華聯產品: Mouse OneArray
Clinical manifestation and molecular genetic characterization of MYH9 disorders.
Platelets 2009, 20(5):289-96. doi: 10.1080/09537100902993022
Currently, the May-Hegglin anomaly (MHA), Sebastian (SBS), Fechtner (FTNS) and Epstein (EPS) syndrome are considered to be distinct clinical manifestations of a single disease caused by mutations of the MYH9 gene encoding the heavy chain of non-muscle myosin IIA (NMMHC-IIA). Manifestations of these disorders include giant platelets, thrombocytopenia and combinations of the presence of granulocyte inclusions, deafness, cataracts and renal failure. We examined 15 patients from 10 unrelated families on whom we performed immunostaining of NMMHC-IIA in blood samples. Polymerase chain reaction (PCR) analysis of selected exons of the MYH9 gene revealed mutations in nine samples with one novel mutation. Results of fluorescence and mutational analysis were compared with clinical manifestations of the MYH9 disorder. We also determined the number of glycoprotein sites on the surface of platelets. Most patients had an increased number of glycoproteins, which could be due to platelet size.
華聯產品: Mouse OneArray
Identification of differentially expressed genes in myocardium of patients with heart failure by human whole genomic oligonucleotide microarray-assisted pathways analysis.
Zhonghua Xin Xue Guan Bing Za Zhi 2009, 37(2):120-125
To identify the differentially expressed gene profiles in myocardium of patients with heart failure using human whole genomic oligonucleotide microarray-assisted pathway analysis. Phalanx whole genomic oligonucleotide microarrays were used to detect the gene expression profiles of myocardium in four patients died of heart failure and 4 brain died patients without heart diseases. The microarray findings were confirmed by real-time quantitative reverse transcriptase-polymerase chain reaction. The genes with a threshold of 1.2 times fold-change were selected and BioCarta Pathway and KEGG (Kyoto Encyclopaedia of Genes and Genomes) pathway databases were used to identify functionallyrelated gene pathways. A total of 2806 genes with differentially expression were detected between the failing and non-failing heart samples,expression changes of 399 genes were more than 2-folds. Eleven pathways were identified by BioCarta pathway database and sixteen pathways were identified by KEGG PATHWAY Database. Genomic microarray-assisted pathway analysis could help to identify gene expression profiles in failing heart.
華聯產品: Mouse OneArray
Effect of hydroxyurea on the promoter occupancy profiles of tumor suppressor p53 and p73.
BMC Biology 2009, 7:35. doi: 10.1186/1741-7007-7-35
The p53 tumor suppressor and its related protein, p73, share a homologous DNA binding domain, and mouse genetics studies have suggested that they have overlapping as well as distinct biological functions. Both p53 and p73 are activated by genotoxic stress to regulate an array of cellular responses. Previous studies have suggested that p53 and p73 independently activate the cellular apoptotic program in response to cytotoxic drugs. The goal of this study was to compare the promoter-binding activity of p53 and p73 at steady state and after genotoxic stress induced by hydroxyurea.We employed chromatin immunoprecipitation, the NimbleGen promoter arrays and a model-based algorithm for promoter arrays to identify promoter sequences enriched in anti-p53 or anti-p73 immunoprecipitates, either before or after treatment with hydroxyurea, which increased the expression of both p53 and p73 in the human colon cancer cell line HCT116-3(6). We calculated a model-based algorithm for promoter array score for each promoter and found a significant correlation between the promoter occupancy profiles of p53 and p73. We also found that after hydroxyurea treatment, the p53-bound promoters were still bound by p73, but p73 became associated with additional promoters that that did not bind p53. In particular, we showed that hydroxyurea induces the binding of p73 but not p53 to the promoter of MLH3, which encodes a mismatch repair protein, and causes an up-regulation of the MLH3 mRNA.These results suggest that hydroxyurea exerts differential effects on the promoter-binding functions of p53 and p73 and illustrate the power of model-based algorithm for promoter array in the analyses of promoter occupancy profiles of highly homologous transcription factors.
華聯產品: Human OneArray
Gene expression profiling in male B6C3F1 mouse livers exposed to kava identifies ?V Changes in drug metabolizing genes and potential mechanisms linked to kava toxicity.
FOOD CHEM TOXICOL 2010, 48(2):686-96. doi: 10.1016/j.fct.2009.11.050
The association of kava products with liver-related health risks has prompted regulatory action in many countries. We used a genome-wide gene expression approach to generate global gene expression profiles from the livers of male B6C3F1 mice administered kava extract by gavage for 14 weeks, and identified the differentially expressed drug metabolizing genes in response to kava treatments. Analyses of gene functions and pathways reveal that the levels of significant numbers of genes involving drug metabolism were changed and that the pathways involving xenobiotics metabolism, Nrf2-mediated oxidative stress response, mitochondrial functions and others, were altered. Our results indicate that kava extract can significantly modulate drug metabolizing enzymes, potentially leading to herb-drug interactions and hepatotoxicity.