-2533T-->A is never shown in the previous references. These data suggested that there exist other unknown genes responsible for the STGD3-like phenotype in the pedigree.


Assuntos
Distrofias Hereditárias da Córnea/genética , Proteínas do Olho/genética , Proteínas de Membrana/genética , Angiografia , Capilares , China , Éxons , Feminino , Genes Dominantes , Humanos , Leucócitos/citologia , Masculino , Mutação , Linhagem , Fenótipo , Reação em Cadeia da Polimerase , Polimorfismo Genético , Doenças Retinianas/genética , Análise de Sequência de DNA
4.
Zhonghua Yi Xue Yi Chuan Xue Za Zhi ; 20(4): 322-4, 2003 Aug.
Artigo em Chinês | MEDLINE | ID: mdl-12903043

RESUMO

OBJECTIVE: To investigate the association between attention-deficit hyperactivity disorder (ADHD) in Han Chinese children and Val158Met polymorphism of catechol-O-methyltransferase (COMT) gene caused by the missense mutation of G158A in exon 4. METHODS: By using polymerase chain reaction-restriction fragment length polymorphisms the Val158Met polymorphism of COMT gene was tested in 117 children with the diagnosis of ADHD as defined by DSM-IV and in 105 healthy controls living in Shanghai. RESULTS: The frequencies of A allele were 25.21% and 23.81% in the ADHD group and the health controls respectively, which showed no significant difference between the two groups (Chi2=0.5197, P>0.05). There was also no significant difference in the distribution of all genotypes of COMT gene between the ADHD patients and the controls (P>0.05). CONCLUSION: It was suggested that for the Han Chinese children with ADHD in this study, there was no association between ADHD and Val158Met polymorphism of COMT gene.


Assuntos
Transtorno do Deficit de Atenção com Hiperatividade/genética , Catecol O-Metiltransferase/genética , Polimorfismo de Nucleotídeo Único , Adolescente , Transtorno do Deficit de Atenção com Hiperatividade/enzimologia , Criança , Éxons/genética , Feminino , Frequência do Gene , Predisposição Genética para Doença/genética , Humanos , Masculino , Reação em Cadeia da Polimerase , Polimorfismo de Fragmento de Restrição
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