产品资讯 > 大鼠表达谱芯片 Rat OneArrayR v2

 
  Rat microarray for gene expression   大鼠表达谱芯片为全新开发的表达谱芯片产品,与其它表达谱系列产品一样, 采用 “一个基因,一个探针” 的设计原理,以 IMPORT 专利技术针对蛋白质编码基因设计高专一性探针, 根据 RefSeq 65Ensembl 76 资料库进行探针的设计, 提供高基因覆盖率的表达谱芯片,以自主的高速布放技术进行芯片生产。
 
 
 
大鼠表达谱芯片 v2 探针内容
探针种类 探针数
  基因探针设计资料库: 20,715
          - RefSeq release 65
          - Ensembl release 76
  控制探针数 992
  总探针数 21,707


  基 因 探 针
 
大鼠表达谱芯片是参考国际公认之 RefSeq 及 Ensembl 序列资料库, 设计长链 60 个碱基寡核酸 (sense-strand) 的基因探针, 内容主要以蛋白质编码基因 (protein-coding gene) 为主, 提供高基因覆盖率并且每一个探针对其来源资料库的目标基因皆具高度专一性,避免非目标基因的杂交影响。

此外,华联专业团队建构 ”华联探针注解搜寻引擎”(PASS) 网站,方便使用者查询各探针相对应于 NCBIEnsembl 资料库的详细注解。
 
   
 

  控 制 探 针
 
 
为确保芯片数据品质,华联技术团队经过一连串的测试及验证,设计一系列的品质控制探针, 以监控完整的芯片实验步骤,包含样本 RNA 完整性、样本 RNA 放大流程、萤光标记效率、芯片杂交、芯片扫描等。
 
 

使用ROA文献 ( 7 )

 PLoS One. 2015, 10(5):e0127352. doi: 10.1371/journal.pone.0127352. eCollection 2015.
 S100A9: A Potential Biomarker for the Progression of Non-Alcoholic Fatty Liver Disease and the Diagnosis of Non-Alcoholic Steatohepatitis 
 Xiaolin Liu, Yongfeng Wang, Yanan Ming, Yanyan Song, Jingyi Zhang, Xiaoyu Chen, Minde Zeng, Yimin Mao
  Abstract
Non-alcoholic fatty liver (NAFL) has the potential to progress to non-alcoholic steatohepatitis (NASH) or to promote type 2 diabetes mellitus (T2DM). However, NASH and T2DM do not always develop coordinately. Additionally, there are no definite noninvasive methods for NASH diagnosis currently. We established rat models of NAFL, NASH, and NAFL + T2DM to recapitulate different phenotypes associated with non-alcoholic fatty liver disease (NAFLD) and its progression. Histologic features of rat livers were scored according to criteria established by the Nonalcoholic Steatohepatitis Clinical Research Network. Microarray was performed to assess gene expression changes in rat livers. We find that gene expression of s100a9 was higher in NAFL group compared with control, and was increased in NASH groups and decreased in NAFL + T2DM group compared with NAFL. In contrast, srebf1, tbx21, and gimap4 only showed limited discriminating abilities in different groups. There is a significant positive correlation between serum levels of S100A9 and NAFLD Activity Score (NAS), the severity of hepatic steatosis, and lobular inflammation (r = 0.80, 0.64 and 0.86, P < 0.001). These findings suggest that S100A9 may be extremely useful in the diagnosis of NASH (AUROC: 0.947, CI: 0.845-1.049). Additionally, serum S100A9 levels displayed a strong correlation with ALT, AST and TBil (r = 0.81, 0.89 and 0.91, P < 0.001) but a weak correlation with FBG, HOMA-IR, TG, and TC (r = -0.41, -0.40, 0.47 and 0.49, P < 0.05). CONCLUSIONS: The results we provide here suggest that S100A9 may be useful as a biomarker for the hepatic and metabolic progression of NAFLD and the non-invasive diagnosis of NASH.
   

 Transactions of Tianjin University. 2014, 20: 451-457. doi: 10.1007/s12209-014-2294-7.
 Transcriptomic Analysis of Aflatoxin B1-Regulated Genes in Rat Hepatic Epithelial Cells
 
 
 Liu Yang, Guanghui Li, Junwen Li, Zhaoli Chen, Jing Ji, Haiyong Wang
  Abstract
Aflatoxins are the most popular hepatotoxicants. Chronic exposure to aflatoxins leads to a wide variety of liver diseases, such as hepatocellular carcinoma. In this study, we analyzed the genome wide expression profiles of aflatoxin B1-induced rat hepatic epithelial cells. The expression of 325, 184 and 199 special genes was altered when exposed to 0.03, 0.1 and 0.2 μmol/L aflatoxin B1 respectively, and 239 genes were commonly expressed. After the functional analysis on these dose-special genes, we determined several key pathways related to hepatotoxicity, such as TGF-beta signaling pathway, tight junction, adherens junction, the regulation of actin cytoskeleton, ErbB signaling pathway, p53 signaling pathway, pathways in cancer and axon guidance. Common genes were mainly associated with focal adhesion, ECM-receptor interaction, and cell adhesion molecules. Gene ontology annotations showed a good concordance with these pathways. The quantitative real-time polymerase chain reaction(PCR) analysis of selected genes showed similar patterns in microarrays. The toxicogenomic study provides a better understanding of molecular mechanisms of aflatoxins.
   

 Journal of Ethnopharmacology. 2014 Jul 19. doi: 10.1016/j.jep.2014.07.022.
 Comparative pharmacokinetics of rhein in normal and loperamide-induced constipated rats and microarray analysis of drug-metabolizing genes
 
 
 Mei-Ling Hou, Li-WenChang, Chi-HungLin, Lie-ChwenLin, Tung-HuTsai
  Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Rhein is a pharmacological active component found in Rheum palmatum L. that is the major herb of the San-Huang-Xie-Xin-Tang (SHXXT), a medicinal herbal product used as a remedy for constipation. Here we have investigated the comparativepharmacokinetics of rhein in normal and constipated rats. Microarray analysis was used to explore whether drug-metabolizing genes will be altered after SHXXT treatment. MATERIALS AND METHODS: The comparative pharmacokinetics of rhein in normal and loperamide-induced constipated rats was studied by liquid chromatography with electrospray ionization tandem mass spectrometry (LC-MS/MS). Gene expression profiling in drug-metabolizing genes after SHXXT treatment was investigated by microarray analysis and real-time polymerase chain reaction (RT-PCR). Results: A validated LC-MS/MS method was applied to investigate the comparative pharmacokinetics of rhein in normal and loperamind-induced constipated rats. The pharmacokinetic results demonstrate that the loperamind-induced constipation reduced the absorption of rhein. Cmax significant reduced by 2.5-fold, the AUC decreased by 27.8%; however, the elimination half-life (t1/2) was prolonged by 1.6-fold. Tmax and mean residence time (MRT) were significantly prolonged by 2.8-fold, and 1.7-fold, respectively. The volume of distribution (Vss) increased by 2.2-fold. The data of microarray analysis on gene expression indicate that five drug-metabolizing genes, including Cyp7a1, Cyp2c6, Ces2e, Atp1b1, and Slc7a2 were significantly altered by the SHXXT (0.5 g/kg) treatment. Conclusion: The loperamide-induced constipation reduced the absorption of rhein. Since among the 25,338 genes analyzed, there were five genessignificantly altered by SHXXT treatment. Thus, information on minor drug-metabolizing genes altered by SHXXT treatment indicates that SHXXT is relatively safe for clinical application.
   

 Journal of Neurosurgery Spine. 2014 Jul 25.
 Nerve growth factor promotes expression of novel genes in intervertebral disc cells that regulate tissue degradation
 
 
 Ting-Hsien Kao, Yi-Jen Peng, Hsi-Kai Tsou, Donald M. Salter, Herng-Sheng Lee
  Abstract
Object: Increased neurotrophin activity in degenerative intervertebral discs (IVDs) is one potential cause of chronic low-back pain (LBP). The aim of the study was to assess if nerve growth factor (NGF) might alter gene expression of IVD cells and contribute to disc degeneration by enhancingexpression or activity of factors that cause breakdown of IVD matrix. Methods: Rat-tail IVD cells were stimulated by NGF and subjected to microarray analysis. Real-time polymerase chain reaction, Western blotting, and immunocytochemistry of rat and human IVD cells and tissues treated with NGF in vitro in the absence or presence of the NGF inhibitor Ro 08-2750 were used to confirm findings of the microarray studies. Phosphorylation of mitogen-activated protein kinase (MAPK) was used to identify cell signaling pathways involved in NGF stimulation in the absence or presence of Ro 08-2750. Results: Microarray analysis demonstrated increased expression of chitinase 3-like 1 (Chi3l1), lipocalin 2 (Lcn2), and matrix metalloproteinase-3 (Mmp3) following NGF stimulation of rat IVD cells in vitro. Increased gene expression was confirmed by real-time polymerase chain reaction with a relative increase in the Mmp/Timp ratio. Increased expression of Chi3l1, Lcn2, and Mmp3 following NGF stimulation was also demonstrated in rat cells and human tissue in vitro. Effects of NGF on protein expression were blocked by an NGF inhibitor and appear to function through the extracellular-regulation kinase 1/2 (ERK1/2) MAPK pathway. Conclusions Nerve growth factor has potential effects on matrix turnover activity and influences the catabolic/anabolic balance of IVD cells in an adverse way that may potentiate IVD degeneration. Anti-NGF treatment might be beneficial to ameliorate progressive tissue breakdown in IVD degeneration and may lead to pain relief.
   

 Journal of Pharmaceutical and Biomedical Analysis. 2014, 96C:231-240. doi: 10.1016/j.jpba.2014.04.001.
 Development of a microdialysis system to monitor lamivudine in blood and liver for the pharmacokinetic application in herbal drug interaction and the gene expression in rats
 
 
 Chia-Ming Lu, Mei-Ling Hou, Lie-Chwen Lin, Tung-Hu Tsai
  Abstract
The aim of study is to develop a novel multiple microdialysis technique coupled to a validated chromatographic system for the measurement of protein-unbound form lamivudine and investigation of its herb-drug interaction in rat blood and liver. Furthermore, gene expression changes of drugmetabolizing enzymes in rat were evaluated by microarray analysis after being treated with a traditional Chinese herbal formulation, Long-Dan-Xie-Gan-Tang (LDXGT). The analyte was separated by a reverse-phase C18 column using the mobile phase comprising methanol and 10mM KH2PO4(15:85, v/v, adjusted to pH 6.0 with NaOH) with the flow rate of 0.8mL/min, and the UV wavelength was set at 270nm. The processes of method validation followed Food and Drug Administration (FDA) guidelines. The pharmacokinetic data demonstrated that the area under the concentration-time curve (AUC) of the lamivudine alone and the LDXGT pretreated group were 532±37.6 and 550±44.2minμg/mL in rat blood after lamivudineadministration (10mg/kg, i.v.) and 682±196 and 642±153minμg/mL in rat liver, respectively. The herb-drug pharmacokinetic interaction showed that with either lamivudine alone or in combination with pretreated with LDXGT, the pharmacokinetic parameters were not significantly changed except the apparent volume of distribution (Vd) at a high dose of lamivudine (30mg/kg). In addition, microarray analysis showed that among 70 altered genes (selection criteria: |Fold change|≧2 and p<0.05), only 11 genes were involved in drug metabolism and indicated that a relatively small portion of drugmetabolizing genes in liver were altered at the genome level after the therapeutic dose of LDXGT treatment. In conclusion, these studies provide constructive information to interpret the herb-drug interactions between lamivudine and a popular Chinese herbal formulation.
   

 Inflammation Research. 2012, 61(12):1395-404. doi: 10.1007/s00011-012-0542-7.
 Mammalian target of rapamycin complex 2 regulates inflammatory response to stress
 
 
 Desmond Mascarenhas, Sheri Routt, Baljit K. Singh
  Abstract
To explore the role of mammalian target of rapamycin 2 (mTORC2) in the activation of inflammatory and oxidative responses in rodent models of acute injury and metabolic stress. The impact of nephrilin, an inhibitor of mTORC2 complex, was assessed in three CD-1 mouse models of acute xenobiotic stress and in a hypertensive Dahl rat model of metabolic stress. Animals received daily subcutaneous bolus injections of saline or 4 mg/kg nephrilin. Tissues were assayed by ELISA, gene arrays and immunohistochemical staining.Nephrilin significantly inhibited elevations in plasma tumor necrosis factor-alpha, kidney substance P, and CX3CR1, and urinary lipocalin-2 [urinary neutrophil gelatinase-associated lipocalin (uNGAL)] in models of acute xenobiotic stress. UCHL1 gene expression levels dropped and plasma HMGB1 levels rose in the rhabdomyolysis model. Both effects were reversed by nephrilin. The inhibitor also blocked diet-induced elevations of uNGAL and albumin-creatinine ratio (UACR) as well as kidney tissue phosphorylation of PKC-beta-2-T641 and p66shc-S36, and reduced dark ring-like staining of nuclei by anti-phos-p66shc-S36 antibody in frozen sections of diseased kidneys from hypertensive Dahl rats fed an 8 % NaCl diet for 4 weeks. Taken together, our results suggest a role for mTORC2 in the inflammatory-oxidative responses to stress.
   

 Hum Gene Ther. 2012, 23(3):255-61. doi: 10.1089/hum.2011.094.
 Improved Function of the Failing Rat Heart by Regulated Expression of Insulin-like Growth Factor-I via Intramuscular Gene Transfer
 
 
 N. Chin Lai, Tong Tang, Mei Hua Gao, Miho Sato, Atsushi Miyanohara, H. Kirk Hammond
  Abstract
Current methods of gene transfer for heart disease include injection into heart muscle or intracoronary coronary delivery, approaches that typically provide limited expression and are cumbersome to apply. To circumvent these problems, we selected a transgene, insulin-like growth factor-I (IGF-I), which may, in theory, have favorable effects on heart function when secreted from a remote site. We examined the feasibility and efficacy of skeletal muscle injection of adeno-associated virus 5 encoding IGF-I under Tet regulation (AAV5.IGFI-tet) to treat heart failure. Myocardial infarction (MI) was induced in rats by coronary occlusion; 1 week later, rats with impaired left ventricular (LV) function received 2×10(12) genome copies (GC) of AAV5.IGFI-tet in the anterior tibialis muscle, and 4 weeks later, were randomly assigned to receive doxycycline in drinking water to activate IGF-I expression (IGF-On; n=10), or not to receive doxycycline (IGF-Off; n=10). Ten weeks after MI (5 weeks after activation of IGF-I expression), LV size and function were assessed by echocardiography and physiological studies. IGF-On rats showed reduced LV end-systolic dimension (p=0.03) and increased LV ejection fraction (p=0.02). In addition, IGF-On rats showed, before and during dobutamine infusion, increases in cardiac output (p=0.02), stroke work (p=0.0001), LV + dP/dt (p<0.0001), LV relaxation (LV - dP/dt; p=0.03), and systolic arterial blood pressure (p=0.0003). Mean arterial pressure and systemic vascular resistance were unchanged. Activation of IGF-I expression reduced cardiac fibrosis (p=0.048), apoptosis (p<0.0001), and caspase-3/7 activity (p=0.04). Serum IGF-I was increased 5 weeks after transgene activation (p=0.008). These data indicate that skeletal muscle injection of AAV5.IGFI-tet enables tetracycline-activated expression, increases serum IGF-I levels, and improves function of the failing heart.